Akademik Veri Yönetim Sistemi
Neurodegenerative Diseases: Pathologies, Mechanisms, and Treatment Strategies, CRC Press, ss.56-64, 2026
Alzheimer's disease (AD) is the most common form of dementia, marked by progressive cognitive decline and brain atrophy. Its hallmark features include extracellular amyloid-β (Aβ) plaques and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein. While early-onset AD is often linked to mutations in APP, PSEN1, and PSEN2, the APOE ε4 allele is a major genetic risk factor in sporadic, late-onset cases. The amyloid hypothesis posits Aβ accumulation as a key pathogenic trigger; however, oxidative stress, cholinergic deficits, and neuroinflammation also play critical roles. Current pharmacological treatments—acetylcholinesterase inhibitors and NMDA receptor antagonists—offer modest symptomatic relief without altering disease progression. Recently, monoclonal antibodies targeting Aβ, such as lecanemab and donanemab, have shown potential in slowing cognitive decline. Non-pharmacological approaches, including cognitive training and regular physical activity, are also being explored to maintain cognitive function. Emerging evidence suggests that the gut–brain axis and gut microbiota dysbiosis may contribute to neuroinflammation and disease progression, revealing new therapeutic targets. Microbiota-based interventions are gaining interest as potential adjunct therapies. Overall, the multifactorial nature of AD calls for integrative treatment strategies that combine conventional and innovative approaches to improve patient outcomes.