Alzheimer's Disease (AD) remains a significant global health challenge, characterized by progressive neurodegeneration and a decline in cognitive abilities such as memory and learning. Despite being the main cause of dementia worldwide, the precise mechanisms that underlie neuronal dysfunction and synaptic plasticity impairment in AD remain elusive. However, while genetic mutations, dietary factors, and immune dysregulation are implicated in AD pathogenesis, the current therapeutic approaches are largely centered around acetylcholinesterase inhibitors (AChEIs). Nevertheless, this cholinergic hypothesis of AD is no longer satisfactory in describing this disease and has demonstrated a limited efficacy. Hence, new treatment approaches should be developed, and that requires us to view AD from a new perspective. Herein, in our review, we present the latest studies that discussed possible AD pathologies and pharmacotherapies. Additionally, we highlight that the emerging treatments that precisely targets brain regions associated with enhancing neuroplasticity have delivered promising results and seem to be more effective than older treatments. Finally, by viewing AD as a complex interplay of various factors that ultimately cause synaptic dysfunction and cognitive decline, we can develop more effective therapeutic interventions and ultimately alleviate the significant burden of this debilitating disease for both patients and their families.
Citation: Nour Kenaan, Zuheir Alshehabi. A review on recent advances in Alzheimer's disease: The role of synaptic plasticity[J]. AIMS Neuroscience, 2025, 12(2): 75-94. doi: 10.3934/Neuroscience.2025006
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Alzheimer's Disease (AD) remains a significant global health challenge, characterized by progressive neurodegeneration and a decline in cognitive abilities such as memory and learning. Despite being the main cause of dementia worldwide, the precise mechanisms that underlie neuronal dysfunction and synaptic plasticity impairment in AD remain elusive. However, while genetic mutations, dietary factors, and immune dysregulation are implicated in AD pathogenesis, the current therapeutic approaches are largely centered around acetylcholinesterase inhibitors (AChEIs). Nevertheless, this cholinergic hypothesis of AD is no longer satisfactory in describing this disease and has demonstrated a limited efficacy. Hence, new treatment approaches should be developed, and that requires us to view AD from a new perspective. Herein, in our review, we present the latest studies that discussed possible AD pathologies and pharmacotherapies. Additionally, we highlight that the emerging treatments that precisely targets brain regions associated with enhancing neuroplasticity have delivered promising results and seem to be more effective than older treatments. Finally, by viewing AD as a complex interplay of various factors that ultimately cause synaptic dysfunction and cognitive decline, we can develop more effective therapeutic interventions and ultimately alleviate the significant burden of this debilitating disease for both patients and their families.
Alzheimer's Disease;
Acetylcholinesterase Inhibitors;
Amyloid Precursor Protein;
Presenilin 1;
Presenilin 2;
Early-Onset Alzheimer's Disease;
Late-Onset Alzheimer's Disease;
Gut Microbiome;
Centeral Nervous System;
Amyloid Precursor Protein;
Neurodegenerative Disorders;
Clonal Hematopoiesis Of Indeterminate Potential;
Blood-Brain Barrier;
Amyloid-Β;
Asparagine Endopeptidase;
Genome-Wide Association Studies;
Hormone Replacement Therapy;
Women's Health Initiative 173 Memory Study;
Mild Cognitive Impairment;
Cognitively Normal Older Adults;
Transcranial Magnetic Stimulation;
Severe Impairment Battery Measurement;
Neuropsychiatric 257 Inventory Measurement;
Alzheimer's Disease Cooperative Study-Activities Of Daily Living Scale;
The Mammalian Sterile 20-Like Kinase 1/2;
N-Methyl-D-295 Aspartate Receptor;
L-Type Voltage-Gated Calcium Ion Channels;
Ryanodine Receptors;
Store-Operated Calcium Entry;
Cholecystokinin;
Alpha7 Nicotinic Acetylcholine Receptor;
Cordycepin Treatment;
Mammalian Target Of Rapamycin;
Camp-Response Element-Binding Protein 342;
Gene Ontology And;
Protein-Protein Interactions;
Long-Term Potentiation;
Post-Synaptic Density Protein 95;
Synaptophysin;
Strong 395 Tetanization Protocol;
Weak Tetanization Protocol;
Plasticity-Related Products;
Familial Alzheimer's Disease;
Dihydroartemisinin–Piperaquine
Cluster algebras were introduced by Fomin and Zelevinsky in [1]. The core idea to define cluster algebra of rank n is that one should have a cluster seed and an operator on cluster seeds, called mutation. Roughly, a cluster seed Σt0 is a collection of variables x1;t0,⋯,xn;t0 (cluster variables) and binomials F1;t0,⋯,Fn;t0 (exchange polynomials). One can apply mutation to a cluster seed to produce a new seed, i.e., new variables and new binomials. Note that the exchange polynomial in cluster algebra is always a binomial. One of the main results in cluster algebras is that they have the Laurent phenomenon [1].
In the theory of cluster algebras, the following are interesting conjectures on seeds of cluster algebras: in a cluster algebra of rank n, (1) each seed is uniquely defined by its cluster; (2) any two seeds with n−1 common cluster variables are connected with each other by one step of mutation. One can refer to [2,3] for detailed proof.
Significant notations of the upper cluster algebra, upper bound and lower bound associated with the cluster seed were introduced by Berenstein, Fomin and Zelevinsky to study the structure of cluster algebras in [4]. There are some theorems of upper bounds and lower bounds: (a) under the condition of coprimeness, the upper bound is invariant under seed mutations; (b) the standard monomials in x1,x′1,…,xn,x′n are linearly independent over ZP if and only if the cluster seed is acyclic; (c) under the conditions of acyclicity and coprimeness, then the upper bound coincides with the lower bound.
Muller showed that locally acyclic cluster algebras coincide with their upper cluster algebras in [5]. Gekhtman, Shapiro and Vainshte in [3] proved (a) for generalized cluster algebras, then Bai, Chen, Ding and Xu demonstrated (c) and the sufficiency of (b) in [6]. Besides, Bai discovered that acyclic generalized cluster algebras coincide with their generalized upper cluster algebras.
Laurent phenomenon (LP) algebras were introduced by Lam and Pylyavskyy in [7], which generalize cluster algebras from the perspective of exchange relations. The exchange polynomials in LP algebras were allowed to have arbitrarily many monomials, rather than being just binomials. It turns out that the Laurent phenomenon also appears in LP algebras [7].
One should note that our method also works for cluster algebras and generalized cluster algebras. We do not talk much about generalized cluster algebras in this paper, and one can refer to [2,6,8,9,10] for details.
In this paper, we first affirm the conjectures on seeds of cluster algebras with respect to LP algebras.
Theorem 1.1. In a LP algebra of rank n,
1) (Theorem 3.1) each LP seed is uniquely defined by its cluster.
2) (Theorem 3.7) any two LP seeds with n−1 common cluster variables are connected with each other by one step of mutation.
Second, we affirm theorems of upper bounds and lower bounds with respect to LP algebras under some conditions, by using the similar methods developed in [4].
Condition 1.2. Let Mk be the lexicographically first monomial in the irreducible polynomial Fk and fk(xi) be the polynomial on xi in R[x2,…,ˆxi,…,ˆxk,…,xn](xi) without constant terms in Fk for any i≠k. Assume that for a LP seed (x,F) of rank n, ∀k∈[1,n], Fk satisfies the following conditions:
(i) ˆFk=Fk.
(ii) Mk is of the form xvk={xvk+1,kk+1⋯xvn,knk∈[1,n−1]1k=n, where vk∈Zn−k≥0 for k∈[1,n−1].
(iii) when x1∈Fk for k≠1, Fk=Mk+fk(x1).
(iv) when x1∉Fk for k≠1 or 2, if there exist an index i in [2,k−1] such that xk∈Mi, then Fk=Mk+fk(xi).
Theorem 1.3. (a) (Theorem 4.9) Under (i) of Condition 1.2, the upper bound is invariant under LP mutations.
(b) (Theorem 4.16) Under (i) and (ii) of Condition 1.2, the standard monomials in x1,x′1,…,xn,x′n form an R-basis for L(Σ).
(c) (Theorem 4.9) Under Condition 1.2, the upper bound coincides with the lower bound.
This paper is organized as follows: In Section 2, some basic definitions are given. In Section 3, we prove Theorem 1.1, and we give the corresponding results and applications in cluster algebras. In Section 4, we affirm Theorem 1.3.
Let a,b be positive integers satisfying a≤b, write [a,b] for {a,a+1,…,b}.
Let R be a unique factorization domain over Z, and the ambient field F be the rational function field in n independent variables over the field of fractions Frac(R). Recall that an element f of R is irreducible if it is non-zero, not a unit, and not be expressed as the product f=gh of two elements g,h∈R which are non-units.
Definition 2.1. A Laurent phenomenon (LP) seed of rank n in F is a pair (x,F), in which
(i) x={x1⋯,xn} is a transcendence basis for F over Frac(R), where x is called the cluster of (x,F) and x1⋯,xn are called cluster variables.
(ii) F={F1,⋯,Fn} is a collection of irreducible polynomials in R[x1,⋯,xn] such that for each i,j∈[1,n], xj∤Fi (Fi is not divisible by xj) and Fi does not depend on xi, where F1,⋯,Fn are called the exchange polynomials of (x,F).
The following notations, definitions and propositions can refer to [7,11].
Let F,N be two rational functions in x1,⋯,xn. Denote by F|xj←N the expression obtained by substituting xj in F by N. And if F involves the variable xi, then we write xi∈F. Otherwise, we write xi∉F.
Definition 2.2. Let (x,F) be a LP seed in F. For each Fj∈F, define a Laurent polynomial ˆFj=Fjxa11⋯xaj−1j−1xaj+1j+1⋯xann, where ak∈Z≥0 is maximal such that Fakk divides Fj|xk←Fk/x′k as an element in R[x1,⋯,xk−1,(x′k)−1,xk+1,⋯,xn]. The Laurent polynomials in ˆF:={ˆF1,⋯,ˆFn} are called the exchange Laurent polynomials.
From the definition of exchange Laurent polynomials, we know that Fj/ˆFj is a monomial in R[x1,⋯,ˆxj,⋯,xn], where ˆxj means xj vanishes in the {x1,⋯,xn}. And ˆFj|xk←Fk/x′k is not divisible by Fk.
Proposition 2.3. (Lemma 2.4 of [7])Let (x,F) be a LP seed in F, then F={F1,⋯,Fn} and ˆF={ˆF1,⋯,ˆFn} determine each other uniquely.
Proposition 2.4. (Lemma 2.7 of [7])If xk∈Fi, then xi∉Fk/ˆFk. In particular, xk∈Fi implies that ˆFk|xi←0 is well defined and ˆFk|xi←0∈R[x±11,⋯,ˆxi,⋯,ˆxk,⋯,x±1n].
Definition 2.5. Let (x,F) be a LP seed in F and k∈[1,n]. Define a new pair
({x′1,⋯,x′n},{F′1,⋯,F′n}):=μk(x,F), |
where x′k=ˆFk/xk and x′i=xi for i≠k. And the exchange polynomials change as follows:
(1) F′k:=Fk;
(2) If xk∉Fi, then F′i:=riFi, where ri is a unit in R;
(3) If xk∈Fi, then F′i is obtained from the following three steps:
(i) Define Gi:=Fi|xk←Nk, where Nk=ˆFk|xi←0x′k. Then we have
Gi∈R[x±11,⋯,ˆxi,⋯,x′k−1,⋯,x±1n]=R[x′1±1,⋯,^x′i,⋯,x′k−1,⋯,x′n±1]. |
(ii) Define Hi to be Gi with all common factors (in R[x1,⋯,ˆxi,⋯,ˆxk,⋯,xn]) removed. Note that Hi is unique up to a unit in R and Hi∈R[x′1±1,⋯,^x′i,⋯,x′k−1,⋯,x′n±1].
