Neurotransmitters and second messengers in aging and Alzheimer's disease.
A substantial loss of cortical cholinergic nerve endings, along with a much more circumscribed cortical degeneration of pyramidal neurons, almost certainly causes glutamatergic hypoactivity in live Alzheimer's patients. These selective pathologies are discussed in terms of therapy. An additional effect of some proposed treatments is emerging as there is evidence that processing pathways for beta-amyloid precursor proteins in cortical pyramidal neurons, a target cell for acetylcholine, are affected by neuronal activity.
Francis
P T
PT
Miriam Marks Department of Neurochemistry, Institute of Neurology, London, United Kingdom.
Webster
M T
MT
Chessell
I P
IP
Holmes
C
C
Stratmann
G C
GC
Procter
A W
AW
Cross
A J
AJ
Green
A R
AR
Bowen
D M
DM
D000375:Aging / Q000502:physiology*; D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002421:Caudate Nucleus / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D006801:Humans; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011712:Pyramidal Tracts / Q000378:metabolism / Q000473:pathology; D015290:Second Messenger Systems / Q000502:physiology*
D018377:Neurotransmitter Agents