Holistic Health Articles and Research Related to Herbal Medicines, Foods and Phytochemicals

Wednesday 30 November 2016

The holistic Prevention, Management and Treatment of Dementia - Free radical causes of Lou Gehrig's disease(Amyotrophic lateral sclerosis)

Kyle J. Norton (Scholar)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.

Dementia

Dementia is defined as neuro degeneration syndrome among elder, affecting memory, thinking, orientation, comprehension, calculation, learning capacity, language, and judgement over 47 millions
of worldwide population, mostly in the West. The evaluation of the syndrome by holistic medicine has been lacking, especially through conventional medicine research and studies.

Causes of dementia

B.4. Lou Gehrig's disease(Amyotrophic lateral sclerosis)
1. Free radicals and Lou Gehrig's disease
Researchers found that glutamate in the synapses enhances the production of free radicals(77) only in motor nerve cells but spares other nerve cells(74)(75) such as cells control senses and other body functions, causing disruption of astrocytes in regulated glutamate levels(76).

2. Antioxidants and Lou Gehrig's disease
a. Vitamin B12 (methylcobalamin)
High doses of vitamin B12 as an antioxidant have shown to improve or slow muscle wasting in the later stages of patients with ALS disease(78)(79).

b. Vitamin E
Vitamin E protected against cell membranes from lipid peroxidation damage(80) in reduced the risk of breakdown of the cell membrane cause of ALS(81).

c. Superoxide dismutase enzyme
Mutations in the superoxide dismutase enzyme can increase the risk ALS(82) in catalyzing the dismutation of superoxide into oxygen and hydrogen peroxide(83).

d. Cerebral cortex
Oxidative stress and DNA alternation triggered neurons damage(84) were found in elevating levels in mice with ALS(85).

e. Amino acids
Diet high in amino acids as antioxidants have shown some promising effect in treating ALS(86)(87).

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References
(74) System xC- is a mediator of microglial function and its deletion slows symptoms in amyotrophic lateral sclerosis mice by Mesci P1, Zaïdi S1, Lobsiger CS1, Millecamps S1, Escartin C2, Seilhean D1, Sato H3, Mallat M1, Boillée S4.(PubMed)
(75) Microglia and motor neurons during disease progression in the SOD1G93A mouse model of amyotrophic lateral sclerosis: changes in arginase1 and inducible nitric oxide synthase by Lewis KE, Rasmussen AL, Bennett W, King A, West AK, Chung RS, Chuah MI1.(PubMed)
(76) Mutant disrupted-in-schizophrenia 1 in astrocytes: focus on glutamate metabolism by Abazyan S1, Yang EJ, Abazyan B, Xia M, Yang C, Rojas C, Slusher B, Sattler R, Pletnikov M.(PubMed)
(77) Glutamate release and free radical production following brain injury: effects of posttraumatic hypothermia by Globus MY1, Alonso O, Dietrich WD, Busto R, Ginsberg MD.(PubMed)
(78) Methyl Vitamin B12 but not methylfolate rescues a motor neuron-like cell line from homocysteine-mediated cell death. by Hemendinger RA1, Armstrong EJ 3rd, Brooks BR.(PubMed)
(79) [Clinical trials of ultra-high-dose methylcobalamin in ALS].[Article in Japanese] by Izumi Y1, Kaji R.(PubMed)
(80) Antioxidant effect of 4-nerolidylcatechol and α-tocopherol in erythrocyte ghost membranes and phospholipid bilayers. by Fernandes KS1, Silva AH, Mendanha SA, Rezende KR, Alonso A.(PubMed)
(81) Vitamin E serum levels and controlled supplementation and risk of amyotrophic lateral sclerosis by Michal Freedman D1, Kuncl RW, Weinstein SJ, Malila N, Virtamo J, Albanes D.(PubMed)
(82) Aggregation propensities of superoxide dismutase G93 hotspot mutants mirror ALS clinical phenotypes by Pratt AJ1, Shin DS1, Merz GE2, Rambo RP3, Lancaster WA4, Dyer KN3, Borbat PP5, Poole FL 2nd4, Adams MW4, Freed JH5, Crane BR2, Tainer JA6, Getzoff ED7.(PubMed)
(83) Hydrogen peroxide induce modifications of human extracellular superoxide dismutase that results in enzyme inhibition by Gottfredsen RH1, Larsen UG, Enghild JJ, Petersen SV.(PubMed)
(84) Oxidative DNA damage and alteration of glutamate transporter expressions in the hippocampal Ca1 area immediately after ischemic insult.by An SJ1, Kang TC, Park SK, Hwang IK, Cho SS, Chung MH, Won MH.(PubMed)
(85) Functional contribution of the transcription factor ATF4 to the pathogenesis of amyotrophic lateral sclerosis.by Matus S1, Lopez E, Valenzuela V, Nassif M, Hetz C.(PubMed)
(86) Amino acids as biomarkers in the SOD1(G93A) mouse model of ALS.by Bame M1, Grier RE, Needleman R, Brusilow WS.(PubMed)
(87) Branched-chain amino acids and amyotrophic lateral sclerosis: a treatment failure? The Italian ALS Study Group.[No authors listed](PubMed)

