S. L. Lowe

TL;DR: Early in the disease evidence of glutamatergic neurone loss is provided by the finding that in many regions of the cerebral cortex the Na+‐dependent uptake of D‐[3H]aspartic acid was almost always lowest in AD subjects compared with control when assessed by a method designed to minimise artifacts and epiphenomena.

TL;DR: No unequivocal measure of the integrity of pyramidal neurones could be established as the content of no amino acid was reduced, the index of the EDAA carrier showed evidence of change in few brain regions and glutaminase activity was subject to unexplained variability.

TL;DR: Losses of choline acetyltransferase activity were observed in all groups of Alzheimer specimens in all areas of brain studied, suggesting that cholinergic under-activity is most closely related to the clinical course of Alzheimer's disease.

TL;DR: Results imply that in the cerebral cortex the agonist site and a site in the cation channel of the receptor are not selectively altered, but that their coupling to a strychnine‐insensitive glycine recognition site is impaired.

TL;DR: The Ca2+-dependent release (K+-stimulated) of putative neurotransmitters has been demonstrated for the first time from brain tissue of depressed patients and the hypothesis of reduced amino acid function in depressive illness is not supported.