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NEUROENDOCRINOLOGY
LETTERS
including
Psychoneuroimmunology, Neuropsychopharmacology,
Reproductive Medicine, Chronobiology
and Human Ethology, ISSN 0172–780X
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NEL
Vol.24 Nos.3/4, Jun-Aug 2003
ORIGINAL ARTICLE
Running
Title:
Testosterone and gonadotropin levels in men with dementia
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2003;
24:203–208
pii: NEL243403A09
PMID: 14523358
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Testosterone and gonadotropin
levels in men with dementia
E.
Hogervorst, M. Combrinck & A. D. Smith
Oxford
Project To Investigate Memory and Ageing, Department of Pharmacology,
University of Oxford, Oxford, U.K.
Submitted:
February 2, 2003
Accepted: March 3, 2003
Key
words:
Alzheimer’s disease, dementia, gonadotropins, LH/FSH,
testosterone
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Abstract
OBJECTIVES:
Sex steroids such as testosterone and estradiol might protect
the brain against Alzheimer’s disease (AD). We previously
found lower levels of testosterone in men with AD compared
with controls. We wanted to assess levels of pituitary gonadotropins
that regulate sex steroid levels, to determine whether primary
or secondary hypogonadism was responsible for low levels of
testosterone in cases.
METHOD:
We included 45 men with AD (McKhann, 1987), 15 men with other
types of dementia and 133 elderly controls from the Oxford
Project to Investigate Memory and Ageing. Gonadotropins (follicle
stimulating hormone or FSH and luteinizing hormone or LH),
sex hormone binding globulin (SHBG, which determines the amount
of free testosterone) and testosterone were measured using
enzyme immunoassays.
RESULTS:
We found no difference in average LH (8.7 ± 9 UI/L),
FSH (13 ± 17 UI/L) or SHBG (44 ± 18 nmol/L)
levels between AD cases and controls. Similar to our earlier
findings, testosterone levels were significantly lower in
men with AD (13 ± 6 nmol/L) compared with controls
(17 ± 8, O.R. = 0.92, 95% C.I. = 0.87 to 0.97, p<0.005).
Results were unchanged when controlled for age, SHBG and gonadotropin
levels.
CONCLUSION:
Although normal, the levels of gonadotropins were inappropriately
low for the levels of testosterone. Our results support a
preliminary conclusion that secondary hypogonadism occurs
in men with AD. This could be a consequence of brain degeneration.
This is contrary to an earlier study (Bowen, 1999) that found
raised levels of gonadotropins in cases with AD, suggesting
primary hypogonadism. Our cohort was younger than theirs and
gonadotropin levels increase with age. We are enlarging our
data set to investigate whether primary hypogonadism occurs
in older cases with AD or whether secondary hypogonadism precedes
cognitive dysfunction in men at risk for AD. If this is true,
testosterone replacement therapy for hypogonadal men at risk
for dementia may be indicated.
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Copyright © Neuroendocrinology Letters 2003
Society of Integrated Sciences
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