Alzheimer’s disease
A closer look at neurodegeneration and mitochondrial dysfunction in cardiac health
Understanding Alzheimer’s Disease
Alzheimer’s disease (AD) is a chronic, progressive neurodegenerative disorder and the most common cause of dementia in the elderly population. It is characterized pathologically by the extracellular accumulation of amyloid-beta (Aβ) plaques and the intracellular formation of neurofibrillary tangles composed of hyperphosphorylated tau protein, predominantly affecting the hippocampus and cerebral cortex.
From Proteinopathy to Memory Loss
These proteinopathies are associated with synaptic dysfunction, neuronal loss, and brain atrophy, particularly in regions involved in memory and cognition. Clinically, AD manifests as insidious onset and gradual progression of memory impairment, followed by deficits in language, visuospatial skills, executive function, and eventually, profound functional dependence.
Genetic Risk and Ongoing Research
While both sporadic and familial forms exist, the majority of cases are late-onset and multifactorial, influenced by genetic risk factors such as the APOE ε4 allele and various environmental contributors. Current therapies provide only symptomatic relief, with ongoing research aimed at identifying disease-modifying interventions targeting amyloid, tau, inflammation, and other pathogenic pathways.
