Delay Dementia - Diseases 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
I. Causes of Dementia
C. Diseases Causes of Dementia
C.1. Alzheimer's disease
Alzheimer's disease is a brain disorder named for German physician Alois Alzheimer. Alzheimer's destroys brain cells, causing problems with memory, thinking and behavior severe enough to affect language communication, memory, lifelong hobbies or social life. Alzheimer's gets worse over time, and it is fatal. Over 1 million people in US alone are currently afflicted by Alzheimer's disease because of degeneration of hippocampus and cerebral cortex of the brain where memory, language and cognition are located. With this mental disorder, brain cells gradually die and generate fewer and fewer chemical signals day by day resulting in diminished of functions. Overtime memory thinking as well as behavior deteriorates. Today, there is no known cure.

C.2. Stroke (Vascular problems)Strokes are caused by uncontrolled diet that is high in saturated and trans fats as a result of bad cholesterol building up in the blood vessels that block the circulation of blood to the body including the brain. If oxygen is not delivered to the brain cells, some cells die off and can not reproduce, then you may get a stroke. Other happen when a blood vessel in the brain ruptures causing the cells in your brain deprived of oxygen that can lead to symptoms of vascular dementia.
In atudy of Prevalence, incidence, and factors associated with pre-stroke and post-stroke dementia: a systematic review and meta-analysis, conducted by University Department of Clinical Neurology, John Radcliffe Hospital, Dr. Pendlebury ST, Rothwell PM. showed that 10% of patients had dementia before first stroke, 10% developed new dementia soon after first stroke, and more than a third had dementia after recurrent stroke. The strong association of post-stroke dementia with multiple strokes and the prognostic value of other stroke characteristics highlight the central causal role of stroke itself as opposed to the underlying vascular risk factors and, thus, the likely effect of optimum acute stroke care and secondary prevention in reducing the burden of dementia.(1)

C.3. Dementia with Lewy bodies
Lewy bodies is defined as a spherical masses that displace other cell components. Abnormal aggregates of protein develop inside nerve cells found in Parkinson's disease (PD), Lewy Body Dementia and some other disorders.(2). In teh study to identify the patterns of diffusivity changes in patients with dementia with Lewy bodies (DLB) and Alzheimer disease (AD) and to determine whether diffusion tensor MRI (DTI) is complementary to structural MRI in depicting the tissue abnormalities characteristic of DLB and AD, the team at Mayo Clinic, found that increased amygdalar diffusivity in the absence of tissue loss in dementia with Lewy bodies (DLB) may be related to microvacuolation, a common pathology associated with Lewy body disease in the amygdala. Diffusivity measurements were complementary to structural MRI, demonstrating that measures of diffusivity on diffusion tensor MRI are valuable tools for characterizing the tissue abnormalities characteristic of Alzheimer disease and DLB.(3)

C.4. Fronto-temporal dementia
Fronto-temporal dementia (FTD) or Pick's disease is defined as the clinical syndrome caused by degeneration of the frontal lobe of the brain. Although early diagnosis of fronto-temporal dementia (FTD) is often difficult because of the non-specific presentation, some researchers showed that the inhibition of reflexive and voluntary saccades appears to be independently processed. A delayed antisaccade task could be useful for the early diagnosis of FTD.(4). Others suggested depression and executive dysfunction triggers the loss of autonomy, the risk of fall and of malnutrition in elderly patients. The clinical significance of this study is that the delineation of specific executive in depressed elderly patients may facilitate the development of effective treatment interventions, including treatment for geriatric depression.(5)


