Molecular mechanisms of Alzheimer's disease | ||||
| Records of Pharmaceutical and Biomedical Sciences | ||||
| Article 14, Volume 6, Issue 3, April 2022, Page 165-171 PDF (531.49 K) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/rpbs.2022.165136.1176 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
Salma Selim  1; Reem Mohamed Hazem2; Norhan Mohamed El-Sayed 3; Hassan Mahmoud Mohamed Elfayoumi1
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| 1Department of Pharmacology and toxicology, Faculty of Dentistry, Sinai University | ||||
| 2Department of Pharmacology and toxicology, Faculty of Pharmacy, Suez Canal University | ||||
| 3Department of Pharmacology & Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia 41522, Egypt | ||||
| Abstract | ||||
| Alzheimer's disease is characterized by cognitive decline, progressive neurodegeneration, the development of amyloid βeta-containing plaques and tau hyperphosphorylated neurofibrillary tangles. Initial signs of the neurodegenerative process in Alzheimer's disease include loss of neurons and synaptic impairment. An imbalance between the amounts of amyloid βeta production, aggregation, and clearance leads to amyloid βeta accumulation due to abnormal cleavage of amyloid precursor protein. Furthermore, abnormal tau phosphorylation, which affects tau structure, distribution, and function in neurons, is recognized as a crucial pathogenic mechanism. The primary question driving current research is "What is the primary mechanism leading to the molecular development of Alzheimer's disease pathology?" This review provides an overview of the current knowledge of the molecular processes that result in the production of amyloid βeta, hyperphosphorylation of tau, and amyloid βeta-induced neurotoxicity, including calcium dyshomeostasis, mitochondrial dysfunction, increased oxidative stress, cholinergic dysfunction, and neuroinflammation, which ultimately lead to neuronal dysfunction and neuronal loss. | ||||
| Keywords | ||||
| Alzheimer's disease; amyloid βeta; hyperphosphorylated tau; oxidative stress | ||||
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