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31 Cards in this Set
- Front
- Back
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what does it mean that dimentia is a syndrome?
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- it is not one disorder
- it is a group of symptoms that can be caused by different diseases & conditions |
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what is an important distinguishing factor between aging and dementia?
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- normal aging it is still possible to learn new things, although with again more time is required
- normal aging does not impeded normal daily activity |
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what is cortical dementia? subcortical?
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- when one area of brain's cortex is effected (memory, language, social behavior, thinking)
- subcortical is when part of brain below cortex are effected (emotions & movement) |
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what does progressive dementia mean?
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- different classification of dementia
- means that dementia gets worse over time, gradually interferes with more cognitive abilities - this is different than sudden loss of ability in more step wise pattern |
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what is primary vs secondary dementia?
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- primary dementia we don't know that the cause is (ex Alzheimer's)
- secondary is dude to physical disease or injury (can be cured if take away stimulus) |
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what are some examples of reversible secondary dementia?
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- infections
- hypothyroidism, hypoglycemia, B12 - medications, hematomas - poisoning - brain tumors - anoxia |
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what is the most common and second most common cause of dementia?
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- most common: alzheimer's disease
- second most common: vascular dementia |
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what is an example of progressive step-wise dementia?
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- vascular dementia (multi-infarct dementia)
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what are some risk factors for multi-infarct dementia?
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- series of small strokes, stepwise manner, sudden changes in ability
- risk factors: diabetes, atherosclerosis, HBP, smoking, strokes |
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what is lewy body dementia?
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- one of most common types of progressive dementia
- caused by build up of lewy-bodies & accumulated alpha-synuclein protein (inside nuclei of neurons) - areas of brain that control memory & motor control - therefore looks like AD & parkinsonian symptoms - live around 7 years after symptoms begin |
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what kind of dementia does alpha-synuclein protein build up cause?
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- lewy body dementia
- present with AD like symptoms & also parkinsonian shuffling gait & flexed posture, etc. |
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what is frontotemporal dementia?
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- 50% inherited
- onset between 40-65 - behavioral changes (socially inappropriate) & problems with language (difficulty making or understanding speech) |
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with young patients what kind of dementia do you have to think about?
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- frontotemporal dementia
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what is dementia pugilistica?
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- CTE
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what are the specific lesions in AD?
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- extraneuronal beta amyloid plaque accumulation
- intraneuronal accumulation of hyperphosphorylated tau (neurofribrillary tangles) |
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what are the specific lesions in frontotemporal dementia?
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- accumulation of hyperphosphorylated tau - pick bodies
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in AD where do the lesions typically appear?
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- tangles initially appear in the hippocampus & spread to cortex
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what is APP? how is it cleaved?
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- amyloid precursor protein (APP) - source of amyloid beta protein
- APP can be processed by beta & gamma secretases to generate Abeta (normally would be processes by alpha secretase) |
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what do teh frontal, parietal, occipital & temporal lobes do in terms of memory? hippocampus?
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- frontal lobes: short term memory
- parietal lobes: sensory information - occipital lobes: visual memory - temporal lobes: memory storage - hippocampus: sens memories to appropriate section of cerebrum & recalls them when necessary |
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what happens to brain volume in AD?
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- atrophy, dilation of the ventricles
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how is familial AD define? Are most of AD inherited?
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- having 2+ family members with AD = 25% of cases
- no majority are genetic & environmental interactions |
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what happens with late-onset familial vs early-onset familial AD?
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- these are both pretty rare, early-onset being <2%
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what is the biggest risk factor for alzheimers?
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- age, more common in women, genetic component, head trauma, vascular disorders, etc.
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what is the genetic basis for early onset AD?
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- mutations in APP & PSEN1 (presenilin) - a component of gamma secretase
- increase Abeta42 |
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what is the strongest genetic risk factor for late onset AD?
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- ApoE allele (normally involved in lipid regulation, but also helps clear beta amyloid from the brain)
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what is the pentrance/prevalence for early onset vs later onset AD genes?
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- earlier onset (APP, PSEN1) = high penetrance, but very little prevalence - higher familial involvement
- late onset (ApoE) - sporadic (less familial involvement), decreased penetrance but increased prevalence |
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what happens with clearance & production of Ab42 in early onset vs late onset AD?
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- early onset: increased production of Ab42
- late onset: decreased clearance of Ab42 |
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what is the amyloid cascade hypothesis?
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- change in Ab metabolism --> oligomerization --> toxic events at synapses --> inflammation --> hyperphosphorylation of tau & formation of tangles
- oligomer --> protofibril --> b-amyloid fibrils |
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what are the two drugs on the market to treat AD symptoms?
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- cholinesterase inhibitors
- NMDA receptor antagonists |
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what is being studied to prevent AD?
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- inhibiting activity of beta secretase
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what is the major problem with gamma secretase inhibitors?
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- gamma-secretase has lots of side effects like interfering with development of blood & Gi tract
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