(iii) Let M be a Laurent monomial in x′1,⋯,^x′i,⋯,x′n with coefficient a unit in R such that F′i:=MHi∈R[x′1,⋯,x′n] and is not divisible by any variable in {x′1,⋯,x′n}. Thus
F′i∈R[x′1,⋯,^x′i,⋯,x′k,⋯,x′n]. |
Then we say that the new pair μk(x,F) is obtained from the LP seed (x,F) by the LP mutation in direction k.
Example 2.6. Let R=Z and F=Q(a,b,c). Consider the LP seed (x,F), where x={a,b,c} and F={b+1, a+c, b+1}. From the definition of exchange Laurent polynomials, we can get ˆFa=Fac,ˆFb=Fb,ˆFc=Fca.
Let (x′,F′)=μa(x,F), then we have a′=^Faa=b+1ac, b′=b, c′=c. From the definition of the LP mutation, the exchange polynomial Fa does not change. Since a∉Fc, we have F′c=b+1 (or up to a unit). Since Fb depends on a, to compute F′b, we need to procedure the above three steps. By (i), we get Na=1a′c and Gb=1a′c+c. By (ii), we get Hb=Gb up to a unit in R. By (iii), M=a′c and F′b=MHb=a′c2+1. Thus the new seed can be chosen to be
(x′,F′)={(a′,b+1),(b,a′c2+1),(c,b+1)}. |
It is not clear a priori that the LP mutation μk(x,F) of a LP seed (x,F) is still a LP seed because of the irreducibility requirement for the new exchange polynomials. But it can be seen from the following proposition that μk(x,F) is still a LP seed in F.
Proposition 2.7. (Proposition 2.15 of [7])Let (x,F) be a LP seed in F, then μk(x,F) is also a LP seed in F.
Proposition 2.8. (Proposition 2.16 of [7])If (x′,F′) is obtained from (x,F) by LP mutation at k, then (x,F) can be obtained from (x′,F′) by LP mutation at k. In this sense, LP mutation is an involution.
Remark 2.9. It is important to note that because of (ii), F′i is defined up to a unit in R. And this is the motivation to consider LP seeds up to an equivalence relation.
Definition 2.10. Let Σt1=(xt1,Ft1) and Σt2=(xt2,Ft2) be two LP seeds in F. Σt1 and Σt2 are equivalent if for each i∈[1,n], there exist ri,r′i which are units in R such that xi;t2=rixi;t1 and Fi;t2=r′iFi;t1.
Denote by [Σt] the equivalent class of Σt, that is, [Σt] is the set of LP seeds which are equivalent to Σt.
Proposition 2.11. (Lemma 3.1 of [7])Let Σt1=(xt1,Ft1) and Σt2=(xt2,Ft2) be two LP seeds in F, and Σtu=μk(Σt2), Σtv=μk(Σt1).If [Σt1]=[Σt2], then [Σtv]=[Σtu].
Let Σt=(xt,Ft) be a LP seed in F. By the above proposition, it is reasonable to define LP mutation of [Σt] at k given by μk([Σt]):=[μk(Σt)].
Definition 2.12. A Laurent phenomenon (LP) pattern S in F is an assignment of each LP seed (xt,Ft) to a vertex t of the n-regular tree Tn, such that for any edge tk_t′,(xt′,Ft′)=μk(xt,Ft).
We always denote by xt={x1;t,⋯,xn;t} and Ft={F1;t,⋯,Fn;t}.
Definition 2.13. Let S be a LP pattern, the Laurent phenomenon (LP) algebra A(S) (of rank n) associated with S is the R-subalgebra of F generated by all the cluster variables in the seeds of S.
If Σ=(x,F) is any seed in F, we shall write A(Σ) to mean the LP algebra A(S) associated with S containing the seed Σ.
Theorem 2.14. (Theorem 5.1 of [7], the Laurent phenomenon) Let A(S) be a LP algebra, and (xt0,Ft0) be a LP seed of A(S). Then any cluster variable xi;t of A(S) is in the Laurent polynomial ring R(t±10):=R[x±11;t0,⋯,x±1n;t0].
Definition 2.15. Let Σ=(x,F) be a LP seed of rank n and k∈[1,n]. A new seed Σ∗=(x∗,F∗) of rank n−1 is defined as follows:
1) let R∗=R[x±1k].
2)x∗=x−{xk}.
3)let F∗={F∗j=Fjxak | j∈[1,n]−k, a is the power of xk in ˆFj/Fj}.
The seed Σ∗ is in fact a LP seed, then Σ∗ is called the freezing of the LP seed Σ at xk. A(Σ∗)⊂F=Frac(R∗[x1,…,^xk,…,xn]) is defined to be the subalgebra generated by all the cluster variables from LP seeds mutation-equivalent to Σ∗. Then A(Σ∗) is called the freezing of the LP algebra A(Σ) at xk.
Example 2.16. Consider the LP seed Σ=(x,F)={(a,b+1),(b,a+c),(c,b+1)} over R=Z from Example 2.6. We produce the freezing of (x,F) at c as follows: first, remove (c,b+1); next, since the powers of c in ^Fa and ^Fb are -1 and 0 respectively, we have F∗a=Fac−1=b+1c and F∗b=Fb. Then the LP seed Σ∗ are {(a,b+1c),(b,a+c)} over Z[c±1].
Proposition 2.17. (Proposition 3.7 of [7])The algebra A(Σ∗) is a LP algebra.
Corollary 2.18. The freezing of the LP seed at xi is compatible with the mutation in direction j for j≠i.
Recall that an integer matrix Bn×n=(bij) is called skew-symmetrizable if there is a positive integer diagonal matrix D such that DB is skew-symmetric, where D is said to be the skew-symmetrizer of B. Bn×n=(bij) is sign-skew-symmetric if bijbji<0 or bij=bji=0 for any i,j∈[1,n]. A sign-skew-symmetric B is totally sign-skew-symmetric if any matrix B′ obtained from B by a sequence of mutations is sign-skew-symmetric. It is known that skew-symmetrizable integer matrices are always totally sign-skew-symmetric.
The diagram for a sign-skew-symmetric matrix Bn×n is the directed graph Γ(B) with the vertices 1,2,⋯,n and the directed edges from i to j if bij>0. Bn×n is called acyclic if Γ(B) has no oriented cycles. As shown in [12], an acyclic sign-skew-symmetric integer matrix B is always totally sign-skew-symmetric.
Let P be the coefficient group, its group ring ZP is a domain [1]. We take an ambient field F to be the field of rational functions in n independent variables with coefficients in ZP.
Definition 2.19. A cluster seed in F is a triplet Σ=(x,y,B) such that
(i) x={x1,⋯,xn} is a transcendence basis for F over Frac(ZP). x is called the cluster of (x,y,B) and {x1⋯,xn} are called cluster variables.
(ii) y={y1,⋯,yn} is a subset of P, where {y1,⋯,yn} are called coefficients.
(iii) B=(bij) is a n×n totally sign-skew-symmetric matrix, called an exchange matrix.
Let (x,y,B) be a cluster seed in F, one can associate binomials {F1,⋯,Fn} defined by
Fj=yj1⊕yj∏bij>0xbiji+yj1⊕yj∏bij<0x−biji. |
{F1,⋯,Fn} are called the exchange polynomials of (x,y,B).
Note that the coefficients and the exchange matrices in a cluster algebra are used for providing the exchange polynomials and explaining how to produce new exchange polynomials when doing a mutation (see Definition 2.20) on a cluster seed.
Definition 2.20. Let Σ=(x,y,B) be a cluster seed in F. Define the mutation of Σ in the direction k∈[1,n] as a new triple Σ′=(x′,y′,B′):=μk(Σ) in F, where
x′i={Fk/xki=kxii≠k.,y′i={y−1ki=kyiymax(bki,0)k(1⨁yk)−bkii≠k., |
and b′ij={−biji=k or j=kbij+sgn(bik)max(bikbkj,0)otherwise. |
It can be seen that μk(Σ) is also a cluster seed and the mutation of a cluster seed is an involution, that is, μk(μk(Σ))=Σ.
Definition 2.21. A cluster pattern S is an assignment of a seed Σt=(xt,yt,Bt) to every vertex t of the n-regular tree Tn, such that for any edge tk_t′,Σ′t′=(xt′,yt′,Bt′)=μk(Σt).
We always denote by xt=(x1;t,⋯,xn;t),yt=(y1;t,⋯,yn;t),Bt=(btij).
Definition 2.22. Let S be a cluster pattern, the cluster algebra A(S) (of rank n) associated with the given cluster pattern S is the ZP-subalgebra of the field F generated by all cluster variables of S.
Theorem 2.23. (Theorem 3.1 of [1], the Laurent phenomenon)Let A(S) be a cluster algebra, and Σt0=(xt0,yt0,Bt0) be a cluster seed of A(S). Then any cluster variable xi;t of A(S) is in the Laurent polynomial ring ZP(t±10):=ZP[x±11;t0,⋯,x±1n;t0].
Example 2.24. Let B=(03−30), then the exchange polynomials of the cluster seed (x,B) are the following two polynomials
F1=x32+1=(x2+1)(x22−x2+1), |
F2=x31+1=(x1+1)(x21−x1+1). |
It is easy to see that the exchange polynomials F1,F2 of (x,B) are both reducible in the above example. Thus the cluster x and the exchange polynomial F of (x,B) can not define a LP seed. From [7], we know that sometimes a cluster algebra defines a LP algebra indeed.
Theorem 2.25. (Theorem 4.5 of [7]) Every cluster algebra with principal coefficients is a Laurent phenomenon algebra.
Theorem 3.1. Let A(S) be a LP algebra of rank n, and (xt1,Ft1),(xt2,Ft2) be two LP seeds of A(S).
1) If there exists a permutation σ of [1,n] and a unit ri∈R such that xi;t2=rixσ(i);t1 for i∈[1,n], then Fi;t2=r′iFσ(i);t1 as polynomials for a certain unit r′i in R.
2) each LP seed is uniquely defined by its cluster.
Proof. For any fixed k∈[1,n], let (xu,Fu)=μk(xt2,Ft2) and (xv,Fv)=μσ(k)(xt1,Ft1), we consider the Laurent expansion of xk;u with respect to xv and the Laurent expansion of xσ(k);v with respect to xu.
From the definition of the LP mutation, we know
xi;u={xi;t2if i≠kˆFk;t2xk;t2if i=k and xi;v={xi;t1if i≠σ(k)ˆFσ(k);t1xσ(k);t1if i=σ(k). | (3.1) |
Since xi;t2=rixσ(i);t1 for i∈[1,n], we have xi;u=rixσ(i);v for i≠k. By (3.1), we get
xk;u=ˆFk;t2(x1;t2,⋯,ˆxk;t2,⋯,xn;t2)/xk;t2=ˆFk;t2(r1xσ(1);t1,⋯,ˆxσ(k);t1,⋯,rnxσ(n);t1)/(rkxσ(k);t1)=ˆFk;t2(r1xσ(1);v,⋯,ˆxσ(k);v,⋯,rnxσ(n);v)/(rkxσ(k);t1);xσ(k);v=ˆFσ(k);t1(x1;t1,⋯,ˆxσ(k);t1,⋯,xn;t1)/xσ(k);t1=ˆFσ(k);t1(x1;v,⋯,ˆxσ(k);v,⋯,xn;v)/xσ(k);t1. |
Thus xk;uxσ(k);v=ˆFk;t2(r1xσ(1);v,⋯,ˆxσ(k);v,⋯,rnxσ(n);v)rkˆFσ(k);t1(x1;v,⋯,ˆxσ(k);v,⋯,xn;v) and we get that
xk;u=xσ(k);vˆFk;t2(r1xσ(1);v,⋯,ˆxσ(k);v,⋯,rnxσ(n);v)rkˆFσ(k);t1(x1;v,⋯,ˆxσ(k);v,⋯,xn;v). | (3.2) |
From the definition of the exchange Laurent polynomial, we know the above equation has the form of
xk;u=xσ(k);vFk;t2(r1xσ(1);v,⋯,ˆxσ(k);v,⋯,rnxσ(n);v)rkFσ(k);t1(x1;v,⋯,ˆxσ(k);v,⋯,xn;v)M, | (3.3) |
where the Laurent monomial M is of the form xm11;v⋯xmσ(k)−1σ(k)−1;vxmσ(k)+1σ(k)+1;v⋯xmnn;v and mj is integer for j∈[1,n]−σ(k). Thus Eq (3.3) is the Laurent expansion of xk;u with respect to xv.
