NMDC221 Session 17: Nervous System Disease Part IV · NMDC221 Session 17: Nervous System Disease...

© Endeavour College of Natural Health endeavour.edu.au 1

NMDC221 Session 17:

Nervous System Disease

Part IV


Recommended Reading

Mahan, LK, & Raymond, JL (14th ed) 2016, Krause’s food & the

nutrition care process, 14th ed, Elsevier, St. Louis, MO.

pp.835-8, 852-63


Topic Summary

Nervous System Disease: Part IV

o Nutritional treatment and consideration of drug-nutrient

interactions for:

• Dementia

• Alzheimer’s disease

• Parkinson’s disease


Dementia


DementiaWhat is Dementia?

o Dementia is a clinical syndrome characterised by a cluster of

symptoms and signs manifested by difficulties in memory,

disturbances in language, psychological and psychiatric changes,

and impairments in activities of daily living. Alzheimer’s disease is a

specific disease entity and is the commonest cause of dementia.’

(Burns, A 2009)

o Common in the elderly (affecting > 15% of persons > 65 yr old and

as many as 40% of persons > 80 yr old).

o May occur at any age and can affect young people as the result of

injury or hypoxia. (Kumar & Clark, 2009)

o Burden of disease - About 12 million people worldwide have

dementia, and this total is likely to increase to 25 million by 2040

(Burns A, 2009).


DementiaDementia is categorized into a few subtypes.:-

Alzheimer’s disease (AD) accounts for about half of the affected population

Vascular dementia (VaD) (20–25%)

Mixed dementia (5–10%),

Parkinson’s disease,

Dementia with Lewy bodies

Physical brain injury

Huntington’s disease

Creutzfeldt–Jacob disease

Frontotemporal dementia/Pick’s disease

Normal pressure hydrocephalus

(Chen, Lin, Chen 2009)

AD is also the most common neurodegenerative disorder and affects 20–30

million individuals worldwide. AD has been further categorized into two forms

according to its onset: sporadic cases (> 95%) with late-onset disease; and

autosomal-dominant mutation cases (< 5%) with early onset.


Dementia

Risks Factors:

o Several factors are related to dementia, e.g. age, ethnicity, sex,

genetic factors (APOE gene for late onset AD & for early-onset

cases, APP, preselin (PS)-1, and PS-2 genes appear most relevant)

o Physical activity, smoking, drug use, education level, alcohol

consumption, body mass index, comorbidity, and environmental

factors (Chen, Lin, Chen 2009)

Signs & symptoms:

o Poor memory and disorientation

o Cognitive impairment (aphasia, apraxia, agnosia, or a loss of

executive functioning).

Unfortunately, the appearance of clinical features suggest there is a

substantial progression of the disease process.

(Kumar & Clark, 2009)


DementiaCauses of Dementia:o Cerebral atrophy - Alzheimer's disease accounts for over 65%.

Other diseases implicated include Parkinson’s disease, Huntington’s disease

o Diffuse vascular disease

o Metabolic insufficiencies – uraemia, liver failure

o Nutritional deficiencies - vitamins B1, B3, B6 & Folate or B12

o Toxic damage – alcohol, solvents, heavy metals

o Head trauma & lesions

o Infections – HIV, neurosyphilis

o Hypothyroidism, hypoparathyroidism



DementiaNutritional Treatment Aims

Support Digestion:

o Address nutritional deficiencies

o Increase absorption (digestive enzymes or lemon water)

o Maintain adequate protein, fibre, fluid intakes (assess hydration)

o Maintain consistent blood glucose levels (eat every 3 hours)

o Assess EFA and saturated fat intake

o Correct any gut dysbiosis: prebiotics, probiotics, anti-microbials,

repairing nutrients

(Sarris & Wardle, 2010)


