July 23, 2010

Should we start exercising early in life to postpone or prevent age-related cognitive decline?

Age-protection, Alzheimer's, Exercise, Memory — Tags: aging, Alzheimr's, cognitive decline, dementia, Exercise — 8:52 am

Exercise during midlife comparing with exercise during late life

Most of the studies into the protective effects of exercise against cognitive decline, dementia, and Alzheimer’s disease, followed the elderly people starting their 65s and watched the results, which were relevant to the beneficial effects in late life. However, there are some results where a large cohort of 65-79-year olds has been followed-up for around 21 years so information about physical activity during midlife was available. Those who who participated in at least “leisure-time physical activity” during midlife had significantly lower risks of dementia or Alzheimer’s disease comparing with those who did not exercise at all [1].

Another study has suggested that physical activity at even earlier ages (physical activity between ages 15 and 25 years was asked retrospectively) can improve or preserve cognitive ability in late life [2]. This cognitive decline risk reduction is at least comparable to the eisks reduction reported in studies of physical activity in older persons. Thus, midlife physical activity might be as important for preventing later cognitive decline as is physical activity at older ages.

Sources

Rovio S, et al. Leisure-time physical activity at midlife and the risk of dementia and Alzheimer’s disease. Lancet Neurol 2005;4:705–11

Dik M, Deeg DJ, Visser M, Jonker C. Early life physical activity and cognition at old age. J Clin Exp Neuropsychol 2003;25:643–53

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July 15, 2010

Resveratrol and curcumin, plant’s own weapons that protect the brain

Alzheimer's, Epilepsy — Tags: curcumin, phytoalexin, Resveratrol — 7:22 am

According to Michael Wong, MD, PhD (1), although there’s a noticeable progress in anti-epileptic drug development, two obstacles remain unchanged for many decades:

1. The number of cases resistant to the best and newest drugs does not decrease

2. The best drugs address symptoms and not the cause of the disease, namely, they might suppress the seizures but they cannot make them disappear. As a result of such a failure, we still have no anti-epileptic therapies.

Recent studies, however, addresses potential neuroprotective and anti-epileptogenic actions of substances naturally occurring in plants. For example, Resveratrol (a phytoalexin) is found in plants such as peanuts and grapes, but it’s especially abundant in red wine. In plants, Resveratrol defends the cells against the consequences of injury, parasitics, and infectious diseases — hence its antiinflammatory, antioxidant, anti-tumor, and, if given to animals, its neuroprotective effects.

In the article “Protective Effect of Resveratrol Against Kainate-Induced Temporal Lobe Epilepsy in Rats” Resveratrol is described as a potent anti-epilepsy agent, which protects against epileptogenesis (not just against seizures) in animal model of temporal lobe epilepsy (2).

Another success story was told about curcumin, which is the major ingredient in the popular Indian spice, tumeric. Tumeric has been used for centuries in parts of India as an herbal therapy; including treatment of Alzheimer’s disease and epilepsy. As resveratrol, curcumin has been shown to inhibit acute seizures. The recent study (3) studied the effect of curcumin on epileptogenesis in a rat model of post-traumatic epilepsy. Curcumin decreased the development of and seizures and improved memory and learning.

1. M Wong. HERBS AND SPICES: UNEXPECTED SOURCES OF ANTIEPILEPTOGENIC DRUG TREATMENTS? Epilepsy Currents, Vol. 10, No. 1 2010 pp. 21–23

2. Protective Effect of Resveratrol Against Kainate-Induced Temporal Lobe Epilepsy in Rats. Wu Z, Xu Q, Zhang

L, Kong D, Ma R, Wang L. Neurochem Res 2009;34(8):1393–1400.

3. Curcumin Protects Against Electrobehavioral Progression of Seizures in the Iron-Induced Experimental Model

of Epileptogenesis. Jyoti A, Sethi P, Sharma D. Epilepsy Behav 2009;14(2):300–308.