Similarly, the following equation is the Laurent expansion of xσ(k);v with respect to xu.
xσ(k);v=xk;uFσ(k);t1(r−11xσ−1(1);u,⋯,ˆxk;u,⋯,r−1nxσ−1(n);u)r−1kFk;t2(x1;u,⋯,ˆxk;u,⋯,xn;u)M−1, | (3.4) |
where M−1 is also a Laurent monomial in R[x±11;u,⋯,ˆxk;u,⋯,x±1n;u] since xi;u=rixσ(i);v for i≠k.
We know that both Fσ(k);t1 ( r−11xσ−1(1);u ,⋯, ˆxk;u ,⋯, r−1nxσ−1(n);u ) Fk;t2 ( x1;u ,⋯, ˆxk;u ,⋯, xn;u ) =Fσ(k);t1 ( x1;v ,⋯, ˆxσ(k);v ,⋯, xn;v ) Fk;t2 ( r1xσ(1);v ,⋯, ˆxσ(k);v ,⋯, rnxσ(n);v ) and Fk;t2 ( r1xσ(1);v ,⋯, ˆxσ(k);v ,⋯, rnxσ(n);v ) Fσ(k);t1 ( x1;v ,⋯, ˆxσ(k);v ,⋯, xn;v ) are Laurent polynomials in
R[x±11;v,⋯,ˆxσ(k);v,⋯,x±1n;v]=R[x±11;u,⋯,ˆxk;u,⋯,x±1n;u] |
by the Laurent phenomenon.
Thus both Fk;t2 ( r1xσ(1);v ,⋯, ˆxσ(k);v ,⋯, rnxσ(n);v ) Fσ(k);t1 ( x1;v ,⋯, ˆxσ(k);v ,⋯, xn;v ) and Fσ(k);t1 ( x1;v ,⋯, ˆxσ(k);v ,⋯, xn;v ) Fk;t2 ( r1xσ(1);v ,⋯, ˆxσ(k);v ,⋯, rnxσ(n);v ) are units in R[x±11;v ,⋯, ˆxσ(k);v ,⋯, x±1n;v].
Because both Fk;t2 and Fσ(k);t1 are irreducible and xj;t2∤Fk;t2, xj;t1∤Fσ(k);t1 for each j∈[1,n], so that both Fk;t2 ( r1xσ(1);v ,⋯, ˆxσ(k);v ,⋯, rnxσ(n);v ) Fσ(k);t1 ( x1;v ,⋯, ˆxσ(k);v ,⋯, xn;v ) and Fσ(k);t1 ( x1;v ,⋯, ˆxσ(k);v ,⋯, xn;v ) Fk;t2 ( r1xσ(1);v ,⋯, ˆxσ(k);v ,⋯, rnxσ(n);v ) are units in R.
Hence
Fk;t2(r1xσ(1);v,⋯,ˆxσ(k);v,⋯,rnxσ(n);v)=r′kFσ(k);t1(x1;v,⋯,ˆxσ(k);v,⋯,xn;v), |
for some unit r′k in R, i.e., Fk;t2(x1;u,⋯,ˆxk;u,⋯,xn;u)=r′kFσ(k);t1(x1;v,⋯,ˆxσ(k);v,⋯,xn;v). Thus Fk;t2=r′kFσ(k);t1 as polynomials, for each k∈[1,n].
Remark 3.2. From the proof of the above theorem, we can see that the choice of the unit ri such that xi;t2=rixσ(i);t1 does not matter when proving Fi;t2/Fσ(i);t1 is a unit in R. Similarly, in the proof which is based on the Laurent phenomenon and need to use the ratio of two exchange polynomials (for example, the proof of Lemma 3.6), we can assume that ri=1.
Next, we will give the proof of the conjecture for cluster algebras that each seed is uniquely defined by its cluster, and main points of proof that are different from the previous one.
Theorem 3.3. Let A(S) be a cluster algebra, and Σtl=(xtl,ytl,Btl),l=1,2 be two cluster seeds of A(S).If there exists a permutation σ of [1,n] such that xi;t2=xσ(i);t1 for i∈[1,n], then
(i) Either yk;t2=yσ(k);t1, bt2ik=bt1σ(i)σ(k) or yk;t2=y−1σ(k);t1, bt2ik=−bt1σ(i)σ(k) for i,k∈[1,n].
(ii) In both cases, Fi;t2=Fσ(i);t1 as polynomials for i∈[1,n].
Proof. By the same method with the proof of Theorem 3.1, the version of the equation (3.2) for the cluster algebra is just
xk;u=xσ(k);vFk;t2(xσ(1);v,⋯,ˆxσ(k);v,⋯,xσ(n);v)Fσ(k);t1(x1;v,⋯,ˆxσ(k);v,⋯,xn;v), | (3.5) |
and note that xi;u=xσ(i);v for any i≠k, we also have
xσ(k);v=xk;uFσ(k);t1(xσ−1(1);u,⋯,ˆxk;u,⋯,xσ−1(n);u)Fk;t2(x1;u,⋯,ˆxk;u,⋯,xn;u). | (3.6) |
We know that Eq (3.5) is the Laurent expansion of xk;u with respect to xv and Eq (3.6) is the Laurent expansion of xσ(k);v with respect to xu. Then by the Laurent phenomenon, both Fk;t2 ( xσ(1);v ,⋯, ˆxσ(k);v ,⋯, xσ(n);v ) Fσ(k);t1 ( x1;v ,⋯, ˆxσ(k);v ,⋯, xn;v ) and Fσ(k);t1 ( xσ−1(1);u ,⋯, ˆxk;u ,⋯, xσ−1(n);u ) Fk;t2 ( x1;u ,⋯, ˆxk;u ,⋯, xn;u ) are Laurent polynomials, and this implies that Fk;t2 ( xσ(1);v ,⋯, ˆxσ(k);v ,⋯, xσ(n);v ) Fσ(k);t1 ( x1;v ,⋯, ˆxσ(k);v ,⋯, xn;v ) is a Laurent monomial in ZP[x±11;v ,⋯, ˆxσ(k);v ,⋯, x±1n;v]. We know that
Fk;t2(xσ(1);v,⋯,ˆxσ(k);v,⋯,xσ(n);v)=yk;t21⊕yk;t2∏bt2ik>0xbt2ikσ(i);v+11⊕yk;t2∏bt2ik<0x−bt2ikσ(i);v, |
Fσ(k);t1(x1;v,⋯,ˆxσ(k);v,⋯,xn;v)=yσ(k);t11⊕yσ(k);t1∏bt1iσ(k)>0xbt1iσ(k)i;v+11⊕yσ(k);t1∏bt1iσ(k)<0x−bt1iσ(k)i;v. |
Because Fk;t2(xσ(1);v,⋯,ˆxσ(k);v,⋯,xσ(n);v)Fσ(k);t1(x1;v,⋯,ˆxσ(k);v,⋯,xn;v) is a Laurent monomial, we must have either yk;t2=yσ(k);t1, bt2ik=bt1σ(i)σ(k) or yk;t2=y−1σ(k);t1, bt2ik=−bt1σ(i)σ(k). In both cases, we have
Fk;t2(xσ(1);v,⋯,ˆxσ(k);v,⋯,xσ(n);v)=Fσ(k);t1(x1;v,⋯,ˆxσ(k);v,⋯,xn;v), |
i.e., Fk;t2(x1;u,⋯,ˆxk;u,⋯,xn;u)=Fσ(k);t1(x1;v,⋯,ˆxσ(k);v,⋯,xn;v). Thus Fk;t2=Fσ(k);t1 as polynomials.
Lemma 3.4. Let A(S) be a skew-symmetrizable cluster algebra with skew-symmetrizer D, and(xt1,yt1,Bt1),(xt2,yt2,Bt2) be two cluster seeds of A(S).If there exists a permutation σ of [1,n] such that xi;t2=xσ(i);t1 for i∈[1,n], then bt2ik=dkdσ(k)bt1σ(i)σ(k).
Proof. Let Pσ be the permutation matrix define by the permutation σ. By the cluster formula (see Theorem 3.5 of [2]), we have Pσ(Bt1D−1)P⊤σ=Bt2D−1. Then Bt2=(PσBt1P⊤σ)(PσD−1P⊤σ)D. The result follows.
By the proof of the first statement and the definition of equivalence for two cluster seeds, we conclude the second statement.
From Theorem 3.3 and Lemma 3.4, we can affirm a conjecture for skew-symmetrizable cluster algebra proposed by Fomin and Zelevinsky in [13], which says every seed of a cluster algebra is uniquely determined by its cluster.
Corollary 3.5. Let A(S) be a skew-symmetrizable cluster algebra with skew-symmetrizer D, and (xt1,yt1,Bt1),(xt2,yt2,Bt2) be two cluster seeds of A(S).If there exists a permutation σ of [1,n] such that xi;t2=xσ(i);t1 for i∈[1,n], then yk;t2=yσ(k);t1, bt2ik=bt1σ(i)σ(k), dk=dσ(k) for any i and k.
The result (1) of Theorem 3.1 shows that when xi;t2=rixσ(i);t1 where i∈[1,n] and ri∈R, then Fi;t2=r′iFσ(i);t1 where r′i∈R. In fact, the proof of result (1) also works for any generalized cluster algebra and any (totally sign-skew-symmetric) cluster algebra with coefficients. The reason is that the proof mainly relies on the Laurent phenomenon and is independent of the form of exchange polynomials. In the meantime, the unit ri such that xi;t2=rixσ(i);t1 can be chosen to be 1 (see Remark 3.2). Although LP algebras, cluster algebras and generalized cluster algebras have different forms of exchange polynomials, and they are not included in each other, they all have the Laurent phenomenon. Thus for cluster algebras or generalized cluster algebras, it is the same method in proving that two clusters up to a permutation imply their corresponding exchange polynomials to be the same up to a permutation.
For cluster algebras or generalized cluster algebras, the equivalence for seeds is defined as two clusters and their corresponding exchange matrices up to a permutation. We know that exchange polynomials are defined by exchange matrices. And exchange polynomials up to a permutation can not imply exchange matrices to be equivalent up to a permutation. So in order to prove the conjecture (1) that each seed is uniquely defined by its cluster, we need to prove that the corresponding exchange matrices are equivalent up to a permutation. For cluster algebras, based on the result that exchange polynomials are the same up to a permutation, we give the proof in Corollary 3.5. For generalized cluster algebras, we will not discuss them more in this article, but will further discuss them in the next work.
Let A(S) be a LP algebra, if there is a seed (xt0,Ft0) of A(S) such that the exchange polynomials in Ft0 are all nontrivial, we say that A(S) is a LP algebra having no trivial exchange relations.
Note that if there is a trivial exchange polynomial in a LP seed (xt0,Ft0), from the definition of LP mutation, this trivial exchange polynomial remain invariant under any sequence of LP mutations. So if A(S) is a LP algebra having no trivial exchange relations, then each exchange polynomial of A(S) is a nontrivial polynomial.
Lemma 3.6. Let A(S) be a LP algebra having no trivial exchange relations, and Σt=(xt,Ft), Σt0=(xt0,Ft0) be two LP seeds of A(S) with xi;t=rixi;t0, where ri is a unit in R for any i≠k. If xk;t=Mxk;t0 for some Laurent monomial M in R[x±11;t0,⋯,ˆxk;t0,⋯,x±1n;t0], then M is a unit in R, and [Σt]=[Σt0].
Proof. Without loss of generality, we assume that ri=1 for i≠k. It does not make difference to the proof.