Dementia

Nutritional Treatment Aims

Support anti-oxidant status

o Increased consumption of antioxidant foods

o Minimise environmental chemical & toxin contact

o Assess homocysteine levels – support B12 & folate

Support neuronal activity

o Support phospholipid maintenance – lecithin, EPA/DHA

o Support the endogenous production of Dopamine, Serotonin, GABA

and Acetylcholine



Dementia


Support liver detoxification & heavy metal chelation

o Assess heavy metal exposure: lead, mercury, aluminum

o Green leafy vegetables, cruciferous vegetables, soluble fiber,

dandelion and other bitter vegetables

o Glycine, cysteine and glutamine for glutathione production

Support cellular metabolism & energy

Improve circulation



Alzheimer's Disease


Alzheimer's Disease

o A common, progressive form of Dementia (50% - 70% of all cases)

that usually occurs during middle age or later.

o Exact cause of Alzheimer’s Disease has not yet been determined

and is difficult to diagnose. However, there is a strong genetic link (

o On autopsy a progressive, loss of cognitive function associated with

an excessive number of senile plaques in the cerebral cortex and

subcortical grey matter, which also contains beta-amyloid and

neurofibrillary tangles.

Signs & Symptoms

o Dementia, poor memory, mood, depression, language impairment,

seizures – later in disease.

(Bryant & Knights, 2011; Kumar & Clark, 2009)


Alzheimer's DiseaseRisk factors :

o Age. Also some studies on parental age at birth, but still inconclusive.

o Sex - AD higher in women compared with men at ages >85 years (Chen,

Lin, Chen 2009)

o Positive family history

o Presence of APO-E4 gene – significant (later AD). A Swedish twin study has

reported that 60–80% of AD is

attributable to genetic effects (Gatz M,

Fratiglioni L, Johansson B, et al 2005)

o Inflammation - recent studies have shown that polymorphisms of one of the

inflammatory genes alone or in combination have comparable effects on AD

risk to those for the APOEe4 allele (Chen, Lin, Chen 2009).


AD Risk Factors Continued:

• Smoking

• Trisomy 21 (Down’s syndrome) – can develop pathological brain changes

after 30-40 yrs age, indistinguishable from Alzheimer’s

• Low Physical Activity (PA) - physical

activity is associated positively with

cognitive function among older

people. Other studies have found that

physical activity is associated with

a reduction of 30–50% in cognitive

decline (Chen, Lin, Chen 2009)

• Trauma to the head

• Heavy metal toxicity – particularly Aluminium

• Oxidative damage to brain tissue – low antioxidants, vascular issues

• Hyper-inflammation

• Circulation disorders – due to impaired vascular integrity



AD – Risk Factors cont.

o Drugs

Benzodiazepine's increase the risk of AD.

However - the following appeared to

reduce the risk:

Statins

HRT

antihypertensive drugs

NDAID’s (Chen. Lin, Chen 2009)

o Alcohol

Alcohol drinking may be protective for AD and dementia, but not for VaD and cognitive decline

(Peters R, Peters J, Warner J, et al. 2008)


Alzheimer's Disease

Therapeutic Actions

Homocysteine

o Recently, a few studies have linked increased levels of

plasma Homocysteine with increased risk of AD and

increased rate of progression.

(Paulionis, Kane, & Meckling, 2005)

o Malouf & Evans (2008) found that “…group of healthy

elderly people with high homocysteine levels, 800

mcg/day folic acid supplementation over three years was

associated with significant benefit in terms of global

functioning…memory storage…and information-

processing speed.”


Alzheimer’s Disease

Therapeutic Actions

Vitamin B3

o Mild to severe Alzheimer’s patients were given 10mg of

NADH. There was a 240% increase in NADH activity

within 2 weeks. This improved mental function, alertness

& memory with increases in dopamine & norepinephrine.

o Global deterioration scale ratings conducted before and

after NADH treatment confirmed significant

improvement. (Demarin et.al 2004)

o Green et.al. (2008) found that nicotinamide was

indicated for early or mild stages of Alzheimer’s disease.


Alzheimer’s DiseaseTherapeutic Actions

Turmeric

o The incidence of Alzheimer disease has been found to be lower

in India and areas with a high traditional consumption of

turmeric.

o The therapeutic effect of turmeric is thought to be associated

with decreased beta-amyloid plaques, delayed degradation of

neurons, metal-chelation, anti-inflammatory, antioxidant and

decreased microglia formation.

o Rodent study found turmeric significantly reduced levels of

soluble and insoluble beta amyloid as well as phosphorylated

Tau protein. Extract 82% curcuminoids dosage 5mg/mouse/day.

