This Article
Right arrow Full Text (PDF)
Right arrow Submit an eLetter
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Bowen, D. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bowen, D. M.

The British Journal of Psychiatry 157: 327-330 (1990)
© 1990 The Royal College of Psychiatrists

Treatment of Alzheimer's disease. Molecular pathology versus neurotransmitter-based therapy

DM Bowen
Miriam Marks Department of Neurochemistry, Institute of Neurology, London.

Cortical inhibitory neurotransmitters, neuropeptides, dopamine and noradrenaline are probably either not selectively or not critically affected in AD. It is, however, likely that a key change is shrinkage or loss of corticocortical pyramidal neurones, which probably use glutamate as their transmitter. This depletion appears to be circumscribed and clinically relevant.


This article has been cited by other articles:


Home page
 Proc. Natl. Acad. Sci. USAHome page
S. Nonaka, C. J. Hough, and D.-M. Chuang
Chronic lithium treatment robustly protects neurons in the central nervous system against excitotoxicity by inhibiting N-methyl-D-aspartate receptor-mediated calcium influx
PNAS, March 3, 1998; 95(5): 2642 - 2647.
[Abstract] [Full Text] [PDF]

Home page
 J PsychopharmacolHome page
N.H.P. Allen and A. Burns
The treatment of Alzheimer's disease
J Psychopharmacol, January 1, 1995; 9(1): 43 - 56.
[PDF]