C.5. Progressive supranuclear palsy
Progressive supranuclear palsy is defined as a condition of a movement disorder occurred as a result of damage to certain nerve cells in the brain that lead to serious and progressive problems with control of gait and balance, including an inability to aim the eyes properly. In a study to observe the progressive supranuclear palsy syndrome (PSPS) and corticobasal syndrome (CBS) and associated with relatively specific patterns of atrophy; the former predominantly involving the brainstem, the latter frontoparietal regions, in a 41 subjects and controls study, by utilizing the technique of voxel-based morphometry to assess both gray and white matter volume loss in six prospectively recruited Hybrids that underwent 3.0 T volumetric head magnetic resonance image scanning to determine the neuroanatomical correlates of the syndrome. he Hybrid group showed imaging features of both PSPS and CBS, with volume loss observed in the brainstem (superior cerebellar peduncle) and cortex (medial and lateral premotor, prefrontal, and motor cortex). As expected, typical patterns of loss were observed in PSPS and CBS.(6)
Others suggested that The patients with CBDS displayed an asymmetric (left > right) pattern of brain atrophy that involved the bilateral premotor cortex, superior parietal lobules, and striatum. Progressive supranuclear palsy was associated with atrophy of the midbrain, pons, thalamus, and striatum, with minimal involvement of the frontal cortex. Midbrain structures were more atrophied in PSP than in CBD, whereas dorsal frontal and parietal cortices were more atrophied in CBD than in PSP. The degree of atrophy of the midbrain and pontine tegmentum and the left frontal eye field differentiated the 2 patient groups with 93% accuracy.(7)

C.6. Korsakoff's syndrome 
Korsakoff's syndrome, named after Sergei Korsakoff, a Russian neuropsychiatris is defined as a neurological disorder as a result of  deficiency of Vitamin B1 (thiamine) in the brain and associated closely to chronic alcohol abuse and/or severe malnutrition. In the study The links between spatial behavior and hippocampal levels of synapsin I and phosphosynapsin in normal rats and in the pyrithiamine-induced thiamine deficiency (PTD) rat model of Wernicke-Korsakoff's syndrome, found that spontaneous alternation performance was impaired in PTD rats and was accompanied by a significant reduction (30%) in phosphorylated synapsin I(8). Other study comfirmed that confirms the widespread neurotoxic effect of chronic alcohol consumption. Only a few cerebral regions, including the medial thalami, mammillary bodies, and corpus callosum, were more severely damaged in KS than in AL. The continuum of macrostructural damage from AL to KS is therefore restricted to key brain structures. Longitudinal investigations are required to determine whether alcoholic patients with medial thalamic volumes that are comparable to those of patients with KS are at increased risk of developing KS.(9). Scientist at the University of Campinas (Unicamp),suggested that self-imposed long-lasting nutritional deprivation is thought to be the main cause of thiamine deficiency and subsequent encephalopathy, but adjunct factors, such as magnesium depletion and chronic alcohol misuse, might have played an important role, especially in the development of Korsakoff's syndrome(10)

C.7. Binswanger's disease
Binswanger disease also known as subcortical vascular dementia  is defined as a type of small vessel vascular dementia caused by microscopic areas of damage to the deep layers of white matter in the brain, including mostly of glial cells and myelinated axons worked to transmit signals from one region of the cerebrum to another and between the cerebrum and lower brain centers. Binswanger's disease frequency increases with age independent of other risk factors, and in nondemented subjects leukoaraiosis is associated with deficits in selected cognitive functions.(11). Other clinical finding associated with Binswanger's disease are varied but typically include a progressive dementia, depression and "subcortical" dysfunction such as gait abnormalities, rigidity and neurogenic bladder. Treatment is largely supportive and includes a discussion about advanced directives, social support and antidepressant therapy. Control of hypertension and aspirin prophylaxis may help prevent further progression of white matter disease.(12)

C.8. Acquired immunodeficiency syndrome (AIDS)
 AIDs is defined as Acquired immunodeficiency syndrome (AIDS) is defined as a condition of the progressive failure of the immune system caused by HIV, a lentivirus.Some researchers suggested that AIDS dementia complex (ADC) pathogenesis may be a multistep process that starts with HIV invasion of CNS by crossing the blood-brain barrier (BBB). It progresses by developing a chronic inflammatory status that can cause dysfunction in neurons and astrocytes that result in apoptotic death. Monocytes-macrophages (M/M) may play an important role by concealing the HIV transfer across the BBB. Furthermore, HIV-infected M/M could produce and release neurotoxic factors(13). Others showed that suggest a possible role for tumor necrosis factor-alpha in the development of neurological dysfunction. Increased levels of tumor necrosis factor-alpha messenger RNA were not associated with increased levels of IL-1 beta messenger RNA, suggesting differential regulation of these monokines in acquired immunodeficiency syndrome(14).


