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Tuesday, 29 October 2013

@Dementia - Deficiency Causes of Dementia

DementiaAbout 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
Causes of Demnetia
A. Deficient cause of dememtia due to aging
1. Vitamin D and 1,25-dihydroxyvitamin D(3) deficiency
Vitamin D levels plays a important role in the pathogenesis of a wide range of non-skeletal, age-associated diseases including cancer, heart disease, type 2 diabetes mellitus and stroke and Low levels of serum 25-hydroxyvitamin D [25(OH)D], a stable marker of vitamin D status, are also associated with increased odds of prevalent cognitive dysfunction, Alzheimer's disease and all-cause dementia in a number of studies, raising the possibility that vitamin D plays a role in the aetiology of cognitive dysfunction and dementia.(1). Other suggested that Vitamin D insufficiency appears to be highly prevalent among older adults. Evidence from epidemiologic studies and small clinical trials suggests an association between 25(OH)D concentrations and systolic blood pressure, risk for CV disease-related deaths, symptoms of depression, cognitive deficits, and mortality.(2)

2. Folic acid with vitamin B12 deficiency
Folates are vitamins essential to the development of the central nervous system. Defiency of Folate can increase the risk of dementia. In the All double-blind placebo-controlled randomized trials, in which supplements of folic acid with or without vitamin B12 were compared with placebo for elderly healthy people or people with any type of dementia or cognitive impairment conducted by Cochrane Dementia and Cognitive Improvement Group, Folic acid plus vitamin B12 was effective in reducing the serum homocysteine concentrations. Folic acid was well tolerated and no adverse effects were reported. More studies are needed.(2)

3. Vitamin B12 deficiency
An association between neuropsychiatric disorders and vitamin B12 deficiency has been recognized since 1849 when pernicious anaemia was first described. Deficiency of Vitamin B12 are found in many elder and might contribute to age-associated cognitive impairment. Scientist at Cochrane Dementia and Cognitive Improvement Group, suggested that Evidence of any efficacy of vitamin B12 in improving the cognitive function of people with dementia and low serum B12 levels is insufficient(4)

4. Vitamin B6 deficiency
In the investigation to assess the efficacy of vitamin B6 supplementation in reducing the risk of developing cognitive impairment by older healthy people, or improving cognitive functioning of people with cognitive decline and dementia, conducted by Cochrane Dementia and Cognitive Improvement Group, found evidence that there is scope for increasing some biochemical indices of vitamin B6 status among older people. More randomized controlled trials are needed to explore possible benefits from vitamin B6 supplementation for healthy older people and those with cognitively impairment or dementia.(5)

5. Deficiciency of Insulin-like growth factor (IGF)-1
Researchers at University of Oklahoma Health Sciences Center, suggested that  Deficiency of this hormone has been reported to influence the genesis of cognitive impairment and dementia in the elderly patients, although  there are studies indicating that cognitive function can be maintained into old age even in the absence of circulating IGF-1 and studies that link IGF-1 to an acceleration of neurological diseases, IGF-1 has a complex role in brain function, synaptic effects appear to be central to the IGF-1-induced improvement in learning and memory(6)

6. Deficiency of Growth hormone and insulin-like growth factor-1 (IGF-1)
In the focus of  age-related decreases in serum growth hormone and IGF-1 as potential mechanisms that may influence cognitive function in the elderly. In rodents, long-term growth hormone/IGF-1 replacement improves learning and memory in aged rats. While the exact mechanism underlying these cognitive improvements is unknown, growth hormone and IGF-1 replacement to aged animals increases neurogenesis, vascular density, and glucose utilization, and alters NMDA receptor subunit composition in brain areas that are implicated in learning and memory(7)

7. GH-deficiency
In the more developed central, GH and IGF-1 are thought to have a variety of functions such as a neuroprotective function, an appetite increasing function, various cognitive functions, and perhaps a blood flow-regulating function. In GH-deficient children and adults, improvement of cognitive functions was observed after the administration of GH. Furthermore, specific cognitive functions in healthy older subjects may improve after increasing GH or IGF-1 levels.(8)

8. Deficiency of cerebrospinal fluid melatonin
Some melatonin is normally secreted directly into the fluid inducing higher levels than in simultaneously sampled blood. Melatonin is carried into the ventricular system via choroid plexus portals. Neural tissue in contact with the ventricular system will have high levels of cellular melatonin. In Alzheimer's disease, inadequate melatonin allows hydroxyl radicals produced by mitochondrial complex IV to damage mitochondria and initiate a cascade of oxygen radicals that causes the neuropathological changes in Alzheimer's disease.(9)

9. Decreased dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) concentrations
DHEA is secreted by the adrenal cortex and is also a neurosteroid. Its sulfate (DHEAS) is the most abundant steroid in circulation. The levels of both are seen to decline in concentration with age. Plasma DHEA concentrations were 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 were 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<or=0.01).(10)

10. Etc.

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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/21790207
(2) http://www.ncbi.nlm.nih.gov/pubmed/20226390
(3) http://www.ncbi.nlm.nih.gov/pubmed/14584018
(4) http://www.ncbi.nlm.nih.gov/pubmed/12918012
(5) http://www.ncbi.nlm.nih.gov/pubmed/14584010
(6) http://www.ncbi.nlm.nih.gov/pubmed/22503992
(7) http://www.ncbi.nlm.nih.gov/pubmed/16024298
(8) http://www.ncbi.nlm.nih.gov/pubmed/15478038
(9) http://www.ncbi.nlm.nih.gov/pubmed/11461164
(10) http://www.ncbi.nlm.nih.gov/pubmed/19665809