Tuesday 29 November 2016

The holistic Prevention, Management and Treatment of Dementia - Free radical causes of Multiple Sclerosis

Causes of dementia

B. Free radical causes of dementia
B.3. Multiple Sclerosis
1. Free radicals and Multiple Sclerosis
Free radical activity is a contributory factors in MS(60) due to proinflammatory cytokines in free radicals production in the peripheral immune and central nervous system (CNS)(60).

2. Antioxidants and Multiple sclerosis
Antioxidants protect the neural tissues from damage against inflammation caused by oxidative stress.
a. TNFalpha
TNFalpha, an imflammatory cytokine showed to associate with MS inhibited by antioxidants(61)) of green tea(62), and curcumin(63).

b. Melatonin
Melatonin functions as an antioxidant has the ability to protect neurons(65)(66) from free radicals cause of lipid peroxidation(64).

c Selenium
Some studies found that the level of selenium in the blood of people with MS was lower than in that of people without(67)(68). In patients with MS, all abnormalities may be normalized by daily intake of selenium(69),

d. Niacin
Niacin acting as antioxidant is a key to the successful treatment of multiple sclerosis, profoundly prevents the degeneration(70) of demyelinated axons and improves the behavioral deficits(71).

e. Vitamin D
Serum of 25(OH)D level showed to regulate expression dynamics of a large gene-gene interaction system in immune modulatory processes of MSactivity(72). According to the study published by the journal Neurology, group receiving vitamin D supplement demonstrated a remarkable 41 percent reduction in new MS events with no meaningful side effects(73).

f. Etc.

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References
(60) Reduction of free radicals in multiple sclerosis: effect of glatiramer acetate (Copaxone) by
Iarlori C1, Gambi D, Lugaresi A, Patruno A, Felaco M, Salvatore M, Speranza L, Reale M.(PubMed)
(61) IL-1, IL-1R and TNFalpha gene polymorphisms in Iranian patients with multiple sclerosis. by
Sarial S1, Shokrgozar MA, Amirzargar A, Shokri F, Radfar J, Zohrevand P, Arjang Z, Sahraian MA, Lotfi J.(PubMed)
(62) Epigalloccatechin-3-gallate inhibits ocular neovascularization and vascular permeability in human retinal pigment epithelial and human retinal microvascular endothelial cells via suppression of MMP-9 and VEGF activation by Lee HS1, Jun JH2, Jung EH3, Koo BA4, Kim YS5.(PubMed)
(63) Curcumin inhibits TNFalpha-induced lectin-like oxidised LDL receptor-1 (LOX-1) expression and suppresses the inflammatory response in human umbilical vein endothelial cells (HUVECs) by an antioxidant mechanism by Lee HS1, Lee MJ, Kim H, Choi SK, Kim JE, Moon HI, Park WH.(PubMed)
(64) [The influence of melatonin on lipid peroxidation and antioxidant enzymes activity during multiply repetitive stress actions].[Article in Russian] by Serikov VS, Liashev IuD.(PubMed)
(65) Melatonin augments hypothermic neuroprotection in a perinatal asphyxia model.by Robertson NJ1, Faulkner S, Fleiss B, Bainbridge A, Andorka C, Price D, Powell E, Lecky-Thompson L, Thei L, Chandrasekaran M, Hristova M, Cady EB,Gressens P, Golay X, Raivich G.(PubMed)
(66) Therapeutic potential of melatonin and its analogs in Parkinson's disease: focus on sleep and neuroprotection.by Srinivasan V1, Cardinali DP, Srinivasan US, Kaur C, Brown GM, Spence DW, Hardeland R, Pandi-Perumal SR.(PubMed)
(67) High dose antioxidant supplementation to MS patients. Effects on glutathione peroxidase, clinical safety, and absorption of selenium. by Mai J1, Sørensen PS, Hansen JC.(PubMed)
(68) Oxidative stress in patients with multiple sclerosis. by Syburra C1, Passi S.(PubMed)
(69) Selenium in chronic neurologic diseases. Multiple sclerosis and Batten's disease by Clausen J1, Jensen GE, Nielsen SA.(PubMed)
(70) The biochemical pathways of central nervous system neural degeneration in niacin deficiency byFu L1, Doreswamy V2, Prakash R2.(PubMed)
(71) Nutrition and performance in children. by Fanjiang G1, Kleinman RE.(PubMed)