Assume that M=r∏i≠kxaii;t0=r∏i≠kxaii;t, where r is a unit in R. If there exists some j≠k such that aj<0, then we consider the LP seed (xw,Fw)=μj(Σt0). From the definition of LP mutation, we know that xi;w=xi;t0 for i≠j and xj;wxj;t0=ˆFj;t0(x1;t0,⋯,ˆxj;t0,⋯,xn;t0). Then we have
xk;t=(r∏i≠kxaii;t0)xk;t0=(r∏i≠j,kxaii;w)x−ajj;wˆF−ajj;t0(x1;w,⋯,ˆxj;w,⋯,xn;w)xk;w, |
which can be written as the following equation, from the definition of the exchange Laurent polynomial.
xk;t=(r∏i≠j,kxaii;w)x−ajj;wLF−ajj;t0(x1;w,⋯,ˆxj;w,⋯,xn;w)xk;w, | (3.7) |
where L is a Laurent monomial in R[x±11;w,⋯,ˆxj;w,⋯,x±1n;w]. Thus Eq (3.7) is the expansion of xk;t with respect to xw. Because A(S) has no trivial exchange relations, Fj;t0 is a nontrivial polynomial. And we know that Fj;t0 is irreducible and xs∤Fj;t0 for each s∈[1,n], thus Eq (3.7) will contradict the Laurent phenomenon. So each aj is nonnegative.
Similarly, by considering that xk;t0=M−1xk;t=(r∏i≠kx−aii;t)xk;t, we can get each −aj is nonnegative. Thus each aj is 0, thus M=r is a unit in R. Then by Theorem 3.1, we have [Σt]=[Σt0].
Theorem 3.7. Let A(S) be a LP algebra of rank n having no trivial exchange relations, and Σt1=(xt1,Ft1), Σt2=(xt2,Ft2) be two LP seeds of A(S). If xi;t1=rixi;t2 holds for any i≠k, where ri is a unit in R, then [Σt1]=[Σt2] or [Σt1]=μk[Σt2], that is, any two LP seeds with n>1 common cluster variables are connected with each other by one step of mutation.
Proof. Without loss of generality, we assume that ri=1 for i≠k. It does not make difference to the proof.
By the Laurent phenomenon, we assume that xk;t2=f(x1;t1,⋯,xn;t1) and xk;t1=g(x1;t2,⋯,xn;t2), where f∈R[x±11;t1,⋯,x±1n;t1] and g∈R[x±11;t2,⋯,x±1n;t2]. Since xi;t1=xi;t2 for any i≠k, we know that xk;t1 entries f with exponent 1 or −1; Thus xk;t2 has the form of xk;t2=L1x±1k;t1+L0, where L1≠0 and L0 are Laurent polynomials in
R[x±11;t1,⋯,ˆxk;t1,⋯,x±1n;t1]=R[x±11;t2,⋯,ˆxk;t2,⋯,x±1n;t2]. |
Let (xu,Fu)=μk(Σt2) and (xv,Fv)=μk(Σt1). From the definition of the LP mutation, we know
xi;u={xi;t2if i≠kˆFk;t2/xk;t2if i=k and xi;v={xi;t1if i≠kˆFk;t1/xk;t1if i=k. |
Thus xk;u=ˆFk;t2(x1;t2,⋯,ˆxk;t2,⋯,xn;t2)/xk;t2=ˆFk;t2(x1;t1,⋯,ˆxk;t1,⋯,xn;t1)L1x±1k;t1+L0. From the definition of the exchange Laurent polynomial, we know the above equation has the form of
xk;u=Fk;t2(x1;t1,⋯,ˆxk;t1,⋯,xn;t1)L1x±1k;t1+L0M, | (3.8) |
where M is a Laurent monomial in R[x±11;t1,⋯,ˆxk;t1,⋯,x±1n;t1]. The above equation is just the expansion of xk;u with respect to xt1. By the Laurent phenomenon, and the fact xk;t1∉Fk;t2(x1;t1,⋯,ˆxk;t1,⋯,xn;t1), we obtain that L0=0 and Fk;t2(x1;t1,⋯,ˆxk;t1,⋯,xn;t1)L1 is a Laurent polynomial in R[x±11;t1,⋯,ˆxk;t1,⋯,x±1n;t1]. Thus we have that xk;t2=L1x±1k;t1 and xk;u has the form of xk;u=˜Mx∓1k;t1, where ˜M is a Laurent polynomial in R[x±11;t1,⋯,ˆxk;t1,⋯,x±1n;t1].
We claim that Fk;t2(x1;t1,⋯,ˆxk;t1,⋯,xn;t1)L1 is actually a Laurent monomial, i.e., ˜M is a Laurent monomial in R[x±11;t1,⋯,ˆxk;t1,⋯,x±1n;t1].
Case (i): xk;t2=L1xk;t1. Then xk;t1=L−11xk;t2, which is the expansion of xk;t1 with respect to xt2. By the Laurent phenomenon, we can get that L1 is a Luarent monomial in
R[x±11;t1,⋯,ˆxk;t1,⋯,x±1n;t1]. |
Then by Lemma 3.6, L1 is a unit in R and [Σt1]=[Σt2].
Case (ii): xk;t2=L1x−1k;t1, in this case, xk;u=˜Mxk;t1. By the same argument in case (i), we can get that ˜M is a Luarent monomial in R[x±11;t1,⋯,ˆxk;t1,⋯,x±1n;t1]. Then by Lemma 3.6, ˜M is a unit in R and [Σt1]=[(xu,Fu)]=[μk(Σt2)]=μk([Σt2]).
Remark 3.8. The same method also works for cluster algebras and one can get the similar result.
The following definitions are natural generalizations of the corresponding notions of cluster algebras in [4].
For i∈[1,n], we define the adjacent cluster xi by xi=(x−{xi})∪{x′i} where the cluster variables xi and x′i are related by the exchange Laurent polynomial ˆFi. Let R[x±1] be the ring of Laurent polynomials in x1,…,xn with coefficients in R.
Definition 4.1. The upper bound U(Σ) and lower bound L(Σ) associated with a LP seed Σ=(x,F) is defined by
U(Σ)=R[x±1]∩R[x±11]∩⋯∩R[x±1n], L(Σ)=R[x1,x′1,…,xn,x′n] |
Thus, L(Σ) is the R-subalgebra of F generated by the union of n+1 clusters x±1,x±11,…,x±1n. Note that L(Σ)⊆A(Σ)⊆U(Σ).
Remark 4.2. The method of the proof of results for LP algebras in this section is a little similar to those for cluster algebras in [4]. The concepts of LP algebras and cluster algebras are essentially different, since LP algebras and cluster algebras are not included with each other. In general, the calculation for LP algebras is more complicated. Now, we give the following three points to explain the specific differences between LP algebras and cluster algebras.
(1) For cluster algebras, the exchange polynomials are binomials. While for LP algebras, those are multinomials, so that the calculation using the exchange polynomials becomes complicated.
(2) For cluster algebras, coprimeness is necessary for the proof of properties for the upper bound and lower bound, and it is easy to check that the coprimeness keeps under mutations for a certain seed. While for LP algebras, the concept of coprimeness is not yet defined. In order to obtain a LP seed with coprimeness, we assume that a LP seed satisfies the condition that ˆFk=Fk for any k. But it is not obvious whether the condition keeps under mutations (see Example 4.12 which shows that the condition does not keep under mutations), so that in the proof that involves mutations and requires that condition, we need to show that the condition keeps under mutations.
(3) In cluster algebras, the acyclic seed has good property that the lexicographically first monomial of its any exchange polynomial Fj is a monomial in {xi|i>j}. While in LP algebras, the concept of the acyclic seed is not yet defined. In order to obtain a LP seed with such good property, we assume that the LP seed satisfies certain conditions, see Condition 1.2.
For any LP seed Σ=(x,F), the following lemma and corollary hold parallel to the corresponding results in [4].
Lemma 4.3.
U(Σ)=n⋂j=1R[x±11,…,x±1j−1,xj,x′j,x±1j+1,…,x±1n]. | (4.1) |
Proof. It is sufficient to show that
R[x±1]∩R[x±11]=R[x1,x′1,x±12,…,x±1n]. |
The inclusion ⊇ is clear, we only need to prove the converse inclusion.
For any y∈R[x±1]∩R[x±11], y is of the form y=N∑m=−Mcmxm1, where M,N∈Z≥0 and cm∈R[x±12,…,x±1n]. If M≥0, it is easy to see that
y∈R[x1,x±12,…,x±1n]⊆R[x1,x′1,x±12,…,x±1n]. |
If MN≠0, from the definition of LP seeds, x1∉ˆF1, then
y|x1←ˆF1x′1=∑Nm=−Mcm(ˆF1x′1)m=∑Mm=1c−mˆF−m1x′m1+∑Nm=0cmˆFm1x′−m1. |
Since y∈R[x±11], y can be written as N′∑p=M′cpxp1 where cp∈R[x±12,…,x±1n], then we have c−mˆF−m1∈R[x±12,…,x±1n]. Thus,
y=M∑m=1c−mˆF−m1x′m1+N∑m=0cmxm1∈R[x1,x′1,x±12,…,x±1n]. |
If N=0, by similar discussion, we have y∈R[x′1,x±12,…,x±1n]⊆R[x1,x′1,x±12,…,x±1n].
Corollary 4.4. For j∈[1,n], y∈R[x±11,…,x±1j−1,xj,x′j,x±1j+1,…,x±1n] if and only if y is of the form y=N∑m=−Mcmxmj where M,N∈Z≥0, cm∈R[x±11,…,^xj±1,…,x±1n] and c−m is divisible by ˆFmj in R[x±11,…,^xj±1,…,x±1n] for m∈[1,M].
Lemma 4.5. Suppose that ˆFj=Fj for j∈[1,2], then R[x1,x±12]∩R[x±11,x2,x′2]=R[x1,x2,x′2].
Proof. The inclusion ⊇ is clear, we only need to prove the converse inclusion. For y∈R[x1,x±12]∩R[x±11,x2,x′2], y is of the form y=∑m∈Zxm1(cm+c′m(x2)+c″m(x′2)), where cm∈R, c′m(x2) and c″m(x′2) are polynomials over R without constant terms.
Let M be the smaller integer such that cM+c′M(x2)+c″M(x′2)≠0. If M≥0, then it is easy to see that y∈R[x1,x2,x′2].
Otherwise, the Laurent expression of y is ∑m∈Zxm1(cm+c′m(x2)+c″m(F2x2)) by the assumption. Let r2 be the sum of monomials in F2 without x1. Then there are nonzero terms with smallest power of x1 in the Laurent expression of y, which are xM1(cM+c′M(x2)+c″M(r2x2))≠0, which contradicts the condition that y∈R[x1,x±12].
Lemma 4.6. Suppose that ˆFj=Fj for j∈[1,2], then
R[x1,x′1,x±12]=R[x1,x′1,x2,x′2]+R[x1,x±12]. |
Proof. The inclusion ⊇ is clear, we only need to prove the converse inclusion. It is enough to show that ∀M,N>0, x′N1x−M2∈R[x1,x′1,x2,x′2]+R[x1,x±12].
By the assumption, we have x2x′2=ˆF2=F2=g(x1)+r2, where g(x1)=m∑i=1gixi1, gi∈R and r2≠0∈R since F2 is not divisible by x1. If g(x1)=0, then x−12=r−12x′2, which implies that x′N1x−M2∈R[x1,x′1,x2,x′2].
Otherwise, let p(x1)=−g(x1)r2∈R[x1], then x2x′2=g(x1)+r2 can be written as
x−12=r−12x′2+p(x1)x−12. |
Repeatedly substituting x−12 in the RHS of the above equation by r−12x′2+p(x1)x−12, we obtain x−12=P(x1,x′2)+pN(x1)x−12, where P(x1,x′2)=r−12x′2N−1∑i=0pi(x1)∈R[x1,x′2].
