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
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
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