A COMPREHENSIVE REVIEW ON THE PATHOPHYSIOLOGY, EXPERIMENTAL MODEL OF ALZHEIMER DISEASE

Alzheimer’s disease is a progressive neurological disorder and the main cause of dementia worldwide. It imposes a substantial socioeconomic and healthcare burden, especially as people age. This article discusses the complex pathophysiology of Alzheimer’s disease, including the β-amyloid cascade, tau hyperphosphorylation, cholinergic dysfunction, excitotoxicity, oxidative stress, chronic neuroinflammation, and neurotransmitter deficits. Genetic variables such as mutations in APP, PSEN1, PSEN2, and the APOE4 allele are reviewed, as well as environmental and metabolic aspects that contribute to both early- and late- onset illnesses. The article summarizes preclinical models used to investigate Alzheimer’s disease, including chemically induced genetically modified and non-genetic models. Each model is useful for assessing treatments and targets distinct disease pathways. A brief overview is also given of recent advancements in gnostic biomarkers and disease-modifying treatments. The article’s overall message highlights the intricacy of Alzheimer disease pathogenesis and the value of a variety of study models in promoting early detection, treatment approaches, and preventative initiatives.