HERBS AND SPICES: UNEXPECTED SOURCES OF ANTIEPILEPTOGENIC DRUG TREATMENTS?

According to Michael Wong, MD, PhD (1), although there’s a noticeable progress in anti-epileptic drug development, two obstacles remain unchanged for many decades.

The number of cases resistant to the best and newest drugs does not decrease
The best drugs address symptoms and not the cause of the disease, namely, they might suppress the seizures but they cannot make them disappear. As a result of such a failure, we still have no anti-epileptic therapies.

Recent studies, however, address potential neuroprotective and anti-epileptogenic actions of substances naturally occurring in plants. For example, Resveratrol (a phytoalexin) is found in plants such as peanuts and grapes, but it’s especially abundant in red wine. In plants, Resveratrol defends the cells against the consequences of injury, parasitics, and infectious diseases — hence its antiinflammatory, antioxidant, anti-tumor, and, if given to animals, its neuroprotective effects.

Sources

M Wong. CURRENT LITERATURE IN BASIC SCIENCE. Epilepsy Currents, Vol. 10, No. 1 2010 pp. 21–23
Protective Effect of Resveratrol Against Kainate-Induced Temporal Lobe Epilepsy in Rats. Wu Z, Xu Q, Zhang
L, Kong D, Ma R, Wang L. Neurochem Res 2009;34(8):1393–1400.
Curcumin Protects Against Electrobehavioral Progression of Seizures in the Iron-Induced Experimental Model of Epileptogenesis. Jyoti A, Sethi P, Sharma D. Epilepsy Behav 2009;14(2):300–308.

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June 28, 2010

Alzheimer’s Facts

Age-protection, Alzheimer's, Brain-Body-Mind — 7:06 am

Alzheimer’s Disease Statistics

• Alzheimer’s affects approximately 4.5 million Americans and is
expected to affect up to 16 million by 2050.
• Alzheimer’s affects approximately 5 percent of men and women
ages 65–74.
• Nearly half of people 85 and older have Alzheimer’s.
• Alzheimer’s must be distinguished from mild cognitive impairment
and normal age-related memory changes.
(National Institute of Aging. Alzheimer’s Disease Information, May 9, 2006)

Physical and mental health: same strategies

Research evidence is accumulating, showing that many of the same strategies for maintaining physical health are also applicable for maintaining brain plasticity and good cognitive functioning throughout the lifespan. These studies reinforce the message that exercise—physical and mental—is an essential part of any comprehensive health program (ALTERNATIVE & COMPLEMENTARY THERAPIES—OCTOBER 2006 pp 222-227)

Exercise and balance for intelligence

Exercise can help maintain balance, and balance in the elderly has been highly correlated with performance measures of mental abilities such as general intelligence, memory, and reaction time. Balance thus serves as a biomarker of cerebroarterial blood flow
and age-related global neurophysiologic status (Neuropsychologia 2006;44:1978–1983).

Meditation and cortex thickness

Magnetic resonance imaging to assess cortical thickness revealed that brain areas—such as the prefrontal cortex involved with memory, attention, and sensory processing—were approximately 5 percent thicker in the subjects who meditated compared with those who did not. This difference was most pronounced in older participants, suggesting that meditation might offset agerelated cortical thinning (Neuroreport 2005;16:1893–1897)

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June 15, 2010

Vitamins C and E, separately or combined

Alzheimer's, Neurones, Supplements — Tags: avitaminosis, cell death, vitamin C, vitamin E, vitamins — 8:43 am

Combined deficiency in vitamins C and E is a risk factor for neuronal death and brain necrosis

Vitamin C easily crosses the blood brain barrier and its transport into the brain is mediated by glucose transporters. Vitamin C concentrations in the brain exceed those in blood by 10-fold. In humans, hypovitaminosis C correlated with brain damage in patients with head trauma (Stroke. 2001;32:898-902). The vitamin C has important functions in the brain, for example, protecting neuronal membranes from oxidative damage acting as a scavenger of free radicals.

