Brain regions affected by Alzheimer's disease

Brain regions affected by Alzheimer's disease (AD) refer to the specific neuroanatomical structures that undergo progressive atrophy and pathological protein accumulation throughout the disease course. Initial degeneration typically starts in the transentorhinal and entorhinal cortex before spreading to the hippocampus, which is essential for the formation of new memories [4, 6, 7]. As AD advances, the pathology extends to the amygdala and the cerebral cortex—particularly the temporal, frontal, and parietal lobes—leading to deficits in language, executive function, and spatial awareness [2, 4, 16]. These areas are characterized by the presence of amyloid-beta plaques and neurofibrillary tau tangles, which are the primary hallmarks of the disease [1, 19]. While these regions themselves are anatomical locations rather than molecular targets, they contain the protein aggregates and dysfunctional neurotransmitter systems that therapeutics aim to modulate [9, 12]. Understanding the spatial progression of damage in these regions is crucial for the development of neuroimaging biomarkers and the delivery of disease-modifying therapies like monoclonal antibodies [15, 20].

Other names

Alzheimer's vulnerable brain regionsAD-affected neuroanatomyLimbic and cortical regions in Alzheimer'sBrain regions showing Alzheimer's pathology

Current pharmacological interventions act within these regions through several mechanisms: acetylcholinesterase inhibition to increase synaptic acetylcholine, NMDA receptor antagonism to mitigate glutamate-induced excitotoxicity, and monoclonal antibody-mediated clearance of amyloid-beta plaques [9, 12, 19, 20].