Genetic and physiological basis of Alzheimer’s disease: A review
Alzheimer's disease (AD) is the primary cause of dementia globally and the most prevalent neurodegenerative disease. Progressive memory loss, cognitive impairment, behavioral abnormalities, and loss of functional independence are its hallmarks. The development of Alzheimer’s disease is strongly associated with both genetic predisposition and physiological dysfunctions within the central nervous system. Modern scientific advances have revealed that multiple genes, including APOE, APP, PSEN1, and PSEN2, contribute to disease susceptibility and progression. Furthermore, the disease's key clinical features include physiological anomalies such amyloid-beta buildup, tau hyper-phosphorylation, neuro-inflammation, oxidative stress, mitochondrial dysfunction, and synaptic degeneration. Additionally, recent research highlights the importance of cellular senescence, non-coding RNAs, and epigenetics in the pathophysiology of AD. Understanding the relationship between genetics and physiology provides new opportunities for early diagnosis and targeted therapeutic interventions. This article reviews the current understanding of the genetic and physiological mechanisms underlying Alzheimer’s disease and discusses modern approaches for diagnosis and treatment.