(72) Molecular mechanism underlying the impact of vitamin D on disease activity of MS.by Munger KL1, Köchert K2, Simon KC1, Kappos L3, Polman CH4, Freedman MS5, Hartung HP6, Miller DH7, Montalbán X8, Edan G9, Barkhof F4, Pleimes D2,Sandbrink R10, Ascherio A1, Pohl C11.(PubMed)

(73) Vitamin D: The Multiple Sclerosis Connection by David Perlmutter, M.D. (The Huffington post)

Monday 28 November 2016

The holistic Prevention, Management and Treatment of Dementia - Free radical causes of Parkinson's disease

Causes of dementia

B. Free radical causes of dementia
B.2. Parkinson's disease
1. Free radicals and Parkinson's disease
Patients with Parkinson's disease have low levels of polyunsaturated fat in the substania nigra(44)(45). Also patients with the disease found to contain waste pigments of lipofusion(46) and other polymers in the neurons(47) where dopamine is most active.

2. Aging and Parkinson's disease
According to Julius-Maximilians-University, physiological aging and OS-dependent aggregation of proteins, accompanied with environment toxins(49) are found to associate to the progression of the disease(48).

3. Antioxidants and Parkinson's disease
Antioxidants play an vital role for patients with Parkinson's disease.
a. Superoxide dismutase
Researcher found that the progression of the disease may be associated with the decrease levels of superoxide dismutase, a antioxidant enzyme(50). According to University of Thessaloniki, patients with advanced Parkinson' diseases showed a statistically significant decrease of SOD activity in whole blood and in red blood cells(51).

b. NADH ubiquinone reductase
Levels of NADH ubiquinone reductase is decreased in the substania
7

nigra(52) in patients with PD, causing neurons apoptosis, but this can be treated with antioxidants Acetyl-L-carnitine (53) and alpha lipoic acid(54).

c. Uric acid
People with a high blood level of the natural antioxidant uric acid have a lower risk of developing Parkinson's disease(55) than do people with lower levels(56), but high levels of uric acid increases the risk of kidney diseases(57) and gout(58).

d. Glutathione
Glutathoine showed to deactivate the harmful product HNE of lipid peroxidation(59).

f. Etc.

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References
(44) Small Amounts of Isotope-reinforced Polyunsaturated Fatty Acids Suppress Lipid Autoxidation by Shauna Hill,a Connor R. Lamberson,b Libin Xu,b Randy To,a Hui S. Tsui,a Vadim V. Shmanai,c Andrei V. Bekish,dAgape M. Awad,a Beth N. Marbois,a Charles R. Cantor,e,f Ned A. Porter,b Catherine F. Clarke,a,* and Mikhail S. Shchepinovf,*(PubMed)
(45) Isotopic reinforcement of essential polyunsaturated fatty acids diminishes nigrostriatal degeneration in a mouse model of Parkinson's disease by Mikhail S. Shchepinova, , Vivian P. Choub, e, , Erik Pollockc, , J. William Langstonb, , Charles R. Cantora, d, , Robert J. Molinaria, , Amy B. Manning-Boğb, e,(ScienceDirect)
(46) Altered lipofuscin pigmentation in the basal nucleus (Meynert) in Parkinson's disease byUlfig N1.(PubMed)