Then we have
x′N1x−M2=x′N1PM(x1,x′2)+x′N1pMN(x1)x−M2+x′N1∑M−1i=1(Mi)(P(x1,x′2))M−i(p(x1)Nx−12)i, | (4.2) |
where the first term of (4.2) that is, x′N1PM(x1,x′2)∈R[x1,x′1,x′2].
For p(x1)=−1r2g(x1)=−1r2m∑i=1gixi1, the smallest power of x1 in pN(x1) is N and the greatest is Nm. Thus we can rewrite pN(x1) in the form xN1(N(m−1)∑i=0pixi1) where pi∈R, implying that for any integer K>0, we have pNK(x1)∈xN1R[x1]. Since x1x′1=ˆF1=F1∈R[x2], we have x′N1pNK(x1)∈R[x1,x2].
Then the middle term of (4.2) is obvious in R[x1,x±12], and the last term of (4.2) is equal to x′N1M−1∑i=1(Mi)(P(x1,F2x2))M−i(p(x1)Nx−12)i∈R[x1,x±12].
Thus we finish the proof.
Proposition 4.7. Suppose that n≥2 and ˆFj=Fj for j∈[1,n], then
U(Σ)=n⋂j=2R[x1,x′1,x±12,…,x±1j−1,xj,x′j,x±1j+1,…,x±1n]. | (4.3) |
Proof. Comparing (4.1) with (4.3), it is sufficient to show that
R[x1,x′1,x2,x′2,x±13,…,x±1n]=R[x1,x′1,x±12,…,x±1n]∩R[x±11,x2,x′2,x±13,…,x±1n]. |
Freeze the cluster variables x3,…,xn and view R[x±13,…,x±1n] as the new ground ring R, then the above equality reduces to
R[x1,x′1,x2,x′2]=R[x1,x′1,x±12]∩R[x±11,x2,x′2]. | (4.4) |
Suppose F1=f(x2)+r1, F2=g(x1)+r2, where r1≠0,r2≠0∈R and f(x2),g(x1) are polynomials over R without constant terms. It is easy to see that Lemma 4.5 and Lemma 4.6 hold for four cases which are: (C1) x2∉F1 and x1∉F2, that is, f(x2)=0 and g(x1)=0; (C2) x2∈F1 and x1∈F2; (C3) x2∉F1 but x1∈F2; (C4) x2∈F1 but x1∉F2. Combining Lemma 4.5 and Lemma 4.6 with the fact that R[x1,x′1,x2,x′2]⊆R[x±11,x2,x′2], we obtain:
R[x1,x′1,x±12]∩R[x±11,x2,x′2]=(R[x1,x′1,x2,x′2]+R[x1,x±12])∩R[x±11,x2,x′2]=R[x1,x′1,x2,x′2]+(R[x1,x±12]∩R[x±11,x2,x′2])=R[x1,x′1,x2,x′2] |
Thus we have (4.4).
Lemma 4.8. For a LP seed (x,F), let x′2 and x″2 be the cluster variables exchanged with x2 in the LP seeds μ2(x,F) and μ2μ1(x,F) respectively, then
R[x1,x′1,x2,x′2,x±13,…,x±1n]=R[x1,x′1,x2,x″2,x±13,…,x±1n]. | (4.5) |
Proof. We can freeze the cluster variables x3,…,xn and view R[x±13,…,x±1n] as the new ground ring R. Then we will prove the following equality can be reduced from (4.5):
R[x1,x′1,x2,x′2]=R[x1,x′1,x2,x″2]. |
We first show that x″2∈R[x1,x′1,x2,x′2].
In (C1), it is easy to see that x″2=rx′2 for certain r∈R, which implies x″2∈R[x1,x′1,x2,x′2].
In (C2), let (x′,F′)=μ1(x,F), then x″2 is obtained by x2x″2=ˆF′2. Recall that x1x′1=ˆF1=F1=f(x2)+r1 and x2x′2=ˆF2=F2=g(x1)+r2, where g(x1)=m∑i=1gixi1, gi∈R and r2≠0∈R. Because F2 depends on x1, from the definition of LP mutations, we have:
1) G2=F2|x1←N2=g(r1x′1)+r2.
2) H2=G2/c, where c is the product of all common factors of giri1 for i∈[1,m] and r2.
3) F′2=MH2=x′m1H2=h(x′1)+r3,
where r3=gmrm1c, h(x′1)=m∑i=1hix′i1, hj={gm−irm−i1/cj∈[1,m−1],r2/cj=m.
By Proposition 2.4, there exist x2 in F′1=F1 in (x′,F′), so that there is no x′1 in F′2/ˆF′2, thus we have ˆF′2=F′2. It follows that
x2x″2=1cr2x′m1+∑m−1j=1hjx′j1+r3=1c(x2x′2−g(x1))x′m1+∑m−1j=1hjx′j1+r3=x2(1cx′2x′m1)−(1cg(x1)x′m1−(∑m−1j=1hjx′j1)−r3), |
where 1cg(x1)x′m1=(m∑i=1gicxi1)x′m1=m∑i=1gic(x1x′1)ix′m−i1=m∑i=1gic(f(x2)+r1)ix′m−i1. Recall that f(x2) is a polynomial in x2 without constant terms, then gmc(f(x2)+r1)m can be written as x2Pm+gmrm1c=x2Pm+r3, where Pm is a polynomial in x2.
For i∈[1,m−1], we have gic(f(x2)+r1)ix′m−i1=x2Pi+giri1cx′m−i1=x2Pi+hm−ix′m−i1, where Pi is a polynomial in x2.
Then 1cg(x1)x′m1−(m−1∑j=1hjx′j1)−r3=x2(m∑i=1Pi), which implies that
x2x″2=x2(1cx′2x′m1−m∑i=1Pi). |
Thus x″2∈R[x1,x′1,x2,x′2].
For (C3) and (C4), it is enough to show for (C3) by symmetry. At this time, F′2 is the same as that in (C2). Since f(x2)=0, (F′1=F1)|x2←F′2/x″2=r1 is not divisible by F′2, so that ˆF′2=F′2. As a consequence, we have x2x″2=x2(1cx′2x′m1). Thus x″2∈R[x1,x′1,x2,x′2].
On the other hand, we can prove similarly that x′2∈R[x1,x′1,x2,x″2]. Then, (4.5) follows truely.
Theorem 4.9. Assume that a LP seed Σ=(x,F) satisfied ˆFj=Fj for j∈[1,n] and Σ′=(x′,F′) is the LP seed obtained from the LP seed Σ by mutation in direction k. Then the corresponding upper bounds coincide, that is, U(Σ)=U(Σ′).
Proof. Without loss of generality, we assume that k=1. Combining Proposition 4.7 and Lemma 4.8, we finish the proof.
Proposition 4.10. If the exchange polynomials of a LP seed satisfy ˆFk=Fk for any k∈[1,n], then Fi≠Fk for any i≠k. Furthermore, any two of the exchange polynomials {Fk|k∈[1,n]}of a LP seed are coprime.
Proof. We will prove by contradiction. If Fi=Fk, then
ˆFi|xk←Fk/x′k=Fi|xk←Fk/x′k=Fk|xk←Fk/x′k=Fk |
for xk∉Fk, implying that Fk divides ˆFi|xk←Fk/x′k, which contradicts the definition of exchange Laurent polynomials.
Besides, since the irreducibility of exchange polynomials for LP seeds, we conclude that the exchange polynomials of a LP seed are coprime under the condition that ˆFk=Fk for any k∈[1,n].
Remark 4.11. When a cluster seed is a LP seed, the coprimeness of the cluster seed is equivalent to the condition that ˆFk=Fk for any k∈[1,n].
Example 4.12. Consider the LP seed (x,F)={(a,b+c),(b,a+c),(c,a+(a+1)b)} over R=Z, which satisfies the condition that ˆFk=Fk for any k∈{a,b,c}. Then the LP seed obtained by mutation at b is
(x′,F′)={(a,1+d),(d,a+c),(c,a+d+1)} |
where d=a+Cb. It is easy to see that ^F′c=F′ca, meaning that the condition that ˆFk=Fk for any k for a LP seed does not keep under mutations.
Definition 4.13. Let Σ=(x,F) be a LP seed, the upper LP algebra ¯A(Σ) defined by Σ is the intersection of the subalgebras U(Σ′) for all LP seeds Σ′ mutation-equivalent to Σ.
Theorem 4.9 has the following direct implication.
Corollary 4.14. Assume that all LP seeds mutation equivalent to a LP seed Σ=(x,F) satisfy the condition that ˆFj=Fj for j∈[1,n], then the upper bound U(Σ) is independent of the choice of LP seeds mutation-equivalent to Σ, and so is equal to the upper LP algebra ¯A(Σ).
Definition 4.15. Let (x,F) be a LP seed. A standard monomial in {xi,x′i|i∈[1,n]} is a monomial that contains no product of the form xix′i.
Let xa=xa11…xann be a Laurent monomial where a∈Zn. For a Laurent polynomial in x1,…,xn, we order the each two terms xa and xa′ lexicographically as follows:
a≺a′ if the first nonzero difference a′j−aj is positive. | (4.6) |
We set the term with the smallest lexicographical order as the first term in a Laurent polynomial.
Theorem 4.16. Assume that a LP seeds Σ=(x,F) satisfies
1) ˆFj=Fj for j∈[1,n].
2) in any Fj, the lexicographically first monomial is of the form
xvj={xvj+1,jj+1⋯xvn,jnj∈[1,n−1]1j=n |
where vj∈Zn−j≥0 for j∈[1,n−1].
Then the standard monomials in x1,x′1,…,xn,x′n form an R-basis for L(Σ).
Proof. The proof is using the same technique as in [4]. We denote the standard monomials in x1,x′1,…,xn,x′n by x(a)=x(a1)1⋯x(an)n, where a=(a1,…,an)∈Zn and
x(ai)i={xaii,ai≥0x′−aii,ai<0. |
Note that x(a) is a Laurent polynomial in x1,…,xn and for any i, we have x(−1)i=x′i=x−1iˆFi=x−1iFi. By the assumption for Fi, it follows that the lexicographically first monomial in x(−1)i is x−1ixvi, then the power of xi in x(ai)i is ai and there is no x1,…,xi−1 in x(ai)i. Then the lexicographically first monomial in x(a) is the product of xaii(ai>0) and xaii(xvi)−ai(ai<0).
We assume that a≺a′ such that ai=a′i for i∈[1,k−1] and ak<a′k. Let P, M and Q be the lexicographically first monomial of k−1∏j=1x(aj)j, x(ak)k and n∏j=k+1x(aj)j respectively. Then the lexicographically first monomial of x(a) is PMQ, similarly that of x(a′) is P′M′Q′.
Since ai=a′i for i∈[1,k−1], we have P=P′=n∏j=1xpjj.
Since ak<a′k and the power of xk in x(ak)k is ak and there is no xi (i∈[1,k−1]) in x(ak)k, we obtain M=xakkn∏j=k+1xmjj and M′=xa′kkn∏j=k+1xm′jj.
And Q=(n∏j=k+1,aj>0xajj)(n∏j=k+1,aj<0xajj(xvj)−aj)=n∏j=k+1xqjj, similarly Q′=n∏j=k+1xq′jj.
It follows that
PMQ=(k−1∏j=1xpjj)(xpk+akk)(n∏j=k+1xpj+mj+qjj), P′M′Q′=(k−1∏j=1xpjj)(xpk+a′kk)(n∏j=k+1xpj+m′j+q′jj). |
Thus PMQ≺P′M′Q′, implying that
if a≺a′, the lexicographically first monomial of x(a)≺that of x(a′). | (4.7) |
The linearly independence of standard monomials over R follows at once from (4.7). Since the product xix′i for any i equals to ^Fi=Fi, which is the linear combination of standard monomials in x1,x′1,…,xn,x′n. Thus they form a basis for L(Σ).
In the following statements, we always assume that Σ=(x,F) is a LP seed of rank n satisfying Condition 1.2.