(Mishra, S, & Palanivelu, K, 2008, Potter, 2010, Shytle RD et al, 2012)


Dementia & Alzheimer’s


Support Digestion:

o Address nutritional deficiencies

o Increase absorption (digestive enzymes or lemon water)

o Maintain adequate protein, fibre, fluid intakes (assess

hydration)

o Maintain consistent blood glucose levels (eat every 3 hours)

o Assess EFA and saturated fat intake

o Correct any gut dysbiosis: prebiotics, probiotics, anti-

microbials, repairing nutrients





Support anti-oxidant status

o Increased consumption of antioxidant foods

o Minimise environmental chemical & toxin contact

o Assess homocysteine levels: elevated in brain tissue of

Alzheimer’s. Support with B12 & folate

Support neuronal activity

o Support phospholipid maintenance – lecithin, EPA/DHA

o Support the endogenous production of Dopamine,

Serotonin, GABA and Acetylcholine.





Support liver detoxification & heavy metal chelation

o Assess heavy metal exposure: lead, mercury, aluminum

o Green leafy vegetables, cruciferous vegetables, soluble

fiber, dandelion and other bitter vegetables

o Glycine, cysteine and glutamine for glutathione

production

Support cellular metabolism & energy

Improve circulation



Dementia & Alzheimer’sNutrient Dosage Therapeutic Actions

5-HTP

Tryptophan

300-4,000mg Depression associated with dementia

Tyrosine

Phenylalanine

400-1500mg

up to

6,000mg)

150-600mg

Dopamine, Adrenaline, Noradrenaline. Alzheimer’s

disease patients have sub-optimal production

Inositol 750-

13,000mg

Secondary messenger for noradrenaline, serotonin and

cholinergic receptors

ACL - Acetyl-L-

Carnitine

500-6,000mg Improves neuronal energetics. Antioxidant for brain

cells. Enhances or mimics acetylcholine function.

Phosphatidyl-

choline

10-300mg Acetylcholine substrate. Found to be broken down faster

in AD Boosts Acetylcholine levels

Phosphatidyl-

serine

100-400mg Main phospholipid found in brain. Increases cell

membrane fluidity.

(Spagnoli et al. 1991; Fugh-Berman &

Cott, 1999; Farber et al. 2000; Hager et al.

2001;Huang et al. 2001; Suzuki et al. 2001)



Nutrient Dosage Therapeutic Actions

Lipoic

acid

200-600mg Recycles anti-oxidants, Improves ATP synthesis –

neuronal energetics, Detoxifies heavy metals, Improves

ageing-related cellular processes – mitochondrial

function

EPA/DHA 1000-

5,000mg

Cell membrane, supports circulation. Supports neuronal

activity. Low DHA levels have been linked to an

increased risk of developing Alzheimer’s disease

Vitamin E 100-1000iu Retards the progression of Alzheimer’s disease by 25%

(clinical trials). Treatment of cultured (test-tube) neurons

with vitamin E protects them from beta-amyloid

(implicated in Alzheimer’s disease) toxicity.

Carnitine 500-6,000mg Improves neuronal energetics

(Fugh-Berman & Cott, 1999; Morris, 2004; Malouf & Evans, 2008)




Vitamin B1 5-150mg Cofactor for ACh (most depleted in Alzheimer’s) & fatty acid

synthesis. Cellular energetics. Deficiency causes dementia

like symptoms

Vitamin B2 10-40mg Cofactor. Activation of B6. Conversion of folate to its

coenzymes; conversion to Tryptophan to niacin & support of

antioxidant activity through FAD & reduced glutathione.

Cellular energetics

Vitamin B3 100-

3000mg

Cofactor. Stimulates GABA without binding to the receptor

sites, an effect likened to that of benzodiazepines. Cellular

energetics. Deficiency causes dementia like symptoms.