C.9.  Creutzfeldt-Jakob disease (CJD)
Creutzfeldt-Jakob disease (CJD) is defined as a form of incurable and invariably fatal, degenerative neurological disorder that leads to a rapid decrease of mental function and movement as a result of  infectious protein called a prion of which can replicate by converting their properly folded counterparts. According to the study of University of Gdańsk, in a report of a female, right-handed, age 68 adiagnosed with the Heidenhain variant of Creutzfeldt-Jakob Disease (HvCJD), over the crucial 6-week period the patient went from "Mild Cognitive Impairment" to a status resembling the final stages of Alzheimer's disease, without any evidence of a CVA, The only aspect of this case that does not fit the usual criteria for the Heidenhain variant is the fact that the patient survived over a year in a persistent vegetative state. Ophthalmologists and family physicians should be aware of the possibility of HvCJD in any patient over 60 presenting with otherwise inexplicable visual disturbances in the absence of significant ocular pathology, even when other symptoms of dementia may not be immediately noticeable(15).


C.10. Parkinson's disease 
Parkinson's disease is defined as condition of  a degenerative disorder of the central nervous system that leads to shaking (tremors) and difficulty with walking, movement, etc. with dementia commonly occurring in the advanced stages of the disease. Scales for Outcomes in Parkinson's Disease Motor and Psychiatric complications, MiniMental State Examination, Clinical Impression of Severity Index, and the Zarit Caregiver Burden Inventory. Patients in all stages of disease were included and 18.38 % were demented. The SEND-PD was responded by patients (86.16 %), caregivers (13.15 %), or both (0.69 %). Three factors (accounting for 66.63 % of the variance) were identified and considered as subscales: Psychotic symptoms, Mood/Apathy, and Impulse control disorders(16)

C.11. Huntington's disease
Huntington's disease is defned as condition of a neurodegenerative genetic disorder that affects muscle coordination and leads to cognitive decline and psychiatric problems(17). In the  investigation to identify cognitive deficits that contribute to functional impairment to support dementia criteria that reflect HD neuropathology. Functional impairment was defined as 80 or below on the FIS. Speed of processing, initiation, and attention measures accounted for 70.0% of the variance in FIS ratings (linear regression) and correctly classified 91.7% of subjects as functionally impaired or intact (logistic regression). A definition of HD dementia that includes cognitive impairment in at least two areas of cognition but does not require a memory deficit, in the context of impaired functional abilities and a deteriorating course, more accurately reflects HD neuropathology and could lead to improved research methods and patient care.(17)

C.12. Motor Neurone disease (MND)
Motor neuron diseases are defined as a group of neurological disorders that affect the motor neurones, located in the central nervous system (or CNS). MND is a multisystem disorder associated with cognitive and behavioural changes which in some instances reaches the criteria for FTD, while a proportion of patients with FTD develop frank MND (18)

C.13. Multiple Sclerosis
is defined as condition of an inflammatory diseasethat cause the damage of the fatty myelin sheaths around the axons of the brain and spinal cord, leading to progressive interference with functions that are controlled by the nervous system such as vision, speech, walking, writing, and memory. there is a report that report that a female patient with severe cognitive presentation at the onset of MS, with dramatically demented evolution, and show MRI examination results. We discuss the published reports of primary cognitive types of MS.(19)

C.14. Obesity
Midlife and late-life obesity my increase the risk of dementia. In 480 persons with incident dementia, 245 with Alzheimer disease (no vascular dementia), and 213 with vascular dementia (with or without Alzheimer disease). In evaluations of midlife obesity, an increased risk of dementia was found for obese (BMI >30) vs normal-weight (BMI 20-25) persons, adjusted for demographics (hazard ratio [HR], 1.39; 95% confidence interval [CI], 1.03-1.87) and for cardiovascular risk factors (1.36; 0.94-1.95). The risk estimates were reversed in assessments of late-life BMI. Underweight persons (BMI <20) had an increased risk of dementia (1.62; 1.02-2.64), whereas being overweight (BMI >25-30) was not associated (0.92; 0.72-1.18) and being obese reduced the risk of dementia (0.63; 0.44-0.91) compared with those with normal BMI.(20)

C. 15. Etc.


Alzheimer's Disease - My Story
This Is A Real Case Study, Written By An Alzheimer's Sufferer
Sharing His Hurts, Frustration And Desperation.

