Lecture 8 Flashcards
What are phonemic fluency and semantic fluency test, and how are they related to Alzheimer’s disease?
Phonemic fluency is the ability to name as many words as possible that start with a specific letter (e.g., words starting with “B”). Semantic fluency involves naming items from a specific category (e.g., animals). These tests are sometimes used to assess cognitive function, and deficits in fluency tasks can be indicative of cognitive impairment, including Alzheimer’s disease.
What is the relationship between Alzheimer’s disease and dementia?
Alzheimer’s disease is a type of dementia. Dementia is a broader term that refers to the gradual loss of brain function due to physical changes in the brain, and Alzheimer’s is one of the specific conditions falling under this category.
How does age influence the risk of developing Alzheimer’s disease?
The risk of developing Alzheimer’s disease increases with age. For example, every five years from age 65 onwards, the risk of developing Alzheimer’s doubles. This is why Alzheimer’s is more common in aging populations.
What are plaques and neurofibrillary tangles in the context of Alzheimer’s disease?
Plaques are clumps of beta-amyloid protein, while neurofibrillary tangles are tangled fibers found in the brains of individuals with Alzheimer’s disease. Both are pathological hallmarks of the condition. Plaques are formed from the accumulation of beta-amyloid protein, and neurofibrillary tangles involve the abnormal tangling of microtubules within neurons.
What is the role of the APOE4 gene in Alzheimer’s disease risk?
The APOE4 gene is associated with an increased risk of developing Alzheimer’s disease. If an individual has a parent with early-onset Alzheimer’s disease and carries the APOE4 gene variant, their risk of developing the disease is elevated. However, not everyone with this gene variant will develop Alzheimer’s, and other factors also play a role.
How does education and social isolation relate to Alzheimer’s disease risk?
Higher levels of education early in life are associated with a reduced risk of developing Alzheimer’s disease. Staying intellectually engaged and continuing education throughout life may contribute to cognitive resilience. Social isolation is considered a risk factor, as maintaining social connections and engagement can have a protective effect on cognitive function.
What role does acetylcholine play in normal brain function, and how is it related to Alzheimer’s disease?
Acetylcholine is a neurotransmitter that carries messages across synapses in the brain. In Alzheimer’s disease, there is a loss of cholinergic projection neurons in the basal forebrain, leading to reduced acetylcholine levels. This deficit in acetylcholine transmission contributes to cognitive impairment.
How do cholinesterase inhibitors (AChE-Is) like Donepezil and Rivastigmine work in the treatment of mild to moderate Alzheimer’s disease?
Cholinesterase inhibitors, such as Donepezil and Rivastigmine, are used to treat mild to moderate Alzheimer’s disease. They work by blocking the action of cholinesterase enzymes, which break down acetylcholine. By inhibiting cholinesterase, these drugs increase the availability of acetylcholine in the brain, allowing it more time to transmit messages between neurons.
What is the role of Amyloid Precursor Protein (APP) in synaptic plasticity, and how is Beta Amyloid (Aβ) produced?
Amyloid Precursor Protein (APP) appears to have a role in synaptic plasticity, which is essential for learning and memory. Beta Amyloid (Aβ) is produced when APP is cleaved by enzymes called secretases, specifically beta and gamma secretases. This cleavage leads to the formation of toxic Beta-Amyloid fragments.
What happens in Alzheimer’s disease when Beta Amyloid is overproduced, and what are the consequences?
In Alzheimer’s disease, Beta Amyloid (Aβ) is overproduced, leading to the formation of fibrillar plaques on the outside surface of cells. These plaques are distributed throughout the cortex and are considered a pathological hallmark of the disease. Beta-Amyloid is sticky and forms toxic clumps or plaques, which may contribute to neurodegeneration.
Why is the location of amyloid plaques in the brain not always closely related to the symptoms of Alzheimer’s disease?
Although amyloid plaques are a characteristic feature of Alzheimer’s disease, their precise location in the brain does not always correlate with the specific cognitive and behavioral symptoms experienced by individuals with the condition. This complexity highlights that Alzheimer’s disease involves multiple pathological processes beyond amyloid plaques.
What has been the status of clinical trials involving drugs targeting Beta Amyloid, such as Aducanumab (2021), in the treatment of Alzheimer’s disease?
Clinical trials of drugs targeting Beta Amyloid, like Aducanumab, have faced challenges and mixed results. As of 2021, clinical trials of some drugs aimed at reducing Beta Amyloid accumulation have been disappointing in terms of their impact on cognitive decline and disease progression. Researchers continue to investigate potential treatments for Alzheimer’s disease.
What is the relationship between the appearance of neurofibrillary tangles (NFTs) and the progression of Alzheimer’s disease?
NFTs, which are composed of aggregated Tau protein, tend to appear initially in the transentorhinal (perirhinal) cortex and then spread to neighboring brain regions as Alzheimer’s disease progresses. This progression of NFTs closely parallels the cognitive deficits and decline observed in individuals with Alzheimer’s disease.
What is the risk of developing Alzheimer’s disease if one of your parents has familial (early-onset) Alzheimer’s?
If one of your parents has familial (early-onset) Alzheimer’s disease due to genetic mutations, there is a 50% chance that you may inherit the mutated gene and be at risk of developing the disease yourself.
What are the three major variations (alleles) of the APOE gene associated with Alzheimer’s disease risk?
The three major variations (alleles) of the APOE gene linked to Alzheimer’s disease risk are APOE2, APOE3, and APOE4. These alleles produce slightly different forms of the Apolipoprotein E (ApoE) protein.