Memory enhancer

(Farber et al. 2000; Demarin et.al. 2004; Morris, 2004; Green, 2008 ; Malouf & Evans 2008)




Vitamin B5

Vitamin B6

Folate

Vitamin B12

20-500mg

10-150mg

500-

5000mcg

300-800mcg

Synthesis of acetylcholine. Deficiency causes dementia

like symptoms

Methylation. Deficiency causes dementia like

symptoms. Lowers high serum homocysteine levels

- increased risk of AD & accelerated progression.

Selenium 200-600mcg Neural Anti-Oxidant. Deficiencies present with low

cognitive function

Taurine 250-2000mg Neuroactive Neurotransmitters. Alzheimer’s disease

patients have depleted levels of taurine in their

cerebrospinal fluid. (Spagnoli et al. 1991; Fugh-Berman & Cott, 1999; Hager et al. 2001; Louzada et.al. 2004; Morris, 2004; Gao et al. 2007)



Drug Action Side Effects Interactions

Acetyl-

cholinesterase

Inhibitors:

Donepezil,

Rivastigmine,

Galantamine

Inhibit acetyl-

cholinesterase

thereby reducing

ACh breakdown at

nicotinic &

muscarinic receptor

sites. Delays

cognitive decline in

the initial stages,

the disease will

progress.

Increased muscle

activity in the eyes

(pupil constriction),

bradycardia,

diarrhoea, muscle

twitching,

bronchoconstriction.

Also hypotension,

increased

lacrimation &

sweating

None listed

(Romi et.al, 2005; Auchus, 2007;; Bullock et.al. 2007; Bryant & Knights, 2011)




NMDA (N-methyl-

d-aspartate)

Antagonist:

Memantine

Selectively blocks

glutamate receptors

(N-methyl-d-

aspartate receptor)

to reduce

overstimulation

(characteristic of

Alzheimer’s). Slows

the progression of

the disease.

Headache,

dizziness, agitation.

Drowsiness,

insomnia.

GIT disturbance

Coughing

None listed

(Auchus, 2007; Bullock et.al. 2007)


Parkinson’s Disease



Chronic disease affecting the basal ganglia of the brain,

with degeneration of dopaminergic receptors in the

substantia nigra. Age is usually 40 yrs+ (can be earlier).

Risk Factors include:

o Neurotoxins

o Poor antioxidant status and high free radical production

oxidising myelin sheaths

o Impaired function of the mitochondria is closely

associated with the progression of Parkinson’s Disease

as seen with significant damage to the mitochondrial

DNA.




Signs & symptoms:

o Loss of smell (early warning sign)

o Restlessness and tremors of the hands mainly at rest. Movement

reduced symptoms.

o Feeling of sluggishness

o Gait is shuffling and stumbling due to loss of centre of gravity.

o Rigidity of skeletal muscles and facial muscles (mask-like

appearance)




Therapeutic Nutritional Considerations:

Folate

o Folate deficiency and hyperhomocysteinemia may contribute to

Parkinson’s disease pathogenesis, decrease dopaminergic neurons

and induced profound motor dysfunctions…” (Chen et. al, 2004, p.

373)

Vitamin B3

o “NADH administration (1.4 mg/Kg) has been useful in PD patients.

An antioxidant, that can stimulate the production of L-dopa in vivo

and dopamine in PC-12 cells, a dopaminergic cell line as well as

ATP.”

(Prasad et.al. 1999)



Therapeutic Actions

Vitamin C & Vitamin E

o Prasad et.al. (1999) found that “…a large community-based study in

the Netherlands has reported that vitamin E consumption was

significantly lower among patients with PD than among controls.” (p.

