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9 Cards in this Set

  • Front
  • Back
Symptoms
*Progressive decline in memory, accompanied from a gradual retreat and frustration with normal activities
* Loss of ability to depict spatial relations
*Perceptual difficulties
*Sequential tasks
Diagnosis
MRI and PET scans show loss of corticles and enlarged ventricles
Pathology (Senile Plaques)
*Senile Plaques - extracellular, exists as a molecular fragment of a large protein found in normal brain
*accumulations of cellular debris surrounding a central core of β-amyloid peptide
*
Pathology (Tangles)
*Intracellular
*Bundles of filamex arranged in a helix - derived from normal structures of neurons
*Usually formed in large neurons of the brain
*Usually linked with abnormal accumulation of protein tau
*Tau is normal brain protein, but AD patients have elevated
* only occur in parts of the brain that control attention and memory
Pathology (Neuronal Cell Loss and changes in morphology)
*Specific loss of ACh-containing neurons (nucleus basalis)
*Decreased brain weight
*Atrophy of the Cortex
*Enlarged Ventricles
*Neuronal loss in hippocampus and the amygdala
Pathology (Loss of ACh neurons)
AcetylCoA+choline =ACh
catalyzed by acetyl transferase (ChAT)
ACh degredation catalyzed by acetyltransferase
Pathology (Loss of ACh Neurons)
ChAT is a marker for ACh containing neurons
AD - Loss of ChAT in Hippocampus and cortex
*Memory and cognitive losses due to loss of ACh containing neurons that originate in the NUCLEUS BASIS, and project to the CORTEX and HIPPOCAMPUS
Smokers have a lower chance of getting AD
Nicotine is an agonist at nicotine ACh receptors
Atypical agonists because they stay bound to receptors for a long period of time, therefore preveinting ACh from binding.
Some sensitization occurs, increasing number or sensitivity of this class ACh receptor
Pharmacological Treatment
Try to compensate for loss of cholinergic neurons

INHIBIT the DEGRADATION of ACh