Another free radical scavenger Vitamin E (-tocopherol) inhibits the amyloid peptide characteristic for Alzheimer’s disease known to induced cell death (Biochemical and Biophysical Research Communications Volume 186, Issue 2, 31 July 1992, Pages 944-950).

The results of a study of Guinea Pigs’s fed either on normal or vitamin-deficient diets showed that while moderate deficiencies of vitamins E or C didn’t result in serious brain changes, their combined moderate deficienciescaused degenerative changes in the guinea pig brains in only 5 days after vitamins were removed from the feed.

Interestingly, the deficiencies in either E or C vitamins had only moderate consequences, but their combination caused severe brain lesions – inflammation, cell death with necrosis and apoptosis and animals’ death (Nutr. 136:1576-1581, June 2006).

Combined deficiency in vitamins C and E is a risk factor for neuronal death and brain necrosis.

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May 28, 2010

Vitamin D and mental health – an easy solution for serious problems?

Alzheimer's, Depression, Prevention, Schizophrenia — Tags: avitaminosis, vitamin D, vitamins — 8:14 am

What is the problem?

Vitamin D deficiency has been linked not only to bone health, but also some types of cancer, lowered immune function, and kidney disease. Recent studies showed that vitamin D may preserve cognitive function exerting its neuroprotective effects via the vitamin D receptors abundantly expressed in regions frequently affected in cases of neurodegenerative diseases such as the hypothalamus, substantia nigra, cortex and hippocampus. An increased incidence of Alzheimer’s disease, schizophrenia and depression (including depression as a symptom of fibromyalgia and chronic fatigue syndrome, Clinical Rheumatology 1434-9949, 26, 4, April 2007) associated with vitamin D deficiency were reported (J Chem Neuroanat 2005;29:21-30.)

What are the causes?

Decreased bioavailability of vitamin D can be caused by malabsorption often present in cystic fibrosis, celiac disease, Whipple’s disease, Crohn’s disease, bypass surgery, and medications that reduce cholesterol absorption. 86,87

Obesity also educes availability of vitamin D locking it in the body fat depots.

Anticonvulsants, glucocorticoids

Inadequate sun exposure including that due to excessive sunscreen use

(N Engl J Med 2007;357:266-81)

Prevention by supplementation

116:2062-72; Primer on the metabolic bone diseases and disorders of mineral metabolism. 6th ed. Washington, DC: American

Society for Bone and Mineral Research, 2006:129-37; Endocrinology. Philadelphia: W.B.Saunders, 2001:1009-28)

What is the problem?

Vitamin D deficiency has been linked not only to bone health, but also some types of cancer, lowered immune function, and kidney disease. Recent studies showed that vitamin D may preserve cognitive function exerting its neuroprotective effects via the vitamin D receptors abundantly expressed in regions frequently affected in cases of neurodegenerative diseases such as the hypothalamus, substantia nigra, cortex and hippocampus. An increased incidence of Alzheimer’s disease, schizophrenia and depression (including depression as a symptom of fibromyalgia and chronic fatigue syndrome, Clinical Rheumatology 1434-9949, 26, 4, April 2007) was proved to be associated with vitamin D deficiency (J Chem Neuroanat 2005;29:21-30.)

What are the causes?

Decreased bioavailability of vitamin D can be caused by malabsorption often present in cystic fibrosis, celiac disease, Whipple’s disease, Crohn’s disease, bypass surgery, and medications that reduce cholesterol absorption.
Obesity also educes availability of vitamin D locking it in the body fat depots.
Anticonvulsants, glucocorticoids
Inadequate sun exposure including that due to excessive sunscreen use

(N Engl J Med 2007;357:266-81)