414)

o Also “…supplemental vitamin E (3,000IU/day) and vitamin C (3,000

mg/day) increased the time interval for requiring L-dopa therapy by

about 2 to 4 years in 75% of patients when compared to historical

controls.” (Prasad et.al. 1999, p. 418)




o Support Digestive system

o Support the Liver and heavy metal chelation – increase sulphur

containing foods (e.g. garlic, onions, eggs) to aid in phase II

sulphation pathways. Sulphate conjugation has been implicated in

disease pathogenesis

o Support anti-oxidant status

o Support cellular energetics

o Support circulation

o Assess hydration levels

(Pizzorno & Murray 2006; Sarris & Wardle, 2010)




Support neurotransmitter synthesis

o Maintain a protein status of 0.8g/kg to aid in dopamine production.

o Note: high amino acid levels can compete with levodopa across the

blood brain barrier, reducing efficacy.

o Fava (Broad) beans have been shown to be high in natural

levodopa – 100g serving = 250mg levodopa)

(Pizzorno & Murray 2006; Sarris & Wardle, 2010)


Parkinson’s DiseaseNutrient Dosage Therapeutic Actions

Vitamin B1 50-200mg Mitochondrial Support, acetylcholine & fatty acid

synthesis

Vitamin B3 100-200 (up

to 3000mg)

Mitochondrial Support Cofactor and memory enhancer

Vitamin B12 500-

2,000mcg

Nerve support. Elevated Homocysteine contributes to

the development of Parkinson’s Disease.

Vitamin C Up to

5,000mg

NTM Cofactor – adrenal NTM. In combination with

vitamin E has been found to slow progression of

Parkinson’s disease

Vitamin E 100-1000iu Antioxidant, commonly deficient in Parkinson’s

disease.

Selenium 200-250mcg Cofactor of glutathione peroxidase, antioxidant

(Prasad et.al. 1999; Chen et.al. 2004; Demarin et.al. 2004; Green, 2008; Malouf & Evans, 2008)




EFA’s 1000-

10,000mg

Parkinson's Disease occurs when the Myelin

Sheaths of Neurons are damaged by Oxidation

Folic Acid 500-

1000mcg

(up to

5000mcg)

Reduce homocysteine levels, implicated in

Parkinson’s exacerbation

Tyrosine 400-6000mg Tyrosine elevated dopamine (precursor) in the CNS

of patients with Parkinson Disease

Phenylalanine 150-600mg Dopamine precursor

Phosphatidyl-

serine

100-400mg Main phospholipid found in brain. Increases cell

membrane fluidity.

Glutathione 100-500mg Antioxidant, commonly low in Parkinson’s patients

(Fugh-Berman & Cott, 1999; Fernstrom, 2000; Suzuki et al. 2001; Chen et.al. 2004; Pizzorno & Murray, 2006;

Malouf et.al. 2008)


Parkinson’s DiseaseDrug Management

o Parkinson’s Disease symptoms present as a depletion of

dopamine. This NT works in equilibrium with

acetylcholine to maintain proper motor function

o Goal of drug therapy is to restore the balance between

dopaminergic and cholinergic function

o This can be accomplished in different ways, including:

• Increasing dopamine levels

• Augmenting dopamine levels with drugs that mimic

dopamine activity

• Suppression of cholinergic activity (reduced ACh).

(Bullock et.al. 2007; Bryant & Knights, 2011)




Levodopa

L-dopa

L-dopa crosses the

blood-brain-barrier &

then converted to

dopamine raising

brain levels.

Dopamine can’t cross

the BBB. Dopa

decarboxylase (L-

dopa to dopamine

conversion) is present

in peripheral tissue =

only 1% of levodopa

reaches the brain.

Peripheral

conversion of

levodopa is

responsible for

most of the

adverse effects

associated with

the drug = nausea,

vomiting, cardiac

arrhythmias,

postural

hypotension.

Vitamin B6: increases

peripheral conversion of

levodopa (co-factor) = less

to cross BBB & increase the

peripheral adverse effects

Calcium, magnesium iron

& zinc: forms insoluble

complex = reduced drug

absorption. Separate by 2

hours

Tyrosine: L-dopa competes

with tyrosine for BBB

uptake. Avoid

(Braun & Cohen 2010; Bryant & Knights, 2011)




Carbidopa;

Sinemet®

Levodopa +

carbidopa

Combined with

levodopa prevents

peripheral conversion

to dopamine

(increased L-dopa

crosses BBB). Lowers

required dose of L-

dopa & reduced drug

adverse effects.

Peripheral

symptoms:

Nausea, vomiting,

cardiac

arrhythmias,

postural

hypotension.