Notation 4.17. We denote by φ:R[x2,x′2,…,xn,x′n]→R[x±12,…,x±1n] the algebra homomorphism defined as the composition φ2∘φ1, where
φ1:R[x2,x′2,…,xn,x′n]→R[x1,x±12,…,x±1n] by xi↦xi and x′i↦Fi/xi.φ2:R[x1,x±12,…,x±1n]→R[x±12,…,x±1n] by x1↦0 and x±1i↦x±1i. |
We denote by Rst[x2,x′2,…,xn,x′n] (resp. Rst[x1,x2,x′2,…,xn,x′n]) the R-linear span (resp. R[x1]-linear span) of the standard monomials in x2,x′2,…,xn,x′n.
Lemma 4.18. R[x2,x′2,…,xn,x′n]=ker(φ)⊕Rst[x2,x′2,…,xn,x′n].
Proof. For any y∈R[x2,x′2,…,xn,x′n], replace xix′i∈y with Fi, then y∈Rst[x1,x2,x′2,…,xn,x′n]. Thus we have R[x2,x′2,…,xn,x′n]⊆Rst[x1,x2,x′2,…,xn,x′n]. It follows that
R[x2,x′2,…,xn,x′n]=ker(φ)+Rst[x2,x′2,…,xn,x′n]. |
Similarly using the tool of the proof of Theorem 4.16, For x(a)∈Rst[x2,x′2,…,xn,x′n], the lexicographically first monomial of φ(x(aj)j) is a Laurent monomial in xj,xj+1,…,xn whose the power of xj is aj, implying that if a≺a′, then the lexicographically first monomial of φ(x(a)) precedes the one of φ(x(a′)).
Then the restriction of φ to Rst[x2,x′2,…,xn,x′n] is injective.
Notation 4.19. Given a Laurent polynomial y∈R[x±11,…,x±1n], we denote by LT(y) as the sum of all Laurent monomials with the smallest power of x1 in the Laurent expansion of y with nonzero coefficient.
The following results parallel to Lemmas 6.4 and 6.5 in [4] can be obtained similarly.
Lemma 4.20. Suppose that y=∑bm=acmxm1 where cm∈Rst[x2,x′2,…,xn,x′n] and ca≠0, then LT(y)=φ(ca)xa1.
Lemma 4.21. R[x1,x±12,…,x±1n]∩R[x±11,x2,x′2,…,xn,x′n]=R[x1,x2,x′2,…,xn,x′n].
Lemma 4.22. Im(φ)=R[x2,x(−)2,…,xn,x(−)n], where x(−)j={x′j,ifx1∉Fjx−1j,otherwise.
Proof. By Condition 1.2, we have φ(x′j)={x′j,if x1∉Fjx−1jMj,otherwise. Thus the inclusion ⊆ is clear.
Let J be the set of indexes j∈[2,n] satisfying x1∉Fj. We set Wj=x−1jMj. To prove the converse inclusion, it is enough to show that x−1j∈ Im(φ) for j∈[2,n]−J.
For m=(m2,…,mn),l=(l2,…,ln)∈Zn−1, let xm be a Laurent monomial in R[x±12,…,x±1n]. Moreover, we set Wl=n∏j=2Wljj. Then we have any xm can be written as Wl satisfying
mj=−lj+∑2≤i<jvjili. |
Define the multiplicative monoid W={xm=Wl|li≥0 for i∈[2,n] and mj≥0 for j∈J}. Then Wl∈W if and only if
(a)lk≥0fork∈[2,n],(b)∑2≤i<jvjili≥lj for j∈J. | (4.8) |
By the equivalence condition (4.8) of Wl∈W, we obtain x−1j∈W for j∈[2,n]−J, implying that it suffices to show that W⊆ Im(φ).
For W=Wl∈W, we prove that W∈ Im(φ) by induction on the degree of W. When deg(W)=0, we have W=1∈R⊆ Im(φ). Assume that deg(W)>0 and for any W′∈W such that deg(W′)<deg(W), then W′∈ Im(φ).
Let j=max{i|li>0 in W}, then we have W/Wj∈W by the equivalence condition (4.8) of Wl∈W. As a consequence, W/Wj∈ Im(φ) under the induction assumption. If j∈[2,n]−J, then Wj∈ Im(φ) so that W=(W/Wj)Wj∈ Im(φ).
Otherwise, since lj>0, there exist i∈[2,j−1] such that vjili>0, where vji≠0 implies that xj∈Mi. Fix such an index i. By (iv) of Condition 1.2, Fj=fj(xi)+Mj and fj(xi)=sj∑t=1rtct, where sj is the number of terms of fj(xi), rt∈R and ct=∏p∈[2,n]−jxγptp satisfying γpt∈Z≥0 and γit≠0.
From the definition of LP mutations and Condition 1.2(i)(ii), we have x′j=x−1jfj(xi)+Wj. By multiplying both sides of that equation by W/Wj, we have
(W/Wj)x′j=x−1jsj∑t=1rtct(W/Wj)+W. |
Since (W/Wj)x′j∈ Im(φ), we only need to show that for t∈[1,sj], x−1jct(W/Wj)∈ Im(φ).
Define W′=Wl′ii⋯Wl′jj, where l′i=1 and l′p=min{lp,∑i≤q<pvpql′q} for p∈[i+1,j]. Because W/W′=Wl22⋯Wli−1i−1Wli−1iWli+1−l′i+1i+1⋯Wlj−l′jj, the equivalence condition (4.8) of W/W′∈W can be written as
(a) for k∈[i,j], lk−l′k≥0;
(b) for k∈J, lk−l′k≤∑2≤h<kvkh(lh−l′h) ⇔ −l′k+∑2≤h<kvkhl′h≤−lk+∑2≤h<kvkhlh.
The inequalities of (a) are immediate from the definition of W′ and the choice of i. And for inequality (b), we discuss in several cases:
1) if k∈[2,i−1], (b) is equivalent to 0≤−lk+∑2≤h<kvkhlh.
2)if k=i, we have ∑2≤h<ivkhl′h=0, (b) is equivalent to −1≤−lk+∑2≤h<kvkhlh.
3)if k∈[i+1,n], when l′k=lk, (b) is equivalent to ∑2≤h<kvkhl′h≤∑2≤h<kvkhlh, when l′k≤lk, l′k=∑2≤h<kvkhl′h, then LHS of (b) is zero.
Since W∈W and inequalities of (a) hold, we have inequality (b) holds for W/W′. Thus W/W′ belongs to W with deg(W/W′)<deg(W), so that W/W′∈ Im(φ).
Then we have
x−1jct(W/Wj)=W⋅∏p∈[2,n]−jxγptp/xvj=(W/W′)⋅(W′⋅(xγ2t2⋯xγj−1,tj−1)⋅(xγj+1,t−vj+1,jj+1⋯xγnt−vnjn))=(W/W′)⋅P |
The claim x−1jct(W/Wj)∈ Im(φ) is a consequence of the statement that P∈R[x2,⋯,xn]. Indeed, R[x2,⋯,xn]⊆ Im(φ).
The only variable with negative power (namely, −1) in W′ is xi, since
W′=W1iWl′i+1i+1⋯Wl′jj=x−1i⋅(xvi+1,i−l′i+1i+1⋅x(∑i≤h<i+2vi+2,h l′h)−l′i+2i+2⋯x(∑i≤h<jvj,h l′h)−l′jj)⋅(x∑i≤h≤jvj+1,h l′hj+1⋯x∑i≤h≤jvnh l′hn)=x−1i⋅Q⋅(xδj+1,tj+1⋯xδntn) |
where δpt=∑i≤h≤jvphl′h for p∈[j+1,n]. Then we have
P=Q⋅(∏q∈[2,i−1]∪[i+1,j−1]xγqtq)⋅xγit−1i⋅(∏p∈[j+1,n]xδpt+γpt−vpjp). |
For i is the fixed index such that γit∈Z>0, γit−1>0, then the power of xi is nonnegative.
For p∈[j+1,n], we have
δpt+γpt−vpj=vpil′i+⋯+vpjl′j+γpt−vpj≥vpj(l′j−1). |
From the definition of W′, we obtain l′j=min{lj,∑i≤q<jvjql′q}, and it is easy to see that lj≥1 and ∑i≤q<jvjql′q=vji+∑i<q<jvjql′q≥vji≥1 by the choice of i and j. Then l′j≥1. Thus the power of xp is nonnegative. Hence the power of any cluster variable is nonnegative. It follows that P∈R[x2,⋯,xn].
By the same technique as in [4], we give the following theorem.
Theorem 4.23. If a LP seed Σ=(x,F) satisfying Condition 1.2, L(Σ)=U(Σ).
Proof. We apply the induction on n, that is, the rank of the LP seed. When n=1, by Lemma 4.3, we have L(Σ)=R[x1,x′1]=U(Σ). Assume that n≥2 and the statement holds for all algebras of rank 2 to n−1. Then we consider about rank n.
By Lemma 4.3, we have
U(Σ)=n⋂j=2R[x±11,…,x±1j−1,xj,x′j,x±1j+1,…,x±1n]⋂R[x1,x′1,x±12,…,x±1n]. |
For the seed Σ′ obtained from Σ by freezing at x1, by the induction assumption, we have L(Σ′)=U(Σ′), that is, n⋂j=2R[x±11,…,x±1j−1,xj,x′j,x±1j+1,…,x±1n]=R[x±11,x2,x′2,…,xn,x′n]. Then it is enough to show that
R[x1,x′1,x±12,…,x±1n]∩R[x±11,x2,x′2,…,xn,x′n]=R[x1,x′1,…,xn,x′n]. | (4.9) |
The inclusion ⊇ is clear, we only need to prove the converse inclusion.
For ∀y∈ LHS of (4.9), let a be the smallest power of x1 in y|xix′i←Fi. Then y can be written as b∑m=acmxm1 where cm∈Rst[x2,x′2,…,xn,x′n]. By Lemma 4.20, we have
LT(y)=φ(ca)xa1∈R[x±11,x±12,…,x±1n]. |
If a≥0, by Lemma 4.21, we have y∈R[x1,…,xn,x′n]⊆ the RHS of (4.9).
Otherwise, we apply the induction on |a|. Since y∈R[x1,x′1,x±12,…,x±1n], by Lemma 4.4 we have φ(ca) is divisible by F|a|1, that is φ(ca)=F|a|1za for certain za∈R[x±12,…,x±1n].
When J=∅, we have Im(φ)=R[x±12,…,x±1n] according to Lemma 4.22. Then za∈ Im(φ).
When J≠∅, we consider the LP seed Σ∗ obtained from Σ by freezing at {xj|j∈[2,n]−J} and removing x1. In view of Lemma 4.22, we have L(Σ∗)=Im(φ). Besides, by the induction assumption, we have L(Σ∗)=U(Σ∗). Using Lemma 4.3, we obtain Im(φ)=⋂j∈JR[x±12,…,xj,x′j,…,x±1n].
For certain j∈J, za can be written as ∑s∈Zcsxsj, where cs∈R[x±12,…,^xj,…,x±1n]. Since F|a|1za=∑s∈Z(csF|a|1)xsj∈ Im(φ)⊆R[x±12,…,xj,x′j,…,x±1n], by Corollary 4.4 csF|a|1 is divisible by F|s|j for s<0. By Proposition 4.10, F1 and Fj are coprime, implying that cs is divisible by F|s|j. Using Corollary 4.4 again, we have za∈R[x±12,…,xj,x′j,…,x±1n].
By the arbitrariness of j∈J, we obtain za∈ Im(φ).
Then there exist c′a∈R[x±12,…,x±1n] such that za=φ(c′a). It implies that
LT(y)=φ(ca)xa1=F|a|1zaxa1=φ(c′a)F|a|1xa1=φ(c′a)x′|a|1. |
Then we have y=b∑m=acmxm1=−1∑m=ac′mx′|m|1+b∑m=0cmxm1∈R[x1,x′1,…,xn,x′n].
