Dementia 1 Flashcards
age associated cognitive changes
difficulty retrieving words and names. slower processing speed. difficulty sustaining attention when faced with competing environmental stimuli. learning something new takes a bigger effort. no functional impairment. harder time multitasking
mild cognitive impairment
memory complaint corroborated by an informant. objective memory impairment for age and education. preserved general cognition. normal activities of daily living. not demented.
amnestic mild cognitive impairment
memory loss not meeting criteria for dementia. progresses to Alzheimers at rate of 10-15% per year, vs. 1-3% incidence in general population. may be earliest phase of AD. no MCI test
DSM-5 criteria for dementia
memory decline/impairment and at least one of the following: aphasia, impaired executive function, apraxia, agnosia. Cognitive deficits must impact social and occupational function. diagnosis must be made in the presence of a clear sensorium.
early onset AD
occurs between age 30-60. rare. familial in most cases. Single gene mutation 1, 14, or 21. 1 has abnormal presenilin 2, 14 has abnormal presenilin 1, and 21 has abnormal amyloid precursor protein.
late onset AD
most common form. develops after age 60. combination of factors likely responsible. chromosome 19 (apolipoprotein E4 gene) implicated. associated with vascular conditions
gross neuropathology of AD
cerebral atrophy, mainly in temporal, parietal, and frontal areas along with ventricular enlargement
microscopic neuropathology of AD
amyloid plaques consisting of extracellular deposits of the beta amyloid peptide (AB). AB deposits in cortical and leptomeningeal arteries and arterioles (amyloid angiopathy). Neurofibrillary tangles and neuropil threads of tau protein. Granulovacuolar degeneration. Hirano bodies
where does AB come from?
derived from transmembrane protein (alzheimer precursor protein or APP). Beta and gamma secretase can cleave APP to form AB40 or AB42. Alzheimers has a high ratio of AB42 to AB40
presenilin
mutations in presenilin are responsible for majority of autosomal dominant AD cases. it is the catalytic component of gamma secretase
what can amyloid getting into the blood vessels cause?
hemorrhage!
major component of NFTs
hyperphosphorylated tau. when tau is hyperphosphorylated, it dissociates from the microtubules and forms paired helical filaments, which bundle together to form NFTs. paired helical filaments are the major component of neurophil threads and are deposited in the dystrophic neurites at the edge of neuritic plaques
frontotemporal lobar degeneration
FTLD Tau is most common. FTLD TDP is related to ALS. FTLD FUS and others are less common. earlier onset compared to AD. named for lobar degeneration, affects anterior frontal and superior temporal lobes, spares the occipital and parietal. very very bad atrophy in frontal lobes. has tau that doesnt conform to nerve shapes, unlike AD