Vitamin B6: (50-

100mg/day) does not

increase extra-cerebral

conversion, thus drug

efficacy is maintained

Iron: binds to form

insoluble complexes.

Reduced drug

bioavailability

(eMims, 2010; Braun & Cohen 2010; Bryant & Knights, 2011)




Selegiline Used in combination with

levodopa in the late stages of the

disease, selegiline inhibits the

activity of the enzyme

monoamine oxidase B (MAO-B),

thereby delaying the breakdown

of naturally occurring dopamine

and dopamine derived from

levodopa.

Nausea, vomiting,

stomach pain

Insomnia,

dizziness, mood

alteration,

dyskinesia.

None listed





Dopamine

Agonists:

Bromocriptine,

Pergolide,

Cabergoline

Directly stimulate the

CNS dopamine (D2)

receptors providing

symptomatic relief.

Used as adjuncts to

levodopa therapy to

prolong effectiveness,

stabilize responses of

and increase tolerance

to levodopa.

Nausea, vomiting,

cardiac

arrhythmias,

postural

hypotension.

None listed





Anti-

cholinergics

Biperiden,

Benztropine

Block the action of

acetylcholine, thereby

helping to restore the

balance between

cholinergic and

dopaminergic activity.

Used in the early

stages of the disease.

Nausea, vomiting,

constipation

Dry skin, dry mouth

Drowsiness

Irritability

None listed




Drug Interaction Considerations

o Natural therapies may be supportive in Parkinson’s

disease, but are not indicated as stand-alone therapies,

given the nature of the disease

o Currently, the only reported integrative interactions relate

to L-dopa, however care should be taken when

prescribing any natural therapies in Parkinson’s disease.

o All nutritional therapies that act on catecholamines,

especially dopamine or acetylcholine pathways, may

theoretically lead to an interaction with the anti-

Parkinson’s drug therapies


References

o Auchus A. (2007). Dementia. Merk manual online for healthcare professionals. Retrieved 13 January 2011 from: 1http://www.merckmanuals.com/professional/sec16/ch213/ch213c.html#sec16-ch213-ch213c-99

o Burns, Alistair. (2009). Dementia. Brit Med J, 2009; 338.

o Braun, L., & Cohen, M. (2015). Herbs & natural supplements: An evidence-based guide (4th ed.). Chatswood, NSW: Elsevier.

o Bryant, B. J., & Knights, K. M. (2015). Pharmacology for health professionals (4th ed.). Chatswood, NSW: Elsevier.

o Bullock, S., Manias, E. & Galbraith, A. (2007). Fundamentals of pharmacology. 5th ed. Pearson, NSW.

o Chen, J., Lin, K., & Chen, Y. (2009). Review Article: Risk Factors for Dementia. Journal Of The Formosan Medical Association, 108754-764. doi:10.1016/S0929-6646(09)60402-2

o Chen, H., Zhang, S. M., Schwarzschild, M. A., Hernán, M. A., Logroscino, G., Willett, W. C., & Ascherio, A. (2004). Folate intake and risk of Parkinson's disease. American Journal Of Epidemiology, 160(4), 368-375.

http://www.merckmanuals.com/professional/sec16/ch213/ch213c.html#sec16-ch213-ch213c-99


Referenceso Demarin, V., Podobnik, S.S., Storga-Tomic, D. & Kay, G. (2004). Treatment

of Alzheimer's disease with stabilized oral nicotinamide adenine dinucleotide: a randomized, double-blind study.’ Drugs under experimental and clinical research. Vol. 30, 1, p. 27-33. Retrieved 24 January 20122 from: http://www.ncbi.nlm.nih.gov/pubmed/15134388

o Douglas Shytle, R., Tan, J., Bickford, P. C., Rezai-zadeh, K., Hou, L., Zeng, J., Roschek, B. (2012). Optimized Turmeric Extract Reduces β-Amyloid and Phosphorylated Tau Protein Burden in Alzheimer’s Transgenic Mice. Current Alzheimer Research, 9(4), 500–506.