(47) Changes within the basal nucleus in Parkinson's disease by Ulfig N1, Braak E, Braak H.(PubMed)
(48) Free radicals in Parkinson's disease by Koutsilieri E1, Scheller C, Grünblatt E, Nara K, Li J, Riederer P.(PubMed)
(49) Considerations on the role of environmental toxins in idiopathic Parkinson's disease pathophysiology by Pan-Montojo F1, Reichmann H2.(PubMed)
(50) Superoxide dismutase overexpression protects dopaminergic neurons in a Drosophila model of Parkinson's disease by Botella JA1, Bayersdorfer F, Schneuwly S.(PubMed)
(51) Superoxide dismutase activity in early and advanced Parkinson's disease by Bostantjopoulou S1, Kyriazis G, Katsarou Z, Kiosseoglou G, Kazis A, Mentenopoulos G.(PubMed)
(52) Quercetin up-regulates mitochondrial complex-I activity to protect against programmed cell death in rotenone model of Parkinson's disease in rats by Karuppagounder SS1, Madathil SK, Pandey M, Haobam R, Rajamma U, Mohanakumar KP.(PubMed)
(53) Behavioral and neurochemical effects of alpha-lipoic Acid in the model of Parkinson's disease induced by unilateral stereotaxic injection of 6-ohda in rat by de Araújo DP1, De Sousa CN, Araújo PV, Menezes CE, Sousa Rodrigues FT, Escudeiro SS, Lima NB, Patrocínio MC, Aguiar LM, Viana GS, Vasconcelos SM.(PubMed)
(54) Acetyl-L-carnitine and α-lipoic acid affect rotenone-induced damage in nigral dopaminergic neurons of rat brain, implication for Parkinson's disease therapy by Zaitone SA1, Abo-Elmatty DM, Shaalan AA.(PubMed)
(55) Association of serum uric acid levels with the progression of Parkinson's disease in Chinese patients by Sun CC1, Luo FF, Wei L, Lei M, Li GF, Liu ZL, LE WD, Xu PY.(PubMed)
(56) Uric acid in Parkinson's disease by Schlesinger I1, Schlesinger N.(PubMed)
(57) Potential role of uric acid in metabolic syndrome, hypertension, kidney injury, and cardiovascular diseases: is it time for reappraisal? by Soltani Z1, Rasheed K, Kapusta DR, Reisin E.(PubMed)
(58) Gout-associated uric acid crystals activate the NALP3 inflammasome. by Martinon F1, Pétrilli V, Mayor A, Tardivel A, Tschopp J.(PubMed)
(59) Lipid mediator interplay: resolvin D1 attenuates inflammation evoked by glutathione-conjugated lipid peroxidation products. by Filep JG1.(PubMed)

Sunday 27 November 2016

The holistic Prevention, Management and Treatment of Dementia - Deficiency Causes of dementia Due to Aging

Deficiency Causes of dementia Due to Aging

1. Vitamin D and 1,25-dihydroxyvitamin D(3) deficiency
Vitamin D levels not only plays an important role in the pathogenesis of many age-associated diseases including cancer, heart disease, type 2 diabetes
mellitus and stroke, but also associate with increased risk of prevalent cognitive dysfunction. According to number of studies, raising vitamin D plays a role in decreased cognitive dysfunction and dementia(24). Evidence from epidemiological also insisted the association between 25(OH)D concentrations and systolic blood pressure, risk for CV disease-related deaths, symptoms of depression, cognitive deficits, and mortality(25).

2. Folic acid with vitamin B12 deficiency
Folates are vitamins essential to the development of the central nervous system. Deficiency of folate can increase the risk of dementia. According to Cochrane Dementia and Cognitive Improvement Group, folic acid plus vitamin B12 were effctive in reducing the serum homocysteine concentrations, with no adverse effects(26).

3. Vitamin B12 deficiency
An association between neuropsychiatric disorders and vitamin B12deficiency has been recognized since 1849. Deficiency of Vitamin B12 are found in many elders and might contribute to age-associated cognitive impairment, according to the Scientist at Cochrane Dementia and Cognitive Improvement Group(27).

4. Vitamin B6 deficiency
Vitamin B6 supplementation showed to reduce the risk of developing cognitive impairment in older healthy people, and improve cognitive functioning of people with cognitive decline and dementia, according the study conducted by Cochrane Dementia and Cognitive Improvement Group(28).