Corollary 4.24. If a LP seed Σ=(x,F) satisfied Condition 1.2, then the standard monomials in x1,x′1,…,xn,x′n form an R-basis of the LP algebra A(Σ).
Proof. It is immediately from Theorem 4.16 and Theorem 4.9.
Example 4.25. Consider the LP seed (x,F)={(a,bcd+1),(b,a+cd),(c,bd+1),(d,1+abc)}, it is easy to see that Condition 1.2 (i) (ii) (iii) hold. Since Mc=1 and b|(Fc−Mc), (iv) of Condition 1.2 holds. Besides, φ: b′↦cdb, c′↦bd+1c=c′, d′↦1d, Then it is clear that d−1∈ Im(φ) and b−1=φ(b′c′d′−d)∈ Im(φ). Thus by Theorem 4.9, we have L(Σ)=U(Σ).
Note that this LP seed is not a cluster seed or a generalized cluster seed for c∈Fa since a∉Fc.
The cluster seed is acyclic if and only if there exist a permutation σ such that for i>j, bσ(i),σ(j)≥0. Renumbering if necessary the indexes of the initial acyclic cluster, we assume that for i>j, bij≥0. Then by the exchange polynomials for cluster algebras, we conclude that the cluster seed is acyclic if and only if for any j, Fj=yj1⊕yj∏i>jxbiji+yj1⊕yj∏i<jx−biji.
Proposition 4.26. Condition 1.2 is equivalent to acyclicity and coprimeness of exchange polynomials for a cluster seed which is a also LP seed.
Proof. When a cluster seed is a LP seed, recall that (i) in Condition 1.2 is equivalent to coprimeness of exchange polynomials by Remark 4.11.
When a cluster seed satisfies the conditions (i) and (ii), for any j∈[2,n−1], since Fj is a binomial, we have Fj=xvj+xbj. If xi∈xbj for some i>j, then xj∈xvi for bjibij<0, which contradicts to the condition (ii). For j=n, Fn=1+xbn. From the definition of exchange polynomials for cluster algebras, we have xbn is of the form x|b1n|1⋯x|bn−1,n|n−1. For j=1, since for any j>1, we have bj1>0 by the above discussion, so that we obtain F1=1+x|b12|2⋯x|b1n|n. Then the cluster seed satisfied the conditions (i) and (ii) is acyclic. Besides, it is easy to see that when a cluster seed is acyclic, it satisfies the conditions (i) and (ii).Thus the conditions (i) and (ii) are equivalent to acyclicity of exchange polynomials.
Under the conditions of acyclicity and coprimeness, the cluster seed in fact satisfies (iii) and (iv) in Condition 1.2.
This project is supported by the National Natural Science Foundation of China (No.12071422 and No.12131015).
The authors declare there is no conflicts of interest.
[1] | 2023 Alzheimer's disease facts and figures. Alzheimers Dement 19: 1598-1695. https://doi.org/10.1002/alz.13016 |
[2] | National Institute on Aging: Alzheimer's Disease Fact Sheet. [cited 2024 May 26]. Available from: https://www.nia.nih.gov/health/alzheimers-and-dementia/alzheimers-disease-fact-sheet |
[3] |
Andrade-Guerrero J, Santiago-Balmaseda A, Jeronimo-Aguilar P, et al. (2023) Alzheimer's Disease: An Updated Overview of Its Genetics. Int J Mol Sci 24: 3754. https://doi.org/10.3390/ijms24043754 ![]() |
[4] |
Chandra S, Sisodia SS, Vassar RJ (2023) The gut microbiome in Alzheimer's disease: what we know and what remains to be explored. Mol Neurodegener 18: 9. https://doi.org/10.1186/s13024-023-00595-7 ![]() |
[5] |
Caldarelli M, Rio P, Marrone A, et al. (2024) Gut-Brain Axis: Focus on Sex Differences in Neuroinflammation. Int J Mol Sci 25: 5377. https://doi.org/10.3390/ijms25105377 ![]() |
[6] | Puderbaugh M, Emmady PD Neuroplasticity, StatPearls [Internet], StatPearls Publishing (2023). Available from: http://www.ncbi.nlm.nih.gov/books/NBK557811/ |
[7] |
Al-Thani HF, Ahmad MN, Younes S, et al. (2021) Genetic Variants Associated With Alzheimer Disease in the 22 Arab Countries: A Systematic Review. Alzheimer Dis Assoc Disord 35: 178-186. https://doi.org/10.1097/WAD.0000000000000447 ![]() |
[8] |
Maisam M, Khan MT, Lodhi MS, et al. (2023) Alzheimer's Disease; Mechanism, Mutations, and Applications of Nano-Medicine. Front Biosci (Landmark Ed) 28: 258. https://doi.org/10.31083/j.fbl2810258 ![]() |
[9] |
Jin P, Li Y, Li Y (2024) Meta-analysis of the association between C9orf72 repeats and neurodegeneration diseases. J Neurogene 38: 1-8. https://doi.org/10.1080/01677063.2024.2343672 ![]() |
[10] |
Bouzid H, Belk JA, Jan M, et al. (2023) Clonal hematopoiesis is associated with protection from Alzheimer's disease. Nat Med 29: 1662-1670. https://doi.org/10.1038/s41591-023-02397-2 ![]() |
[11] | National Institute on AgingStudy reveals how APOE4 gene may increase risk for dementia (2021). [cited 2024 December 25]. Available from: https://www.nia.nih.gov/news/study-reveals-how-apoe4-gene-may-increase-risk-dementia |
[12] |
Smith CJ, Ashford JW (2023) Apolipoprotein ɛ4-Associated Protection Against Pediatric Enteric Infections Is a Survival Advantage in Pre-Industrial Populations. J Alzheimers Dis 93: 907-918. https://doi.org/10.3233/JAD-221218 ![]() |
[13] |
Huggins LKL, Min SH, Kaplan S, et al. (2023) Meta-Analysis of Variations in Association between APOE ɛ4 and Alzheimer's Disease and Related Dementias Across Hispanic Regions of Origin. J Alzheimers Dis 93: 1095-1109. https://doi.org/10.3233/JAD-221167 ![]() |
[14] |
Oriá RB, Smith CJ, Ashford JW, et al. (2024) Pros and Cons of APOE4 Homozygosity and Effects on Neuroplasticity, Malnutrition, and Infections in Early Life Adversity, Alzheimer's Disease, and Alzheimer's Prevention. J Alzheimers Dis 100: S179-S185. https://doi.org/10.3233/JAD-240888 ![]() |
[15] |
Liew Y, Retinasamy T, Arulsamy A, et al. (2023) Neuroinflammation: A Common Pathway in Alzheimer's Disease and Epilepsy. J Alzheimers Dis 94: S253-S265. https://doi.org/10.3233/JAD-230059 ![]() |
[16] |
Chatterjee A, Kumar S, Roy Sarkar S, et al. (2024) Dietary polyphenols represent a phytotherapeutic alternative for gut dysbiosis associated neurodegeneration: A systematic review. J Nutr Bioche 129: 109622. https://doi.org/10.1016/j.jnutbio.2024.109622 ![]() |
[17] |
González Cordero EM, Cuevas-Budhart MA, Pérez Morán D, et al. (2022) Relationship Between the Gut Microbiota and Alzheimer's Disease: A Systematic Review. J Alzheimers Dis 87: 519-528. https://doi.org/10.3233/JAD-215224 ![]() |
[18] |
Bello-Corral L, Alves-Gomes L, Fernández-Fernández JA, et al. (2023) Implications of gut and oral microbiota in neuroinflammatory responses in Alzheimer's disease. Life Sci 333: 122132. https://doi.org/10.1016/j.lfs.2023.122132 ![]() |
[19] |
Chu Z, Han S, Luo Y, et al. (2024) Targeting gut-brain axis by dietary flavonoids ameliorate aging-related cognition decline: Evidences and mechanisms. Crit Rev Food Sci Nut 64: 10281-10302. https://doi.org/10.1080/10408398.2023.2222404 ![]() |
[20] | Waheed Janabi AH, Kamboh AA, Saeed M, et al. (2020) Flavonoid-rich foods (FRF): A promising nutraceutical approach against lifespan-shortening diseases. Iran J Basic Med Sci 23: 140-153. https://doi.org/10.22038/IJBMS.2019.35125.8353 |
[21] |
Uchida K, Meno K, Korenaga T, et al. (2024) Effect of matcha green tea on cognitive functions and sleep quality in older adults with cognitive decline: A randomized controlled study over 12 months. PLoS One 19: e0309287. https://doi.org/10.1371/journal.pone.0309287 ![]() |
[22] |
Ghorat F, Sepidarkish M, Saadattalab F, et al. (2024) The clinical efficacy of Olibanum gum chewing in patients with Mild-to-Moderate Alzheimer disease: A randomized Parallel-Design controlled trial. Neuropsychopharmacol Rep 44: 109-114. https://doi.org/10.1002/npr2.12398 ![]() |
[23] |
Galluzzi S, Marizzoni M, Gatti E, et al. (2024) Citrus supplementation in subjective cognitive decline: results of a 36-week, randomized, placebo-controlled trial. Nutr J 23: 135. https://doi.org/10.1186/s12937-024-01039-8 ![]() |
[24] |
Xiang L, Wang Y, Liu S, et al. (2023) Targeting Protein Aggregates with Natural Products: An Optional Strategy for Neurodegenerative Diseases. Int J Mol Sci 24: 11275. https://doi.org/10.3390/ijms241411275 ![]() |
[25] | Summat R, Waiwut P, Daodee S, et al. (2025) Phytomedicine Potential of Oroxylum indicum Root and Its Constituents: Targeting Alzheimer's Disease. Plants (Basel) 14: 223. https://doi.org/10.3390/plants14020223 |
[26] |
Laukkanen T, Kunutsor S, Kauhanen J, et al. (2017) Sauna bathing is inversely associated with dementia and Alzheimer's disease in middle-aged Finnish men. Age Ageing 46: 245-249. https://doi.org/10.1093/ageing/afw212 ![]() |
[27] |
Hunt AP, Minett GM, Gibson OR, et al. (2020) Could Heat Therapy Be an Effective Treatment for Alzheimer's and Parkinson's Diseases? A Narrative Review. Front Physiol 10: 1556. https://doi.org/10.3389/fphys.2019.01556 ![]() |
[28] |
Heinonen I, Laukkanen JA (2018) Effects of heat and cold on health, with special reference to Finnish sauna bathing. Am J Physiol Regul Integr Comp Physiol 314: R629-R638. https://doi.org/10.1152/ajpregu.00115.2017 ![]() |
[29] |
Lopez-Lee C, Torres ERS, Carling G, et al. (2024) Mechanisms of sex differences in Alzheimer's disease. Neuron 112: 1208-1221. https://doi.org/10.1016/j.neuron.2024.01.024 ![]() |
[30] |
Yeung CHC, Au Yeung SL, Kwok MK, et al. (2023) The influence of growth and sex hormones on risk of alzheimer's disease: a mendelian randomization study. Eur J Epidemiol 38: 745-755. https://doi.org/10.1007/s10654-023-01015-2 ![]() |
[31] |
Lv W, Du N, Liu Y, et al. (2016) Low Testosterone Level and Risk of Alzheimer's Disease in the Elderly Men: a Systematic Review and Meta-Analysis. Mol Neurobio 53: 2679-2684. https://doi.org/10.1007/s12035-015-9315-y ![]() |
[32] |
Mills ZB, Faull RLM, Kwakowsky A (2023) Is Hormone Replacement Therapy a Risk Factor or a Therapeutic Option for Alzheimer's Disease?. Int J Mol Sci 24: 3205. https://doi.org/10.3390/ijms24043205 ![]() |
[33] |