Prevention by supplementation

Most experts agree that current recommendations for daily intake of vitamin D are in fact inadequate: without adequate sun exposure, children and adults require approximately 800 to 1000 IU per day (J Clin Invest 2006; 116:2062-72; Primer on the metabolic bone diseases and disorders of mineral metabolism. 6th ed. Washington, DC: American Society for Bone and Mineral Research, 2006:129-37; Endocrinology. Philadelphia: W.B.Saunders, 2001:1009-28)

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April 29, 2010

Caffeine protect against neurodegeneration in Alzheimer’s disease

Alzheimer's, Foods for the Brain, Prevention — Tags: Alzheimr's, amyloid-beta, caffein, coffee, dementia, insulin — 1:48 pm

Caffeine, the most widely consumed behaviourally active substance in the western world (Pharmacol Rev 51 1999: 83–133), has neuroprotective effects in cases of hypoxia and ischaemia (Brain Res Rev 33 2000: 258–274). Does caffeine protect against neurodegeneration in Alzheimer’s disease as it does in Parkinson’s? Researchers from Faculty of Medicine of Lisbon, Portugal, tested the hypothesis that average daily caffeine intake in the period of 20 years before the diagnosis could be lower than caffeine intake in age- and sex-matched healthy people and showed that indeed, people who was diagnosed with Alzheimer’s consumed an average 74 mg (less than one cup) while the controls had about 200 mg.

“These results, if confirmed with future prospective studies, may have a major impact on the prevention of AD,” concluded the researchers (Eur J Neurology, Volume 9, Issue 4, 2002: 377–382).

In a Canadian study, daily coffee intake decreased the risk of Alzheimer’s by 31% during a 5-year followup in 65-year old people [Am J Epidemiol 2002, 156, 445-453.]. The Finland, Italy and the

Netherlands Elderly (FINE) Study showed that elderly men drinking three cups of coffee daily had the least cognitive decline [Eur J Clin Nutr 2007, 61, 226-232]. Tea drinking (Am J Epidemiol, 2004, 159, 959-967.], or flavonoid intake from tea has not been associated with a reduced risk of dementia.

The low coffee consumers in mid-life had the highest occurrence of dementia and Alzheimer’s at late-life, and the highest scores on the depression scale (J Alzheimer’s Disease 16: 2009, 85–91).

Caffeine, the most widely consumed behaviourally active substance in the western world (Pharmacol Rev 51 1999: 83–133), has neuroprotective effects in cases of hypoxia and ischaemia (Brain Res Rev 33 2000: 258–274). Does caffeine protect against neurodegeneration in Alzheimer’s disease as it does in Parkinson’s? Researchers from Faculty of Medicine of Lisbon, Portugal, tested the hypothesis that average daily caffeine intake in the period of 20 years before the diagnosis could be lower than caffeine intake in age- and sex-matched healthy people and showed that indeed, people who was diagnosed with Alzheimer’s consumed an average 74 mg (less than one cup) while the controls had about 200 mg. ”These results, if confirmed with future prospective studies, may have a major impact on the prevention of Alzheimer’s,” concluded the researchers (Eur J Neurology, V 9, Issue 4, 2002: 377–382).

In a Canadian study, daily coffee intake decreased the risk of Alzheimer’s by 31% during a 5-year followup in 65-year old people (Am J Epidemiol 2002, 156, 445-453.). The Finland, Italy and the Netherlands Elderly (FINE) Study showed that elderly men drinking three cups of coffee daily had the least cognitive decline (Eur J Clin Nutr 2007, 61, 226-232). Tea drinking (Am J Epidemiol, 2004, 159, 959-967.), or flavonoid intake from tea has not been associated with a reduced risk of dementia. The low coffee consumers in mid-life had the highest occurrence of dementia and Alzheimer’s at late-life, and the highest scores on the depression scale (J Alzheimer’s Disease 16: 2009, 85–91).

