| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
From the Mental Illness Research, Education, and Clinical Center (MIRECC) (Drs. Peskind and Raskind) and Geriatric Research, Education, and Clinical Center (GRECC) (Drs. Wilkinson and Schellenberg), VA Puget Sound Health Care System; and Departments of Psychiatry and Behavioral Sciences (Drs. Peskind, Wilkinson, Petrie, and Raskind) and Medicine (Dr. Schellenberg), University of Washington School of Medicine, Seattle.
Address correspondence and reprint requests to Dr. E.R. Peskind, Mental Illness Research, Education, and Clinical Center (116MIRECC), VA Puget Sound Health Care System, 1660 S. Columbian Way, Seattle, WA 98108; e-mail: peskind.elaine{at}seattle.va.gov
BACKGROUND: Increased hypothalamic–pituitary–adrenal (HPA) axis activity manifested by elevated cortisol levels is observed in AD and may contribute to AD by lowering the threshold for neuronal degeneration. Presence of the APOE-
4 allele increases risk for AD. Increased cortisol concentrations in apoE-deficient mice suggest that APOE genotype may influence cortisol concentrations in AD.
METHODS: The authors measured cortisol levels in CSF and determined APOE genotypes for 64 subjects with AD and 34 nondemented older control subjects.
RESULTS: CSF cortisol was significantly higher in AD than in control subjects. CSF cortisol concentrations differed with respect to APOE genotype in both subjects with AD (4/4 > 3/4 > 3/3) and normal older control subjects (3/4 > 3/3 > 2/3). Comparison of CSF cortisol concentrations within the 3/4 and 3/3 genotypes revealed no differences between AD and control subject groups.
CONCLUSIONS: Higher CSF cortisol concentrations were associated with increased frequency of the APOE-4 allele and decreased frequency of the APOE-2 allele in AD subjects relative to control subjects. This effect of APOE genotype on HPA axis activity may be related to the increased risk for AD in persons carrying the APOE-4 allele and decreased risk for AD in persons carrying the APOE-2 allele.
This article has been cited by other articles:
|
|
 |
|
  K.-F. Lau, W.-M. Chan, M. S. Perkinton, E. L. Tudor, R. C. C. Chang, H.-Y. E. Chan, D. M. McLoughlin, and C. C. J. Miller Dexras1 Interacts with FE65 to Regulate FE65-Amyloid Precursor Protein-dependent Transcription J. Biol. Chem., December 12, 2008; 283(50): 34728 - 34737. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. A. Beydoun, A. Lhotsky, Y. Wang, G. D. Forno, Y. An, E. J. Metter, L. Ferrucci, R. O'Brien, and A. B. Zonderman Association of Adiposity Status and Changes in Early to Mid-Adulthood With Incidence of Alzheimer's Disease Am. J. Epidemiol., November 15, 2008; 168(10): 1179 - 1189. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. S. Wilson, J. A. Schneider, P. A. Boyle, S. E. Arnold, Y. Tang, and D. A. Bennett Chronic distress and incidence of mild cognitive impairment Neurology, June 12, 2007; 68(24): 2085 - 2092. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. N. Green, L. M. Billings, B. Roozendaal, J. L. McGaugh, and F. M. LaFerla Glucocorticoids Increase Amyloid-beta and Tau Pathology in a Mouse Model of Alzheimer's Disease. J. Neurosci., August 30, 2006; 26(35): 9047 - 9056. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Freeman, V. Roca, F. Guggenheim, T. Kimbrell, and W.S.T. Griffin Neuropsychiatric Associations of Apolipoprotein E Alleles in Subjects With Combat-Related Posttraumatic Stress Disorder J Neuropsychiatry Clin Neurosci, November 1, 2005; 17(4): 541 - 543. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. G. Baker, N. N. Ekhator, J. W. Kasckow, B. Dashevsky, P. S. Horn, L. Bednarik, and T. D. Geracioti Jr. Higher Levels of Basal Serial CSF Cortisol in Combat Veterans With Posttraumatic Stress Disorder Am J Psychiatry, May 1, 2005; 162(5): 992 - 994. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. F. Schatzberg Recent Studies of the Biology and Treatment of Depression Focus, January 1, 2005; 3(1): 14 - 24. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Grundman Weight Loss in the Elderly May Be a Sign of Impending Dementia Arch Neurol, January 1, 2005; 62(1): 20 - 22. [Full Text] [PDF]
|
|
|
|
|
|
R. J. Caselli, E. M. Reiman, J. G. Hentz, D. Osborne, and G. E. Alexander A Distinctive Interaction Between Chronic Anxiety and Problem Solving in Asymptomatic APOE e4 Homozygotes J Neuropsychiatry Clin Neurosci, August 1, 2004; 16(3): 320 - 329. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. J.-F. de Quervain, R. Poirier, M. A. Wollmer, L. M.E. Grimaldi, M. Tsolaki, J. R. Streffer, C. Hock, R. M. Nitsch, M. H. Mohajeri, and A. Papassotiropoulos Glucocorticoid-related genetic susceptibility for Alzheimer's disease Hum. Mol. Genet., January 1, 2004; 13(1): 47 - 52. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Raber, G. Bongers, A. LeFevour, M. Buttini, and L. Mucke Androgens Protect against Apolipoprotein E4-Induced Cognitive Deficits J. Neurosci., June 15, 2002; 22(12): 5204 - 5209. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. O. Sass, P. Heinz-Erian, W. Hogler, C. W. Wilkinson, and E. R. Peskind Increased CSF cortisol in AD is a function of APOE genotype Neurology, October 23, 2001; 57(8): 1522 - 1523. [Full Text] [PDF]
|
|
Read all Correspondence
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
