Final answer:
Abnormal, age-related structural changes in neurons, as seen in Alzheimer's disease, involve the formation of amyloid plaques and neurofibrillary tangles that lead to neuron death and cognitive impairments. Proteins such as beta-amyloid and hyperphosphorylated tau play key roles in the development of these changes. The resulting brain degeneration has a profound impact on memory, mood, and personality functions.
Step-by-step explanation:
Research on abnormal, age-related structural changes in neurons shows that diseases like Alzheimer's disease (AD) involve significant neurodegeneration. Key features of this condition include the buildup of amyloid plaques and neurofibrillary tangles within the brain. These changes are linked to synapse loss and neuron death, which have profound effects on cognitive functions such as memory, mood, and personality.
Two major pathological hallmarks of AD are hyperphosphorylated tau tangles and beta-amyloid (AĆ) plaques. The plaques interfere with glutamate transport, potentially leading to excitotoxicity, and influence the presence and activity of glutamate receptors. Recent studies suggest that these abnormal protein accumulations disrupt the normal cellular processes critical for neuron communication, leading to memory impairment and dementia. Additionally, the degeneration of corticostriatal connections may contribute to the reduced cognitive abilities often seen in the elderly.
Other neurodegenerative diseases, such Parkinson's disease, are similarly associated with misfolded or malfunctioning proteins, leading to toxic effects on specific brain cells and regions. Overall, these findings underline the complexity of neurodegenerative disorders and the multifaceted ways in which they affect the central nervous system.