One possible mechanism could involve insulin and degrading enzyme that degrades both insulin and amyloid-beta, the most suspected cause of Alzheimer’s (CNS Drugs 17, 2009, 27-45). Another mechanism is via adenosine receptors (caffein mimics effects of adenosine). It has been shown in mice that both caffeine and adenosine prevent amyloid-beta induced cognitive decline (Exp Neurol 203, 2007, 241-245).

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April 28, 2010

Walking away from dementia

Age-protection, Alzheimer's, Exercise, Prevention — Tags: Alzheimr's, dementia, Exercise, walking — 9:31 am

If we could delay the onset of dementia by 2 years, we could reduce its risks by as much as 25% — all other things being equal — and one of the most effective and simple ways is physical activity (Am J Public Health 1998;88:1337– 42). Drs Rockwood and Middleton from Dalhousie University, Halifax, Canada, analyzed 7 studies of exercise effects on risks of dementia and concluded that, without exception, 65 to 93 years old men and women who exercise the most have a lower risk of dementia relative to those who exercise the least. (Alzheimer’s & Dementia 3 2007; S38–S44)

Another, large-scale study found a significant dose-response relationship between physical activity and cognitive function was conducted as part of the Nurses’ Health Study in 18,766 women (JAMA 2004;292:1454–61). After about 10 or more years, when the women were 70 to 81 years old, those reporting the most physical activity scored higher on several baseline tests of cognitive function. During the 2 years of additional follow up, there were again significant trends for a dose-response relationship in which those reporting the most physical activity exhibited the least decline in cognitive function (JAMA 2004;292:1454–61).

Higher activity levels might not be necessary for the benefit (Alzheimer Dis Assoc Disord 2004; 18:57– 64) – an increase of 30-minutes aerobic exercise frequency from 3 to 5 times per week did not result in a proportional decrease of cognitive decline in a group of 1146 women 65 years old or older.

However, for those in the higher-intensity exercise group, that worked out at least moderate intensity (more vigorously than walking), or for longer durations each day (Med Sci Sports Exerc 2001;33:772–7.) chances of cognitive impairment, Alzheimer’s, or all-cause dementia were lower (Arch Neurol 2001;58:498 –504).

Even walking was associated with a “dose-dependent” risk reduction: those walked at an easy pace for at least 1.5 hours per week had significantly higher cognitive scores than those walking less than 40 minutes per week. Higher activity levels might not be necessary for the benefit (Alzheimer Dis Assoc Disord 2004; 18:57– 64) – an increase of 30-minutes aerobic exercise frequency from 3 to 5 times per week did not result in a proportional decrease of cognitive decline in a group of 1146 women 65 years old or older.

Related:

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April 21, 2010

Metabolic syndrome and mental health

Alzheimer's, Brain Basics, Brain Metabolism, Schizophrenia — Tags: hippocampus, metabolic syndrome, type 3 diabetes — 7:54 am

The metabolic syndrome’s area of influence seems to be growing startlingly fast. Latest research revealed its link to mental health problems. Researchers discovered that insulin resistance can be “in your head” and created a new medical term, the “type 3 diabetes” referring to the newly discovered insulin receptors in the brain.

Researchers at Rhode Island Hospital showed that insulin resistance is tied to neurodegeneration. A drop in insulin production in the hippocampus — the part of the brain responsible for memory — can contribute to early stages of Alzheimer’s disease. In the frontal cortex of the brain, a major area affected by Alzheimer’s, the levels of insulin receptors and the brain’s ability to respond to insulin decreased.

Whether or not an insulin shortage causes a breakdown in brain cell communication, which would explain another brain disease, schizophrenia, remains unknown, but people with schizophrenia are at least twice as likely to develop Type 2 diabetes. ”There’s a whole series of steps that may prevent the schizophrenic brain from responding to insulin,” said Dr Altar of the Psychiatric Genomics Center in Boston, which is now focusing on potential treatments for schizophrenia.