5. Deficiency of Insulin-like growth factor (IGF)-1and growth hormones
Deficiency of Insulin-like growth factor (IGF)--1 hormone may contribute to the genesis of cognitive impairment and dementia in the elderly patients. Old age, in the absence of circulating IGF-1, a hormone with a complex role in brain function has seen to link to an acceleration of neurological diseases(29) Growth hormone and IGF-1 replacement showed to increase neurogenesis, vascular density, and glucose utilization, and alter NMDA receptor subunit composition in brain areas implicated learning and memory, in animal (30)and children(31) studies.

8. Deficiency of cerebrospinal fluid melatonin
Melatonin plays an essential role in ventricular system via choroid plexus portals. In Alzheimer's disease, inadequate melatonin increases risk of the neuropathological changes due to hydroxyl radicals cause of damage mitochondria and initiated cascade of oxygen radicals(32).

9. Decreased dehydroepiandrosterone (DHEA)
Dehydroepiandrosterone sulfate (DHEAS) concentrations
DHEA, a neurosteroid secreted by the adrenal cortex. is also a neurosteroid. The levels of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) concentrationsare decline in concentration with age(33).

10. Etc.

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References(24) Vitamin D, cognitive dysfunction and dementia in older adults by Dickens AP1, Lang IA, Langa KM, Kos K, Llewellyn DJ.(PubMed)
(25) Extraskeletal effects of vitamin D in older adults: cardiovascular disease, mortality, mood, and cognition by Barnard K1, Colón-Emeric C.(PubMed)
(26) Folic acid with or without vitamin B12 for cognition and dementia by Malouf M1, Grimley EJ, Areosa SA.(PubMed)
(27) Vitamin B12 for cognition by Malouf R1, Areosa Sastre A.(PubMed)
(28) The effect of vitamin B6 on cognition by Malouf R1, Grimley Evans J.(PubMed)
(29) Aging, synaptic dysfunction, and insulin-like growth factor (IGF)-1 by Deak F1, Sonntag WE.(PubMed)
(30) Growth hormone and insulin-like growth factor-1 (IGF-1) and their influence on cognitive aging by Sonntag WE1, Ramsey M, Carter CS.(PubMed)
(31) The role of the somatotropic system in cognition and other cerebral functions by Creyghton WM1, van Dam PS, Koppeschaar HP.(PubMed)
(32) Alzheimer's disease: roles for mitochondrial damage, the hydroxyl radical, and cerebrospinal fluid deficiency of melatonin by Maurizi CP1.(PubMed)
(33) Decreased dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS)

Saturday 26 November 2016

The holistic Prevention, Management and Treatment of Dementia - Free radical causes of dementia

Free radical causes of dementia

B.1. Alzheimer’s disease
1. Free radical and Alzheimer’s disease
Free radicals causes of Alzheimer’s disease is well defined in many researches(34). Oxidative stress-induced injury involved the selective modification of different intracellular proteins may lead to the neurofibrillary degeneration of neurons in the brain(34a)(34b).

2. Antioxidants and Alzheimer’s disease
a. Docosahexaenoic acid (DHA)
Change of brain aging in DHA metabolism, was found in patients with Alzheimer's disease(34c)(34d). DHA, a naturally occurring component found in every cell membrane with ability to increase phosphatidylserine(35)(35a) is important in decreased production of proinflammatory omega-6 eicosanoids causes of Alzheimer's disease(35b) and in improved the memory of animals with Alzheimer's disease by suppressing oxidative damage in the brain(41).

b. Vitamin E
Vitamin E reduced generalized inflammation, may slow the decline of mental and physical abilities in people with Alzheimer's disease (AD) over the long term(36). Also vitamin E inhibited cells damage and cells death caused by beta-amyloid(36a)(36b), which is toxic to brain cells(36c).

c. Phosphatidylserine
Patients who had Alzheimer’s disease taken100 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 without(37)(40).

d. Antioxidants
Antioxidant are found at much lower levels for patients with Alzheimer’s disease(38), such as serum of vitamin A, C, E, zinc and transfferin. Carotenoids are fat-soluble antioxidants that may protect polyunsaturated fatty acids, such as n-3 fatty acids from oxidation(39)

e. Muscarinic cholinergic receptors
Alzheimer’s disease patients showed to exhibit the significant loss of muscarinic cholinergic receptors neurons(42) causes of reduced volume of neural transmission that can lead to loss of memory(43).

