Alzheimer's Disease and Neuroinflammation: Exploring Cellular and Molecular Mechanisms

Alzheimer’s disease is a progressive neurodegenerative disorder characterized by cognitive decline, memory impairment, and behavioral changes. It is the most common cause of dementia, primarily affecting the elderly population. The pathological hallmarks of Alzheimer’s disease include extracellular amyloid-beta plaques, intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein, neuroinflammation, and synaptic dysfunction. This review explores the cellular and molecular mediators involved in the progression of Alzheimer’s disease, highlighting the role of amyloid-beta accumulation, tau pathology, neuroinflammatory responses mediated by microglia and astrocytes, oxidative stress, and inflammatory mediators. A deeper understanding of these cellular and molecular mechanisms is crucial for developing targeted therapeutic strategies to slow or halt disease progression.