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Human Physiology
TOPIC – Alzheimer’s disease
Key Takeaway: “The information from ChatGPT includes both scientific and general content. However, the lack of clarity and/or accuracy in this data restricts its usefulness for learning purposes.”
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Chat-GPT Prompt: Act as a graduate student in a medical biotechnology program at a Canadian University studying human physiology course, and explain the question with relevant references and citations in APA 7th edition style format.
Question: For Alzheimer disease, where do the Aβ peptides and tau aggregates are formed in the brain?
Chat GPT Response:
Title: Formation of Aβ Peptides and Tau Aggregates in Alzheimer’s Disease Pathology
As a graduate student in a medical biotechnology program at a Canadian University studying human physiology, I am pleased to provide you with an explanation of where the Aβ peptides and tau aggregates are formed in the brain in relation to Alzheimer’s disease, supported by relevant references and citations in APA 7th edition style format.
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the accumulation of abnormal protein aggregates in the brain, primarily amyloid-beta (Aβ) plaques and tau neurofibrillary tangles (NFTs). The formation of Aβ peptides and tau aggregates occurs within specific regions of the brain, contributing to the cognitive decline observed in affected individuals.
Formation of Aβ Peptides:
Aβ peptides are derived from the amyloid precursor protein (APP) through sequential proteolytic cleavages by β-secretase and γ-secretase enzymes. The accumulation of Aβ peptides leads to the formation of insoluble amyloid plaques, one of the hallmark pathological features of AD. These plaques are primarily composed of Aβ42, a longer form of Aβ peptide, which has been implicated in the neurotoxic effects observed in AD.
Aβ peptides are initially formed in various brain regions, particularly in areas associated with memory and cognition. The two major brain regions where Aβ peptides are prominently generated are the neocortex and the hippocampus. Studies have shown that Aβ peptides accumulate first in neocortical regions, such as the frontal cortex, before spreading to other brain regions as the disease progresses (Selkoe & Hardy, 2016). The hippocampus, a vital structure for memory formation, is also significantly affected early in AD, leading to memory impairment.
Formation of Tau Aggregates:
Tau aggregates, on the other hand, are primarily composed of hyperphosphorylated tau protein. In healthy neurons, tau protein stabilizes microtubules and assists in maintaining the neuron’s cytoskeletal structure. However, in AD, tau becomes hyperphosphorylated, leading to its misfolding and subsequent aggregation into paired helical filaments (PHFs) and NFTs.
The formation of tau aggregates begins in the entorhinal cortex and the transentorhinal region, which are closely connected to the hippocampus. These regions are critical for memory and spatial navigation. As the disease progresses, tau pathology spreads to other brain regions, including the hippocampus and neocortex (Braak & Braak, 1991). This progressive spread of tau aggregates correlates with the clinical progression of cognitive decline in AD.
In summary, Aβ peptides and tau aggregates, the hallmark pathological features of Alzheimer’s disease, are formed in specific regions of the brain. Aβ peptides are initially generated in the neocortex and hippocampus, while tau aggregates form in the entorhinal cortex and transentorhinal region before spreading to other brain areas. The accumulation of these abnormal protein aggregates contributes to the neurodegeneration and cognitive decline observed in AD.
References:
- Selkoe, D. J., & Hardy, J. (2016). The amyloid hypothesis of Alzheimer’s disease at 25 years. EMBO Molecular Medicine, 8(6), 595-608.
- Braak, H., & Braak, E. (1991). Neuropathological stageing of Alzheimer-related changes. Acta Neuropathologica, 82(4), 239-259.
Last Updated November 20, 2024
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