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24 Cards in this Set

  • Front
  • Back
Major gross change
cortical atrophy
Regions of brain involved
medial temporal lobe, including hippocampus, entorhinal cortex and amygdala, are involved early in the course and are usually severely atrophied in the later stages
Major microscopic findings
neuritic plaques
neurofibrillary tangles
neuronal loss
gliosis
Neuritic plaques
location
protein
dystrophic neurites around central amyloid core (extracellular)
protein: Abeta (40 or 42)
specific to Alzheimers
Neuritic tangles
location
protein
within neurons
hyperphosphorylated tau
not specific to Alzheimers
Neuritic plaque Abeta how is it formed?
Abeta 40 or 42 is from beta-secretase followed by gamma-secretase action on APP (Amyloid precursor protein); Abeta aggregates and is directly toxic to neurons
cells surrounding neuritic plaque?
microglial cells and reactive astrocytes
what is a diffuse plaque?
amyloid core (Abeta protein) without surrounding neuritic reaction, usually in cerebral and cerebellar cortex and basal ganglia; likely an early form of neuritic plaque
Other proteins in neuritic plaque besides Abeta amyloid?
complement cascade components, pro-inflammatory cytokines, α1-antichymotrypsin, and apolipoproteins
condition with early onset Alzheimers?
Trisomy 21 Downs syndrome bc APP (amyloid precursor protein) is on chr 21
What are ghost or tombstome tangles?
Neurofibrillary tangles are resistant to degradation and ghosts remain after death of neuron (remember tangles are intracellular)
location of neurofibrillary tangles?
cortical neurons, especially in the entorhinal cortex, pyramidal cells of hippocampus, amygdala, basal forebrain, and raphe nuclei
What is tau?
axonal microtubule-associated protein that enhances microtubule assembly
Other components in tangles besides tau?
MAP2 (another microtubule-associated protein) and ubiquitin
Other micorscopic pathology of Alzheimers besides plaques and tangles?
Cerebral amyloid angiopathy (CAA), Granulovacuolar degeneration, Hirano bodies
What is cerebral amyloid angiopathy?
Cerebral amyloid angiopathy (CAA) is an almost invariable accompaniment of Alzheimer disease; however, it can also be found in brains of individuals without AD (see Fig. 28-18B ). Vascular amyloid is predominantly Aβ40, as is also the case when CAA occurs without AD. .
What is granulovacuolar degeneration?
Granulovacuolar degeneration is the formation of small (∼5 μm in diameter), clear intraneuronal cytoplasmic vacuoles, each of which contains an argyrophilic granule. While it occurs with normal aging, it is most commonly found in great abundance in hippocampus and olfactory bulb in AD.
What are Hirano bodies?
Hirano bodies, found especially in AD, are elongated, glassy, eosinophilic bodies consisting of paracrystalline arrays of beaded filaments, with actin as their major component. They are found most commonly within hippocampal pyramidal cells.
Assessment of plaques and tangles to dx Alzheimers
Plaques are assessed semiquantitatively (absent, sparse, moderate, abundant) in each cortical area, while tangles are assessed based on how widespread they are in the brain.[38,][39] These assessments are combined in the current NIA-Reagan criteria to provide an estimate of the likelihood that AD pathology caused a particular patient's dementia
Progression of pathologic changes (finding plaques and tangles) in Alzheimers
earliest in the entorhinal cortex, then spread through the hippocampal formation and isocortex, and then extend into the neocortex
Causes of the majority of early-onset familial Alzheimers
two presenilins (PS1 on chromosome 14 and PS2 on chromosome 1). These mutations lead to a gain of function, such that the γ-secretase complex generates increased amounts of Aβ, particularly Aβ42
ApoE relation to Alzheimers?
ApoE (chr 19)
dosage of the ε4 allele increases the risk of AD and lowers the age of onset of the disease
promotes Aβ generation and deposition
plaques histopath
starburst
tangles histopath
comet tail or flame