For the series of Alzheimer's disease, visit http://medicaladvisorjournals.blogspot.com/2012/01/alzheimers-disease.html

For Other Health articles visit http://medicaladvisorjournals.blogspot.com/
 


Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/19782001
(2) http://en.wikipedia.org/wiki/Lewy_body
(3) http://www.ncbi.nlm.nih.gov/pubmed/20513818
(4) http://www.ncbi.nlm.nih.gov/pubmed/16227556
(5) http://www.ncbi.nlm.nih.gov/pubmed/19748373
(6) http://www.ncbi.nlm.nih.gov/pubmed/22519566
(7) http://www.ncbi.nlm.nih.gov/pubmed/16401739
(8) http://www.ncbi.nlm.nih.gov/pubmed/22507301
(9) http://www.ncbi.nlm.nih.gov/pubmed/22496200
(10) http://www.ncbi.nlm.nih.gov/pubmed/20646296
(11) http://www.ncbi.nlm.nih.gov/pubmed/7604429
(12) http://www.ncbi.nlm.nih.gov/pubmed/9861880
(13) http://www.ncbi.nlm.nih.gov/pubmed/16540457
(14) http://www.ncbi.nlm.nih.gov/pubmed/8498837
(15) http://www.ncbi.nlm.nih.gov/pubmed/17179914
(16) http://www.ncbi.nlm.nih.gov/pubmed/22527230 
(17) http://en.wikipedia.org/wiki/Huntington%27s_disease
(18) http://www.ncbi.nlm.nih.gov/pubmed/20629124
(19) http://www.ncbi.nlm.nih.gov/pubmed/20031302
(20) http://www.ncbi.nlm.nih.gov/pubmed/19273752

Delay Dementia - Free Radical Causes of Dementia

Dementia
Human aging is a biological process, no one can stop, but delay it. It is possible that one person looks younger than his or her biological if engages in healthy living life style and eating healthily by increasing the intake of good healthy food such as whole grain, fruits, vegetables, beans and legumes, etc. and reducing the consumption of harmful foods, such as saturated fat, trans fat, artificial ingredients, etc.. 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

Causes of Dementia
B. Free radical causes of dementia
B.1. Alzheimer’s disease
1. Free radical and Alzheimer’s disease
Free radicals causes Alzheimer’s disease is well defined in many researches. In a study of protein oxidation in the brain in Alzheimer's disease by using immunohistochemistry and two-dimensional fingerprinting of oxidatively modified proteins (two-dimensional Oxyblot) together to investigate protein carbonyl formation in the Alzheimer's disease brain, researchers found that oxidative stress-induced injury may involve the selective modification of different intracellular proteins may lead to the neurofibrillary degeneration of neurons in the brain. (source)

2.  Antioxidants and Alzheimer’s disease
a. Docosahexaenoic acid (DHA)
Researchers found that DHA increases phosphatidylserine, a naturally occurring component found in every cell membrane of the body and improves the memory of animals with Alzheimer's disease by suppressing oxidative damage in the brain.

b. Vitamin E
In a study, researcher found that vitamin E, and drugs that reduce generalized inflammation, may slow the decline of mental and physical abilities in people with Alzheimer's disease (AD) over the long term. Also vitamin E inhibits cells damage and cells death caused by beta-amyloid, which is toxic to brain cells.

c. PhosphatidylserineIn one double-blind, placebo-controlled study, patients who had Alzheimer’s disease who took 300 milligrams per day (mg/day) of phosphatidylserine scored significantly better on standardized memory tests at the end of the 12-week trial period than patients who received placebo.

d. Antioxidants
Antioxidant are found at much lower levels for patients with Alzheimer’s disease, such as serum of vitamin A, C, E, zinc and transfferin.

e. Muscarinic cholinergic receptors
researchers found that Alzheimer’s disease patients exhibit the significant loss of muscarinic cholinergic receptors neurons that cause the reduced volume of neural transmission leading to the loss of memory.

f. Etc.