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References
(34) Possible causes of Alzheimer's disease: amyloid fragments, free radicals, and calcium homeostasis by Hölscher C1.(PubMed)
(34a) PROTEIN OXIDATION IN THE BRAIN IN ALZHEIMER'S DISEASE M. Y. AKSENOV,a,d* M. V. AKSENOVA,a,b D. A. BUTTERFIELD,a,c J. W. GEDDESa,d and W. R. MARKESBERYa,b a Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40536, US.(Pergamon)
(34b) Interactions between β-amyloid and central cholinergic neurons: implications for Alzheimer's disease by Satyabrata Kar, Stephen P.M. Slowikowski, David Westaway, and Howard T.J. Mount(PubMed)
(34c) The Impact of Cholesterol, DHA, and Sphingolipids on Alzheimer's Disease by Marcus O. W. Grimm, Valeri e C. Zimmer, 1 Johannes Lehmann, Heike S. Grimm, and Tobias Hartmann (PubMed)
(34d) DHA Improves Cognition and Prevents Dysfunction of Entorhinal Cortex Neurons in 3xTg-AD Mice Dany Arsenault,1,2 Carl Julien,1,2 Cyntia Tremblay,2 and Frédéric Calon1,2,(PubMed)
(35) Administration of DHA-PS to aged mice was suitable for increasing hippocampal PS and DHA ratio by Ohkubo T1, Tanaka Y.(PubMed)
(35a) Neuronal specific increase of phosphatidylserine by docosahexaenoic acid.by Guo M1, Stockert L, Akbar M, Kim HY.(PubMed)
(35b) Docosahexaenoic acid (DHA), an essential fatty acid for the proper functioning of neuronal cells: their role in mood disorders By Alfonso Valenzuela B. ( University of Chile)
(36) Vitamin E for Alzheimer's dementia and mild cognitive impairment by Farina N1, Isaac MG, Clark AR, Rusted J, Tabet N.(PubMed)
(36a)Inflammatory mediator and beta-amyloid (25-35)-induced ceramide generation and iNOS expression are inhibited by vitamin E by Ayasolla K1, Khan M, Singh AK, Singh I.(PubMed)
(36b) Vitamin E but not 17beta-estradiol protects against vascular toxicity induced by beta-amyloid wild type and the Dutch amyloid variant by Muñoz FJ1, Opazo C, Gil-Gómez G, Tapia G, Fernández V, Valverde MA, Inestrosa NC.(PubMed)
(36c) Parkin protects against mitochondrial toxins and beta-amyloid accumulation in skeletal muscle cells by Rosen KM1, Veereshwarayya V, Moussa CE, Fu Q, Goldberg MS, Schlossmacher MG, Shen J, Querfurth HW.(PubMed)
(37) Soybean-Derived Phosphatidylserine Improves Memory Function of the Elderly Japanese Subjects with Memory Complaints by Akito Kato-Kataoka,1,* Masashi Sakai,1 Rika Ebina,1 Chiaki Nonaka,2 Tsuguyoshi Asano,3 and Takashi Miyamori4(PubMed)
(38) Oxidative stress involving changes in Nrf2 and ER stress in early stages of Alzheimer's disease by Mota SI1, Costa RO1, Ferreira IL1, Santana I2, Caldeira GL3, Padovano C3, Fonseca AC3, Baldeiras I4, Cunha C5, Letra L5, Oliveira CR4, Pereira CM6, Rego AC7.(PubMed)
(39) Nutritional biomarkers in Alzheimer's disease: the association between carotenoids, n-3 fatty acids, and dementia severity by Wang W1, Shinto L, Connor WE, Quinn JF.(PubMed)
(40) The effect of soybean-derived phosphatidylserine on cognitive performance in elderly with subjective memory complaints: a pilot study by Yael Richter, Yael Herzog, Yael Lifshitz, Rami Hayun, and Sigalit Zchut(PubMed)
(41) Action of long-chain fatty acids on protein kinase C activity: comparison of omega-6 and omega-3 fatty acids.by Holian O1, Nelson R.(PubMed)
(42) Interactions between β-amyloid and central cholinergic neurons: implications for Alzheimer's disease by Satyabrata Kar, Stephen P.M. Slowikowski, David Westaway, and Howard T.J. Mount(PubMed)
(43) Chapter 12Memory Impairments Associated with Stress and Aging by Carmen Sandi.(PubMed)

Friday 25 November 2016

The holistic Prevention, Management and Treatment of Dementia - Types of dementia

Types of dementia

1. Alzheimer's disease

Alzheimer's disease is a brain disorder named for German physician Alois Alzheimer(1). 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(2). Over 1 million people in US alone are currently afflicted by Alzheimer's disease because of degeneration of hippocampus and cerebral cortex(3) of the brain where memory, language and cognition(4) 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(5), caused by diminished quality of acetylcholine due long term alcohol abused may result of cognitive dysfunction(6) causes of language difficulty, memory loss, concentration problem, and anxiety- and depression-like behaviors(8),reduced moblile skills because of lacking reaction in muscular activity and refection(7).

