Chapter 10 Flashcards
1
Q
dementia
A
loss of cognitive ability
2
Q
Alzheimer’s disease (AD)
A
- leading cause of dementia
- degeneration of the brain, especially the cortex and limbic system (hippocampus)
- sulci especially wide, indicating degeneration of the cortex
3
Q
preclinical AD
A
- no symptoms
- measurable brain changes
4
Q
mild cognitive impairment due to AD
A
- very mild symptoms that do not interfere with everyday activities
- measurable brain changes plus subtle problems with memory and thinking
5
Q
mild AD
A
- symptoms interfere with some everyday activities
- memory problems (especially new memories), word finding difficulties, trouble with planning/organization
6
Q
moderate AD
A
- symptoms interfere with many everyday activities
- memory problems (personal history), feeling moody and/or withdrawn, wandering/getting lost, personality changes (e.g., suspiciousness and delusions)
7
Q
severe AD
A
- symptoms interfere with most everyday activities
- loss of awareness (of recent events and surroundings), difficulty with communication, vulnerable to infections (especially pneumonia)
8
Q
dementia memory lapses
A
- not recognizing family members
- forgetting to serve meal just prepared
- substituting inappropriate words
- getting lost in own neighborhood
9
Q
key characteristics of AD
A
- cognitive deficits: profound memory loss (anterograde/retrograde), language (anomic, empty, circumlocutory), visuospatial disturbance
- behavioral deficits: no significant early changes in personality, unawareness or denial of illness, psychosis
- no sensory or motor deficits
- age of onset 70s-80s
10
Q
pathology of AD
A
- neurofibrillary tangles (tau protein)
- amyloid plaques (beta amyloid)
11
Q
beta-amyloid plaques (senile plaques)
A
- large amyloid precursor proteins (APP) are cut into fragments called beta-amyloid fragments via the enzyme beta-secretase
- the fragments clump into plaques outside of the cell and destroy dendrites, reducing dendritic branching affecting cognition
- they also initiate an immune response from the microglia that also increase the spread of plaques killing neurons
12
Q
neurofibrillary tangles
A
- inside of the neuron
- microtubules are bound together with tau proteins
- if tau proteins change their structure, the microtubules fall apart
- the tau proteins clumps together in tangles, killing the neuron
13
Q
cytoskeleton of neuron
A
- gives the neuron its shape
“bones” are: - microtubules: big, run longitudinally down neurites, made of tubulin, microtuble-associated proteins (MAPs) regulate microtuble assembly and function; changes in MAPs called tau implicated in AD
- microfilaments: solid, thinner, actin
- neurofilaments: intermediate filaments, individual long protein molecules
14
Q
microtubule-associated proteins (MAPs)
A
- tau/MAPs can function as cross-bridges connecting microtubules
- can affect microtubule rigidity
- brain uses a transport system to help move around the nutrients it needs; system is made of proteins like railroad tracks guiding trains guide nutrients where they need to go; proteins that keep the tracks straight are tau proteins
15
Q
causes of AD
A
- genetics (likely several genes)
- immune responses initiated by microglia
- sleep imbalance
16
Q
genetics of AD
A
- amyloid precursor protein (APP) (familiar early onset of AD)
- presenilin (PS) 1 and 2 (familial early onset of AD)
- Down’s Trisomy 21
- ApoE4 increases risk of late onset of AD