Aging and Neurodegeneration Flashcards
(26 cards)
Canadian Age Demographic
Average age of Canadians is going up, we will need to change strategies in career planning, medical system, and technology development
Are younger adults good at forecasting the experiences of older adults?
I don’t think that younger adults are good because they have not yet experienced the things that older adults have
also changes that come with aging are different between individuals
4 physical changes with aging
Volume loss: varies across structures (frontal, basal G, temporal). Shrinks 5% per decade after 40, accelerating after 70
Neurotransmitter depletion: dopamine and serotonin levels decline
Decreased cerebral blood flow
Acuumulation of white matter damage
Normal brain changes
Small degree of alzheimers pathology, some neuronal loss
Abnomal brain changes
Mild cognitive impairments
What counts as MCI?
Changes that are serious to be noticed by others
Cognitive difficulties in excess of normal aging
MCI can represent alzheimers disease prodrome
Can include higher levels of forgetfulness
Common socioeconomic changes of aging
Smaller but intentionally chosen social networks with higher proportion of emotionally close partners
Greater emotional stability and emotional complexity in daily life
Normal aging in memory performance and activities of daily living
Long-term, working memory will decline over time, large drop in the 70s
MCI
Changes in attention and memory serious enough to be noticed by the person, friends, and family
Activities of daily living are fine
Symptoms of Alzheimers Disease
Earlier symptoms include confusion, irritability, anxiety, and deterioration of speech
Later symptoms difficulties with even simple responses or behaviours
Make memory and activites of daily living poor
Identify symptoms of AD
Earlier symptoms: confusion, irritability, anxiety, and deterioration of speech
Later symptoms difficulties with even simple responses or behaviours
Predictors of AD from MCI
Older age, APOE e4 status
Medial temporal lobe atrophy on MRI, Positive amyloid on PET scan,
Molecular markers in CSF
Apo-E e4 status
If you carry two copies of the APOE, then you are more likely develop AD early compared to non-carriers and one copy carriers
3 defining structural changes of AD
Neurofibrillary tangles, amyloid plaques, volume loss
What are Neurofibrillary tangles?
Tau proteins are hyperphosphorylated, misfolded, and built up
Act as prions that cause fatal damage
Inside the cell, compromising the cell structure
What are amyloid plaques?
Beta amyloid proteins take on large collapsed forms, building up in the extracellular space
Kills cells on the inside. Typical collapses are taken away by the body, but excess protein collapsing builds up.
Volume loss relative to AD
Progressive loss of both cells and synapses, first in medial temporal lobe structures involved in memory
includes: etorhinal cortex, amygdala, hippocampus
Amyloid cascade hypothesis
Amyloid plaques are primary symptoms, and cause other symptoms.
Trisomy 21 - down syndrome: people have more chromosome, where amyloid proteins are made. 100% of people with down syndrome will develop amyloid plaques
Problem with amyloid cascade hypothesis
Some people have plaques without cognitive consequences
Amyloid drugs don’t cure AD
Neurofibrillary hypothesis
Misfolded tau is causal agent
Tau pathology correlates with dognitive impairment better than beta amyloid
Problem with neurofibrillary hypothesis
Tau mutations alone do not cause beta amyloids
Treatments for AD
Cholinergic agonists, NMDA receptor antagonist, target modifiable risk factors
Cholinergic Agonists
Prevents decline in learning and memory
NMDA receptor antagonist
Reduces actions of glutamate, preventing damage to neurons