o Farber, S.A., Slack, B.E. & Blusztajn, J.K. (2000). Acceleration of phosphatidylcholine synthesis and breakdown by inhibitors of mitochondrial function in neuronal cells: a model of the membrane defect of Alzheimer’s disease.’ Journal of the federation of American societies for experimental biology. Vol. 14, p. 2198 – 2206. Retrieved 24 January 2011 from: http://www.fasebj.org/content/14/14/2198.abstract

o Fernstrom, J.D. (2000). Can nutrient supplements modify brain function?’ American journal of clinical nutrition. 71, 6, 1669s-1673s.

o Fugh-Berman , A & Cott, JM 1(999). Dietary supplements and natural

products as psychotherapeutic agents. Psychosomatic medicine, Vol.

61, No. 5, pp.712-28.

http://www.ncbi.nlm.nih.gov/pubmed/15134388

http://www.fasebj.org/content/14/14/2198.abstract


References

o Gao, S., Jin, Y., Hall, K.S., Liang, C., Unverzagt, F.W., Ji, R., Murrell et al. (2007).

Selenium Level and Cognitive Function in Rural Elderly Chinese. American

journal of epidemiology. Vol. 165. Iss. 8, p. 955-965. Viewed 29 March 2018

from: http://aje.oxfordjournals.org/content/165/8/955.abstract

o Gatz, M., Fratiglioni, L., Johansson, B., Berg, S., Mortimer, J. A., Reynolds, C. A., &

Pedersen, N. L. (2005). Complete ascertainment of dementia in the Swedish

Twin Registry: the HARMONY study. Neurobiology Of Aging, 26(4), 439-

447.

o Green, K. N., Steffan, J. S., Martinez-Coria, H., Sun, X., Schreiber, S. S., Thompson,

L. M., & LaFerla, F. M. (2008). Nicotinamide restores cognition in Alzheimer's

disease transgenic mice via a mechanism involving sirtuin inhibition and

selective reduction of Thr231-phosphotau. The Journal Of Neuroscience: The

Official Journal Of The Society For Neuroscience, 28(45), 11500-11510.

doi:10.1523/JNEUROSCI.3203-08.2008

o Hager, K., Kenklies, M., & McAfoose, J. (2008). Alpha-lipoic acid as a new treatment

option for Alzheimer's disease--a 48 months follow-up analysis. Alternative

Medicine Review, (1), 74.

http://aje.oxfordjournals.org/content/165/8/955.abstract


Referenceso Huang, W., Alexander, G.E., Chang, L., Shetty, H.U., Krasuski, J.S.,

Rapoport, S.I. & Schapiro, M.B. (2001). Brain metabolite concentration

and dementia severity in Alzheimer’s disease. Neurology. 57, 4, 626-

634.

o Kumar, P. & Clark, M. (2009). Clinical medicine (7th ed). Edinburgh,

Scotland: Saunders Elsevier.

o Healthnotes Releases A -Z Guide to Drug-Herb-Vitamin Interactions, A

Comprehensive Reference for Consumers. (2000) PR Newswire.

o Lininger SW (1999). A-Z Guide to Drug-Herb-Vitamin Interactions. Healthnotes. Three Rivers Press. New York

o Louzada, P. R., Paula Lima, A. C., Mendonca-Silva, D. L., Noël, F., De Mello, F. G., & Ferreira, S. T. (2004). Taurine prevents the neurotoxicity of beta-amyloid and glutamate receptor agonists: activation of GABA receptors and possible implications for Alzheimer's disease and other neurological disorders. FASEB Journal: Official Publication Of The Federation Of American Societies For Experimental Biology, 18(3), 511-518.

o Luchsinger JA, Tang MX, Siddiqui M, et al (2004). Alcohol intake and risk of

dementia. J Am Geriatr Soc, vol 52:540–6.


