Outline the major pathological features of Alzheimer's disease and how they relate to cognitive decline.

Outline the major pathological features of Alzheimer's disease and how they relate to cognitive decline.

• A. The disease is caused exclusively by demyelination of white matter tracts.
• B. Lewy bodies are the primary pathology causing Alzheimer’s-like symptoms.
• C. Neurofibrillary tangles occur without amyloid-beta plaques and explain all symptoms.
• D. Amyloid-beta plaques and tau neurofibrillary tangles disrupt synaptic function and neuronal viability; hippocampal and deep cortical atrophy lead to memory impairment and later executive dysfunction.

Answer: (D)

Alzheimer's disease is defined by two key protein abnormalities: amyloid-beta plaques outside neurons and tau neurofibrillary tangles inside neurons. These pathological changes disrupt how neurons communicate and how they transport essential nutrients and signals along their axons, leading to synaptic dysfunction and ultimately neuron death. The damage starts in the hippocampus and nearby medial temporal regions, including the entorhinal cortex, which are crucial for forming and retrieving new memories. As the disease progresses, atrophy spreads to deep cortical areas, especially in temporal, parietal, and then frontal regions, which broadens the cognitive impact to include language, visuospatial skills, and eventually executive functions. This pattern explains why memory impairment appears early and becomes more global over time as the affected brain regions expand. In essence, the combination of plaques and tangles undermines neural networks, and the resulting hippocampal and deep cortical atrophy tracks closely with the observed cognitive decline.

Alzheimer's disease is defined by two key protein abnormalities: amyloid-beta plaques outside neurons and tau neurofibrillary tangles inside neurons. These pathological changes disrupt how neurons communicate and how they transport essential nutrients and signals along their axons, leading to synaptic dysfunction and ultimately neuron death. The damage starts in the hippocampus and nearby medial temporal regions, including the entorhinal cortex, which are crucial for forming and retrieving new memories. As the disease progresses, atrophy spreads to deep cortical areas, especially in temporal, parietal, and then frontal regions, which broadens the cognitive impact to include language, visuospatial skills, and eventually executive functions. This pattern explains why memory impairment appears early and becomes more global over time as the affected brain regions expand. In essence, the combination of plaques and tangles undermines neural networks, and the resulting hippocampal and deep cortical atrophy tracks closely with the observed cognitive decline.