3. Dementia due to long-term alcohol abuse
Dementia is common in patients with alcoholism(9). Most classic is the Korsakoff's dementia resulted in extremely poor short term memory(10) and often associated with the memory losses of confabulations due to diminished processing resources and/or an encoding or retrieval deficit(11).

4. Multi-infarct dementia
Also known as vascular dementia, is the second most common form of dementia after Alzheimer's disease in older adults caused by different mechanisms all results in vascular lesions(12) of the brain(13).

5. Dementia associated with Parkinson's disease
Parkinson disease (PD) is a disabling, progressive condition, causes of cognitive deficits due to the interruption of frontal-subcortical loops that facilitate cognition and parallel the motor loop(15)(16) due to loss of substantia nigra pars compacta (SNc) dopamine (DA) neurons(14).

6. Creutzfeldt-Jakob disease (CJD)
People who have eaten contaminated beef(18) for many years may be infected without even knowing it. Creutzfeldt-Jakob disease is a quickly progressing and fatal disease consisted of dementia(19), muscle abnormal functions(17).

7. Subdural hematoma
It is the accumulation of blood beneath the outer cover of the brain resulted from the rupture of blood vessel(20)(21). Subdural hemorrhages may increase intracranial pressure(22), causing compression and damage to delicate brain tissue. Acute subdural hematoma has a high mortality rate(23).

Other types of dementia include metabolic disorders, dementia due to long-term substance abuse, hypothyroidism, and hyperethyroidism.

References
(1) Alzheimer's disease (Wikipedia)
(2) Understanding dementia in the sociocultural context: a review by Cipriani G1, Borin G2.(PubMed)
(3) What is normal in normal aging? Effects of aging, amyloid and Alzheimer's disease on the cerebral cortex and the hippocampus by Fjell AM1, McEvoy L2, Holland D3, Dale AM4, Walhovd KB5; Alzheimer's Disease Neuroimaging Initiative.(PubMed)
(4) Does degree of gyrification underlie the phenotypic and genetic associations between cortical surface area and cognitive ability? by Docherty AR1, Hagler DJ Jr2, Panizzon MS3, Neale MC4, Eyler LT5, Fennema-Notestine C6, Franz CE3, Jak A7, Lyons MJ8, Rinker DA9, Thompson WK10, Tsuang MT11, Dale AM12, Kremen WS13.(PubMed)
(5) Acetylcholine facilitates recovery of episodic memory after brain damage by Croxson PL1, Browning PG, Gaffan D, Baxter MG.(PubMed)
(6) Postsynaptic activity reverses the sign of the acetylcholine-induced long-term plasticity of GABAA inhibition by Domínguez S1, Fernández de Sevilla D2, Buño W3.(PubMed)
(7) Induction of dystrophin-associated proteins together with nicotinic acetylcholine receptors by denervation in the absence of dystrophin in skeletal muscles of mdx mice by Mitsui T1, Kawai H, Kawajiri M, Kunishige M, Aki K, Saito S.(PubMed)
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Thursday 24 November 2016

Antioxidants: The Summary

Kyle J. Norton(Scholar, Master of Nutrients), all right reserved.
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.

Human aging is a biological process, no one can stop, but delay it. It is possible that one person has a physiological younger than his or her biological if one 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.

The Summary

Aging is a natural process, no one can stop but delay it. Over last 20+ years, researchers found that free radicals have played a majors role in the progression of aging process as they damage every cells of the whole body. One of the majoy cause of free radical is that of setting a chain reaction, if left unchecked, it can cause death of the cells, triggering the attack to the adjacent cells. At the middle age, due to weakened immune system, damage of body organs and reduced levels of antioxidants, our health is deteriorate and aging progressed at a fast rate, it is up to you to delay it by eating healthy, living a healthy style, exercise, etc. if you want to look younger than you biological age, live longer, healthier and diseases free.

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