B.2. Parkinson's disease
1. Free radicals and Parkinson's disease
Researcher found that patients with Parkinson's disease have low levels of polyunsaturated fat in the substania nigra than other part of the brain, but higher levels of lipid peroxidation as indication of higher levels of malonaldehyde. Also patients with the disease found to contain waste pigments of lipofusion and other polymers in the neurons where dopamine is most active.

2. Antioxidants and Parkinson's disease
Antioxidants play an vital role for patients with Parkinson's disease, as researchers found the prohression of the disease accompany with reduction of antioxidants in the affected parts of the brain.
a. Superoxide dismutase
Researcher found that the progression of the disease may be associated with the decrease levels of superoxide dismutase, a antioxidant enzyme.

b. NADH ubiquinone reductase
Researcher found that the levels of NADH ubiquinone reductase is decreased in the substania nigra due to its inhibitors, leading to apoptosis, but can be retreated with antioxidants Nacetylcysteine and alpha lipoic acid.

c. Uric acid
Researchers at the University of Hawaii recently reported that people with a high blood level of the natural antioxidant uric acid have a lower risk of developing Parkinson's disease than do people with lower levels, but high levels of uric acid increases the risk of kidney diseases and gout.

d. Vitamin C
Vitamin C is one of powerful and effective antioxidant in scavenging hydroxyl radicals as it enters the cerebrospinal fluid thus protecting against Parkinson's disease or slowing down the progression of the disease.

e. Glutathione
Researcher found that glutathoine is one of the antioxidant which can help to deactivate the harmful product HNE of lipid peroxidation.

f. Etc.

B.3. Multiple Sclerosis
1. Free radicals and Multiple Sclerosis
a. The DeVine theory suggested that free radical activity is a contributory factors in MS, theory suggestive that immune system and free radical cooperation cause the generation of in the myelin itself that deteriorates the myelin shealts.

b. Cooper theory went on step further by suggested that free radicals actually initiate MS, by damaging the myelin, leading to initiating and promoting of activity of T-cells.

c. Etc.

4. Antioxidants and Multiple sclerosis
Antioxidants can help protect the neural tissue from damage that reduce the risk of inflammation result in lessening the risk of oxidative stress.
a. TNFalpha
An imflammatory cytokine has been associated with MS is inhibited by antioxidants of green tea, and others such as curcumin, quercetin, etc.

b. Melatonin
Melatonin functions as an antioxidant and has the ability to protect neurons from free radicals cause of lipid peroxidation.

c Selenium
Some studied found that the levels of selenium in the blood of people with MS was lower than in that of people without MS.

d. Niacin
Niacin acts as antioxidant is a key to the successful treatment of multiple sclerosis, researchers at Harvard Medical School found that Niacin profoundly prevents the degeneration of demyelinated axons and improves the behavioral deficits.

e. Vitamin D
A study published in a recent issue of the journal Neurology, the group receiving the vitamin D demonstrated a remarkable 41 percent reduction in new MS events with no meaningful side effects.

f. Etc.

B.4. Lou Gehrig's disease
1. Free radicals and Lou Gehrig's disease
Researchers found that glutamate in the synapses enhances the production of free radicals compounds only in motor nerve cells but spares other nerve cells such as cells control senses and other body functions, causing to more production of free radicals and leading to disrupting of the surrounding support cells, called astrocytes, which regulate glutamate levels.