Referenceso Malouf, R. & Grimley Evans, J. (2008). Folic acid with or without vitamin B12 for the

prevention and treatment of healthy elderly and demented people.’ Cochrane database of systemic reviews. Retrieved 24 January 2011 from:

http://www2.cochrane.org/reviews/en/ab004514.html

o Mishra, S., & Palanivelu, K. (2008). The effect of curcumin (turmeric) on Alzheimer's disease: An overview. Annals Of Indian Academy Of Neurology, (1).

o Morris, M.C. (2004). Diet & Alzheimer’s disease: what the evidence shows.’ Medscape general medicine. Vol. 6, No. 1. Retrieved 24 January 2011 from: http://www.medscape.com/viewarticle/466037

o Mukamal KJ, Kuller LH, Fitzpatrick AL (2003). Prospective study of alcohol

consumption and risk of dementia in older adults. 2003;289:1405–13.

o Osiecki, H. (2014). The Nutrient Bible (7th ed.). Eagle Farm, QLD: Bioconcepts

Publishing.

o Peters R, Peters J, Warner J (2008). Alcohol, dementia and cognitive decline in the

elderly: a systematic review. Age Ageing. 37:505–12.

o Pizzorno, J., & Murray, M. (2006). Textbook of Natural Medicine (3rd ed). St. Louis,

MO: Churchill Livingstone.

http://www2.cochrane.org/reviews/en/ab004514.html

http://www.medscape.com/viewarticle/466037


References

o Potter, P.E. (2010). Investigational medications for treatment of patients with Alzheimer disease.’ Journal of the American osteopathic association. Vol. 110, Iss. 9, Suppl. 8, p 27-36. Retrieved 11 January 2011 from:file:///C:/Users/staff/Desktop/Working/Research/Alzeimers%20Parkinsons/Investigations%20in%20AD.htm

o Prasad, K.N., Cole, W.C. & Kumar, B. (1999). Multiple antioxidants in the prevention

and treatment of Parkinson's disease.’ Journal of the American college of

nutrition, Vol. 18, No. 5, p. 413–423 viewed 26/01/11:

http://www.jacn.org/cgi/reprint/18/5/413

o Romi, F., Gilhus, N. E., & Aarli, J. A. (2005). Myasthenia gravis: clinical,

immunological, and therapeutic advances. Acta Neurologica Scandinavica,

111(2), 134-141.

o Reuben, D. B., Judd-Hamilton, L., Harris, T. B., & Seeman, T. E. (2003). The

associations between physical activity and inflammatory markers in high-

functioning older persons: MacArthur Studies of Successful Aging. Journal

Of The American Geriatrics Society, 51(8), 1125-1130.

o Sarris, J & Wardle, J (2010) Clinical naturopathy. Churchill Livingstone Elsevier,

Chatswood, NSW.

C:/Users/staff/Desktop/Working/Research/Alzeimers Parkinsons/Investigations in AD.htm

http://www.jacn.org/cgi/reprint/18/5/413


References

o Spagnoli, A., Lucca, U., Menasce, G., Bandera, L., Cizza, G., Forloni et al.

(1999). Long‐term acetyl‐L‐carnitine treatment in Alzheimer's disease’

Neurology. Vol. 41, Iss. 11, p. 1726. Retrieved from:

http://www.neurology.org/content/41/11/1726.short

o Suzuki, S., Yamatoya, H., Sakai, H., Kataoka, A., Furushiro, M. & Kudo, S.

(2001). Oral administration of soybean lecithin transphosphatidylated

phosphatidylserine improves memory impairment in aged rats.’

Journal of nutrition. Vol. 131, p. 12951-2956. Viewed 24/01/11:

http://jn.nutrition.org/content/131/11/2951.full

http://www.neurology.org/content/41/11/1726.short


COMMONWEALTH OF AUSTRALIA

Copyright Regulations 1969

WARNING

This material has been reproduced and communicated to you by or on behalf of the Australian College of Natural Medicine Pty Ltd (ACNM) trading as Endeavour College of Natural Health, FIAFitnation, College of Natural Beauty, Wellnation - Pursuant Part VB of the Copyright Act 1968 (the Act).

The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act.

Do not remove this notice.

NMDC221 Session 17: Nervous System Disease Part IV · NMDC221 Session 17: Nervous System Disease...

Documents

Transcript of NMDC221 Session 17: Nervous System Disease Part IV · NMDC221 Session 17: Nervous System Disease...