WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience
 QUICK SEARCH:   [advanced]


     
-


HOME
  |  
SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

Electronic Letters to:

Neurobiology of Disease:
Kim N. Green, Lauren M. Billings, Benno Roozendaal, James L. McGaugh, and Frank M. LaFerla
Glucocorticoids Increase Amyloid-beta and Tau Pathology in a Mouse Model of Alzheimer’s Disease
J. Neurosci. 2006; 26: 9047-9056 [Abstract] [Full text] [PDF]
*eLetters: Submit a response to this article

Electronic letters published:

[Read eLetter] This could be due to a reduced DHEA to cortisol ratio...
James M. Howard   (21 June 2007)

This could be due to a reduced DHEA to cortisol ratio... 21 June 2007
  Top
James M. Howard,
Biologist, independent
1037 North Woolsey Avenue, Fayetteville, Arkansas 72701

Send letter to journal:
Re: This could be due to a reduced DHEA to cortisol ratio...

jmhoward{at}anthropogeny.com James M. Howard

In 1985, I first suggested that Alzheimer's disease may be due to low DHEA (1). In the same place, I suggested that cortisol evolved to counteract the effects of DHEA and that this is the basis of the "fight or flight" mechanism. This may explain why prolonged exposure to cortisol is so harmful because this means that DHEA is not exerting sufficient effects to counteract the negative effects of cortisol. DHEA naturally begins to decline around age twenty, reaching very low levels in aging while cortisol levels do not decline as dramatically. This may explain the findings of Green, et al.

1."A Theory of the Control of the Ontogeny and Phylogeny of Homo sapiens bythe Interaction of Dehydroepiandrosterone and the Amygdala," Copyright 1985, James Michael Howard, Fayetteville, Arkansas, Registration No. TXu 220 580

-
-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help

-
Copyright 2009 by Society for Neuroscience ONLINE ISSN: 1529-2401
-