Sources:

Dementia and Geriatric Cognitive Disorders, 2007;23:29-34
JAMA. 2004; 292:2237-2242
J Alzheimer’s Disease; March 2005
J Alzheimer’s Disease; November 2005

Related:

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March 16, 2010

Free radicals are to blame for Alzheimer’s and Parkinson’ s diseases

Alzheimer's, Oxidative damage, Parkinson's — 5:55 pm

Brain and free radicals Logically speaking, anti-oxidants are substances that fight oxidants. Then what are oxidants? They are chemicals producing unstable form of oxygen, which make them deadly for some life forms and dangerous for the others. To name just two, chlorine and chloramines are oxidants and are used for disinfection – killing the microbes.

Now, antioxidants are chemicals (naturally occurring or synthesized) that absorb or scavenge and finally neutralize oxidants also known as free radicals. High levels of free radicals may eventually lead to damage of bodily cells and is believed are responsible for many diseases.

It is agreed upon that free radicals are to blame for diseases associated with long lasting oxidant stress: cardiovascular disease, diabetes, the most common forms of cancer, eye diseases, neurological diseases, infectious diseases, and rheumatoid arthritis, adult respiratory distress syndrome, drug induced lung lesions, chronic obstructive pulmonary diseases, asthma, emphysema, interstitial fibrosis, Alzheimer’s disease, and Parkinson’ s disease. (Stockholm, Swedish Council of Technology Assessment in Health Care)

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Epilepsy Drugs May Treat Alzheimer’s and Parkinson’s

Alzheimer's, Epilepsy, Parkinson's — 8:37 am

(WebMD) A group of drugs used to treat epilepsy may also treat Alzheimer’s and Parkinson’s disease.

New research shows treatment with T-type calcium channel blockers, used to treat epilepsy, protected nerve cells from the brains of mice that can be damaged by neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease.

Researchers say there aren’t any effective medications that protect brain cells from age-related damage and degeneration. If these findings hold up under further study in humans, they could lead to a new class of more effective treatments for age-related neurological diseases.

Calcium-signaling pathways play an important role in the survival of nerve cells (neurons) in the brain. As people age, this process can become disrupted and can lead to cognitive and functional decline.

Researchers say that opens up the possibility of using chemicals like calcium channel blockers that are involved in the calcium-signaling process to protect the nerve cells from death.

The study, published in Molecular Neurodegeneration, looked at the effects of treatment with calcium channel blockers on the brain cells of mice.

Researchers found neurons showed an increase in viability after treatment with the calcium channel blockers over both the long term and short term.

“Our data provides implications for the use of this family of anti-epileptic drugs in developing new treatments for neuronal injury, and for the need of further studies of the use of such drugs in age-related neurodegenerative disorders,” says researcher Jianxin Bao, PhD, of Washington University in St. Louis, in a news release.

(WebMD) A group of drugs used to treat epilepsy may also treat Alzheimer’s and Parkinson’s disease.

New research shows treatment with T-type calcium channel blockers, used to treat epilepsy, protected nerve cells from the brains of mice that can be damaged by neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease.

Researchers say there aren’t any effective medications that protect brain cells from age-related damage and degeneration. If these findings hold up under further study in humans, they could lead to a new class of more effective treatments for age-related neurological diseases. Calcium-signaling pathways play an important role in the survival of nerve cells (neurons) in the brain. As people age, this process can become disrupted and can lead to cognitive and functional decline.

Researchers say that opens up the possibility of using chemicals like calcium channel blockers that are involved in the calcium-signaling process to protect the nerve cells from death. The study, published in Molecular Neurodegeneration, looked at the effects of treatment with calcium channel blockers on the brain cells of mice.

Researchers found neurons showed an increase in viability after treatment with the calcium channel blockers over both the long term and short term.

“Our data provides implications for the use of this family of anti-epileptic drugs in developing new treatments for neuronal injury, and for the need of further studies of the use of such drugs in age-related neurodegenerative disorders,” says researcher Jianxin Bao, PhD, of Washington University in St. Louis, in a news release.

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