How Hormones Influence the Early Onset of Dementia as We Age, Scientists Reveal

Kyle J. Norton

Dementia
About 5-8% of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age.

Dementia is the loss of mental ability that is severe enough to interfere with people’s every life and Alzheimer’s disease is the most common type of dementia in aging people.

American typical diet contains high amount of saturated and trans fat, artificial ingredients with less fruits and vegetable which can lead to dementia and other kind of diseases.

As we age, productions of hormone decrease gradually that can effect the cognitive function, leading to dementia.

According to Eric R. Braverman, MD in the article of Hormones Dementia, numerous studies have linked hormone supplementation as protective in the development of dementia regardless of whether or not these hormones are deficient but more so when they are deficient.

Growth hormone beginning from age 30 in both men and women, estrogen loss beginning at age 40 in women, testosterone loss beginning at age 40 in men and DHEA loss beginning in both men and women at age 50.

The loss of luteinizing and sex binding globulin hormones may also be associated with the development of dementia with age(1)

The Impacts
1. Growth hormone
A report at the Universidad de Barcelona, Barcelona showed that there is a physiological decline of the growth hormone (GH)/insulin-like growthfactor-I (IGF-I) axis with ageing, and the possibility that the GH/IGF-I axis is involved in cognitive deficits has been recognized for several years.

The results of several studies addressing the deficiency of growth hormone (GH) in induction of dementia include
* Superimposable response of GH to GHRH than response of GH to GHRH in healthy individuals.

* Blunted GH to GHRH response in AD patients

* Higher GH concentrations in the morning; greater increase of GH to GHRH in AD patients than in controls(2).

Other reported that evidence favoring this idea stems from the ability of both hormones to stimulate beta amyloid release from neurons as well as by the stimulatory effect that IGF-I exerts on brain amyloid clearance.

In addition, insulin and IGF-I levels are altered in Alzheimer’s patients and, probably in close association to these changes, cell sensitivity towards insulin–and possibly also IGF-I–is decreased in these patients.(3)

2. Estrogen
In the research of the association of decreased levels of estrogen and dementia, scientist at the Kings College London suggested that the positive effects of estrogen are most robust in young women and in older women who had initiated ET around the time of menopause(4).

Other study supported the hypothesis that estrogen-replacement therapy is associated with a reduced prevalence of Alzheimer’s disease in postmenopausal women.

Prospective clinical trials are required to enable women and their physicians to weigh risks and benefits of estrogen-replacement therapy for the prevention of dementia(5)

3. Testosterone 
In a study of a group of 28 older men with either subjective memory loss or dementia, researchers found that serum total testosterone and sex hormone binding globulin (SHBG) correlated inversely with plasma levels of amyloid beta peptide 40.
According to the Fremantle Hospital study,  lower androgen levels are associated with increased plasma Abeta40 in older men with memory loss or dementia.

These results suggested that subclinical androgen deficiency enhances the expression of Alzheimer’s disease-related peptides in vivo(6).

4. DHEA
Kyushu University, in the study of a decreased concentration of dehydroepiandrosterone sulfate (DHEA-S) in patients with Alzheimer’s disease (AD), found that patients with AD and patients with CVD were found to have lower concentration of serum DHEA-S and a lower DHEA-S/DHEA ration compared to normal control individuals.

Also, according to the final report, no significant difference was observed in the concentration of serum DHEA-S or the DHEA-S/DHEA ratio between patients with AD and those with CVD.

These results suggest that reduced concentrations of serum DHEA-S may not be unique to AD, but instead reflect a common phenomenon in dementing diseases(7).

Other study in the assessed plasma DHEA and DHEAS levels in AD sufferers (n=72) and compared them to age-matched controls (n=72) showed that Plasma DHEA concentrations are significantly lower in AD patients compared to control (4.24+/-0.4 ng/ml for AD; 3.38+/-0.3 ng/ml for control, p=0.027, Mann-Whitney 1-tailed)

And DHEA levels are significantly correlated to DHEAS levels in both control and AD conditions (Spearman’s rho correlation coefficient=0.635 in controls and 0.467 in AD, p

Spearman’s rho correlation coefficient is a method used to measure  the relationship between two variables using a monotonic function.
5. Sex-hormone binding globulin 
There are evidence in the literature suggests that gonadotropins may be involved in processes in contribution to the etiology/pathogenesis of AD such as inflammation, cholesterol homeostasis, and insulin status.

Here we examine the potential mechanisms by which gonadotropins could influence neurodegenerative processes.(9)

6. Luteinizing hormone (LH)
Some researchers suspected that that another hormone of the hypothalamic-pituitary-gonadal axis, luteinizing hormone (LH), may be a major factor in AD pathogenesis.

In cell culture, LH increased amyloidogenic processing of amyloid-beta protein precursor, and in animal models of AD, pharmacologic suppression of LH and FSH reduced plaque formation.

Given the evidence supporting a pathogenic role for LH in AD, a trial of leuprolide acetate, which suppresses LH release, has been initiated in patients.(10)

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Sources
(1) http://www.pathmed.com/faq/?p=409 
(2) http://www.ncbi.nlm.nih.gov/pubmed/18537700
(3) http://www.ncbi.nlm.nih.gov/pubmed/15094079
(4) http://www.ncbi.nlm.nih.gov/pubmed/20840280
(5) http://www.ncbi.nlm.nih.gov/pubmed/9566385
(6) http://www.ncbi.nlm.nih.gov/pubmed/14624021
(7) http://www.ncbi.nlm.nih.gov/pubmed/8732462
(8) http://www.ncbi.nlm.nih.gov/pubmed/19665809
(9) http://www.ncbi.nlm.nih.gov/pubmed/16785601