Chou YH, Sundman M, Ton That V, et al. (2022) Cortical excitability and plasticity in Alzheimer's disease and mild cognitive impairment: A systematic review and meta-analysis of transcranial magnetic stimulation studies. Ageing Res Rev 79: 101660. https://doi.org/10.1016/j.arr.2022.101660 ![]() |
[34] |
Hulshof LA, van Nuijs D, Hol EM, et al. (2022) The Role of Astrocytes in Synapse Loss in Alzheimer's Disease: A Systematic Review. Front Cell Neurosci 16: 899251. https://doi.org/10.3389/fncel.2022.899251 ![]() |
[35] |
Gowda P, Reddy PH, Kumar S (2022) Deregulated mitochondrial microRNAs in Alzheimer's disease: Focus on synapse and mitochondria. Ageing Res Rev 73: 101529. https://doi.org/10.1016/j.arr.2021.101529 ![]() |
[36] |
Malvaso A, Gatti A, Negro G, et al. (2023) Microglial Senescence and Activation in Healthy Aging and Alzheimer's Disease: Systematic Review and Neuropathological Scoring. Cells 12: 2824. https://doi.org/10.3390/cells12242824 ![]() |
[37] |
Ashford JW (2015) Treatment of Alzheimer's Disease: The Legacy of the Cholinergic Hypothesis, Neuroplasticity, and Future Directions. J Alzheimers Dis 47: 149-156. https://doi.org/10.3233/JAD-150381 ![]() |
[38] | Winslow BT, Onysko MK, Stob CM, et al. (2011) Treatment of Alzheimer disease. Am Fam Physician 83: 1403-1412. |
[39] | NHSTreatment: Alzheimer's disease (2024). [cited 2024 June 03]. Available from: https://www.nhs.uk/conditions/alzheimers-disease/treatment/ |
[40] |
Varadharajan A, Davis AD, Ghosh A, et al. (2023) Guidelines for pharmacotherapy in Alzheimer's disease - A primer on FDA-approved drugs. J Neurosci Rural Pract 14: 566-573. https://doi.org/10.25259/JNRP_356_2023 ![]() |
[41] |
Schneider LS, Dagerman KS, Higgins JP, et al. (2011) Lack of evidence for the efficacy of memantine in mild Alzheimer disease. Arch Neurol 68: 991-998. https://doi.org/10.1001/archneurol.2011.69 ![]() |
[42] |
Yaghmaei E, Pierce A, Lu H, et al. (2023) A causal inference study: The impact of the combined administration of Donepezil and Memantine on decreasing hospital and emergency department visits of Alzheimer's disease patients. PLoS One 18: e0291362. https://doi.org/10.1371/journal.pone.0291362 ![]() |
[43] |
Chen Y, Lai M, Tao M (2024) Evaluating the efficacy and safety of Alzheimer's disease drugs: A meta-analysis and systematic review. Medicine (Baltimore) 103: e37799. https://doi.org/10.1097/MD.0000000000037799 ![]() |
[44] |
Tan CC, Yu JT, Wang HF, et al. (2014) Efficacy and safety of donepezil, galantamine, rivastigmine, and memantine for the treatment of Alzheimer's disease: a systematic review and meta-analysis. J Alzheimers Dis 41: 615-631. https://doi.org/10.3233/JAD-132690 ![]() |
[45] |
Stepan J, Heinz DE, Dethloff F, et al. (2024) Inhibiting Hippo pathway kinases releases WWC1 to promote AMPAR-dependent synaptic plasticity and long-term memory in mice. Sci Signal 17: eadj6603. https://doi.org/10.1126/scisignal.adj6603 ![]() |
[46] |
Hemenway CS, Heitman J (1999) Calcineurin. Structure, function, and inhibition. Cell Biochem Biophys 30: 115-151. https://doi.org/10.1007/BF02737887 ![]() |
[47] |
Zeng J, Hu XF, Sun DS, et al. (2024) Alzheimer-like behavior and synaptic dysfunction in 3 × Tg-AD mice are reversed with calcineurin inhibition. Exp Brain Res 242: 1507-1515. https://doi.org/10.1007/s00221-024-06841-8 ![]() |
[48] |
Tan YZ, Fei DD, He XN, et al. (2019) L-type voltage-gated calcium channels in stem cells and tissue engineering. Cell Prolif 52: e12623. https://doi.org/10.1111/cpr.12623 ![]() |
[49] | ScienceDirect TopicsN Methyl-D-Aspartate Receptor-an overview (2021). [cited 2024 May 29]. Available from: https://www.sciencedirect.com/topics/medicine-and-dentistry/n-methyl-d-aspartate-receptor |
[50] |
Ramakrishna S, Radhakrishna BK, Kaladiyil AP, et al. (2024) Distinct calcium sources regulate temporal profiles of NMDAR and mGluR-mediated protein synthesis. Life Sci Alliance 7: e202402594. https://doi.org/10.26508/lsa.202402594 ![]() |
[51] |
Zhang N, Sui Y, Jendrichovsky P, et al. (2024) Cholecystokinin B receptor agonists alleviates anterograde amnesia in cholecystokinin-deficient and aged Alzheimer's disease mice. Alzheimers Res Ther 16: 109. https://doi.org/10.1186/s13195-024-01472-1 ![]() |
[52] |
De Jaco A, Bernardini L, Rosati J, et al. (2017) Alpha-7 Nicotinic Receptors in Nervous System Disorders: From Function to Therapeutic Perspectives. Cent Nerv Syst Agents Med Chem 17: 100-108. https://doi.org/10.2174/1871524916666160729111446 ![]() |
[53] |
Upadhayay S, Mehan S (2021) Targeting Nrf2/HO-1 anti-oxidant signaling pathway in the progression of multiple sclerosis and influences on neurological dysfunctions. Brain Disorders 3: 100019. https://doi.org/10.1016/j.dscb.2021.100019 ![]() |
[54] |
Yuan F, Jiang L, Li Q, et al. (2021) A Selective α7 Nicotinic Acetylcholine Receptor Agonist, PNU-282987, Attenuates ILC2s Activation and Alternaria-Induced Airway Inflammation. Front Immunol 11: 598165. https://doi.org/10.3389/fimmu.2020.598165 ![]() |
[55] | Cao K, Xiang J, Dong YT, et al. (2022) Activation of α7 Nicotinic Acetylcholine Receptor by its Selective Agonist Improved Learning and Memory of Amyloid Precursor Protein/Presenilin 1 (APP/PS1) Mice via the Nrf2/HO-1 Pathway. Med Sci Monit 28: e933978. https://doi.org/10.12659/MSM.933978 |
[56] |
Wang Y, Leak RK, Cao G (2022) Microglia-mediated neuroinflammation and neuroplasticity after stroke. Front Cell Neurosci 16: 980722. https://doi.org/10.3389/fncel.2022.980722 ![]() |
[57] |
Jiao L, Yu Z, Zhong X, et al. (2023) Cordycepin improved neuronal synaptic plasticity through CREB-induced NGF upregulation driven by MG-M2 polarization: a microglia-neuron symphony in AD. Biomed Pharmacother 157: 114054. https://doi.org/10.1016/j.biopha.2022.114054 ![]() |
[58] |
Tuli HS, Sandhu SS, Sharma AK (2014) Pharmacological and therapeutic potential of Cordyceps with special reference to Cordycepin. 3 Biotech 4: 1-12. https://doi.org/10.1007/s13205-013-0121-9 ![]() |
[59] |
Formolo DA, Cheng T, Yu J, et al. (2022) Central Adiponectin Signaling - A Metabolic Regulator in Support of Brain Plasticity. Brain Plast 8: 79-96. https://doi.org/10.3233/BPL-220138 ![]() |
[60] |
Yan XD, Qu XS, Yin J, et al. (2022) Adiponectin Ameliorates Cognitive Behaviors and in vivo Synaptic Plasticity Impairments in 3xTg-AD Mice. J Alzheimers Dis 85: 343-357. https://doi.org/10.3233/JAD-215063 ![]() |
[61] |
Rojas M, Chávez-Castillo M, Bautista J, et al. (2021) Alzheimer's disease and type 2 diabetes mellitus: Pathophysiologic and pharmacotherapeutics links. World J Diabetes 12: 745-766. https://doi.org/10.4239/wjd.v12.i6.745 ![]() |
[62] |
Kang P, Wang Z, Qiao D, et al. (2022) Dissecting genetic links between Alzheimer's disease and type 2 diabetes mellitus in a systems biology way. Front Genet 13: 1019860. https://doi.org/10.3389/fgene.2022.1019860 ![]() |
[63] |
Cai HY, Yang D, Qiao J, et al. (2021) A GLP-1/GIP Dual Receptor Agonist DA4-JC Effectively Attenuates Cognitive Impairment and Pathology in the APP/PS1/Tau Model of Alzheimer's Disease. J Alzheimers Dis 83: 799-818. https://doi.org/10.3233/JAD-210256 ![]() |
[64] |
Santana DA, Smith MAC, Chen ES (2023) Histone Modifications in Alzheimer's Disease. Genes (Basel) 14: 347. https://doi.org/10.3390/genes14020347 ![]() |
[65] |
Levinsky AJ, McEdwards G, Sethna N, et al. (2022) Targets of histone H3 lysine 9 methyltransferases. Front Cell Dev Biol 10: 1026406. https://doi.org/10.3389/fcell.2022.1026406 ![]() |
[66] |
Han JLT, Pang KKL, Ang SRX, et al. (2021) Inhibition of lysine methyltransferase G9a/GLP reinstates long-term synaptic plasticity and synaptic tagging/capture by facilitating protein synthesis in the hippocampal CA1 area of APP/PS1 mouse model of Alzheimer's disease. Transl Neurodegener 10: 23. https://doi.org/10.1186/s40035-021-00247-0 ![]() |
[67] |
Asih PBS, Rozi IE, Dewayanti FK, et al. (2022) Efficacy and safety of dihydroartemisinin-piperaquine for the treatment of uncomplicated Plasmodium falciparum and Plasmodium vivax malaria in Papua and Sumatra, Indonesia. Malar J 21: 95. https://doi.org/10.1186/s12936-022-04101-0 ![]() |
[68] |
Zhao Y, Long Z, Ding Y, et al. (2020) Dihydroartemisinin Ameliorates Learning and Memory in Alzheimer's Disease Through Promoting Autophagosome-Lysosome Fusion and Autolysosomal Degradation for Aβ Clearance. Front Aging Neurosci 12: 47. https://doi.org/10.3389/fnagi.2020.00047 ![]() |
[69] |
Xia L, Pang Y, Li J, et al. (2021) Dihydroartemisinin Induces O-GlcNAcylation and Improves Cognitive Function in a Mouse Model of Tauopathy. J Alzheimers Dis 84: 239-248. https://doi.org/10.3233/JAD-210643 ![]() |
[70] |
Herrmann N, Ruthirakuhan M, Gallagher D, et al. (2019) Randomized Placebo-Controlled Trial of Nabilone for Agitation in Alzheimer's Disease. Am J Geriatr Psychiatry 27: 1161-1173. https://doi.org/10.1016/j.jagp.2019.05.002 ![]() |
[71] |
van den Elsen GA, Ahmed AI, Verkes RJ, et al. (2015) Tetrahydrocannabinol for neuropsychiatric symptoms in dementia: A randomized controlled trial. Neurology 84: 2338-2346. https://doi.org/10.1212/WNL.0000000000001675 ![]() |
[72] |
Stone NL, Murphy AJ, England TJ, et al. (2020) A systematic review of minor phytocannabinoids with promising neuroprotective potential. Br J Pharmacol 177: 4330-4352. https://doi.org/10.1111/bph.15185 ![]() |
[73] |
Davidson M, Stanciu GD, Rabinowitz J, et al. (2025) Exploring novel therapeutic strategies: Could psychedelic perspectives offer promising solutions for Alzheimer's disease comorbidities?. Dialogues Clin Neurosci 27: 1-12. https://doi.org/10.1080/19585969.2025.2480566 ![]() |
1. | Junyuan Huang, Xueqing Chen, Fan Xu, Ming Ding, Some properties of generalized cluster algebras of geometric type, 2024, 660, 00218693, 270, 10.1016/j.jalgebra.2024.07.013 |