2. Antioxidants and Lou Gehrig's disease
a. Vitamin B12 (methylcobalamin)
Researcher found that high doses of vitamin B12 (25 mg) as an antioxidant have been shown to improve or slow muscle wasting in the later stages of patients with ALS disease.

b. Vitamin E
Vitamin E beside helps to protect cell membranes from lipid peroxidation damage that reduce the risk of breakdown of the cell membrane, causing ALS.

c. Superoxide dismutase enzyme
Research found that mutations in the superoxide dismutase enzyme can increase the risk ALS in catalyzing the dismutation of superoxide into oxygen and hydrogen peroxide.

d. Cerebral cortex
Researcher found that oxidative protein damage and DNA alternation were found in elevating levels in the cerebral cortex of those with sporadic ALS.

e. Amino acids
study found that diet high in amino acids as antioxidants have shown some promising effect in treating ALS.

f. Etc.

B.5. Etc.

Alzheimer's Disease - My Story
This Is A Real Case Study, Written By An Alzheimer's Sufferer
Sharing His Hurts, Frustration And Desperation.

For the series of Alzheimer's disease, visit http://medicaladvisorjournals.blogspot.com/2012/01/alzheimers-disease.html

For Other Health articles visit http://medicaladvisorjournals.blogspot.com/

Delay 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.
Alzheimer's Disease - My Story
This Is A Real Case Study, Written By An Alzheimer's Sufferer
Sharing His Hurts, Frustration And Desperation.

For the series of Alzheimer's disease, visit http://medicaladvisorjournals.blogspot.com/2012/01/alzheimers-disease.html

For Other Health articles visit http://medicaladvisorjournals.blogspot.com/
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

Delay Dementia - Types of Dmentia

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

Types of dementia
1. Alzheimer's disease
 Alzheimer's disease is a brain disorder named for German physician Alois Alzheimer. Alzheimer's destroys brain cells, causing problems with memory, thinking and behavior severe enough to affect language communication, memory, lifelong hobbies or social life. Alzheimer's gets worse over time, and it is fatal. Over 1 million people in US alone are currently afflicted by Alzheimer's disease because of degeneration of hippocampus and cerebral cortex of the brain where memory, language and cognition are located. With this mental disorder, brain cells gradually die and generate fewer and fewer chemical signals day by day resulting in diminished of functions. Overtime memory thinking as well as behavior deteriorates. Today, there is no known cure.

2. Absence of acetylcholine
 If the nerves located in front of the brain perish, causing diminished quality of acetylcholine resulting in language difficulty, memory loss, concentration problem and reduced moblile skills because of lacking reaction in muscular activity and refection.

3. Dementia due to long-term alcohol abuse
 Dementia is common in patients with alcoholism. Most classic is the Korsakoff's dementia resulting in extremely poor short term memory and often associated with the memory losses are confabulations.

4. Multi-infarct dementia
Also known asvascular dementia , is the second most common form of dementia after Alzheimer's disease in older adults. It is caused by different mechanisms all resulting in vascular lesions in the brain.

5. Dementia associated with Parkinson's disease
 Parkinson disease (PD) is a disabling, progressive condition. It is a cognitive deficits due to the interruption of frontal-subcortical loops that facilitate cognition and that parallel the motor loop.

6. Creutzfeldt-Jakob disease (CJD)
People who have eaten contaminated beef many years may be infected without even knowing it. Creutzfeldt-Jakob disease is a quickly progressing and fatal disease that consists of dementia, muscle twitching and spasm.

7. Subdural hematoma
It is the accumulation of blood beneath the outer covering of the brain that result from the rupture of blood vessel. Subdural hemorrhages may cause an increase in tracranial pressure, which can cause compression of and damage to delicate brain tissue. Acute subdural hematoma has a high mortality rate.

There are many types of dementia such as metabolic disorders, dementia due to long-term substance abuse, hypothyroidism, and hyperethyroidism.

Alzheimer's Disease - My Story
This Is A Real Case Study, Written By An Alzheimer's Sufferer
Sharing His Hurts, Frustration And Desperation.

For the series of Alzheimer's disease, visit http://medicaladvisorjournals.blogspot.com/2012/01/alzheimers-disease.html

For Other Health articles visit http://medicaladvisorjournals.blogspot.com/