Alzheimers prevention

Vascular & Mixed Dementia

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Vascular dementia, as its name suggests, is caused by poor blood flow, produced by a single, localized stroke, or series of strokes.

It is the second most common dementia, accounting for perhaps 17% of dementias. It also co-occurs with Alzheimer's in 25-45% of cases. Although there are other types of dementia that also co-occur with Alzheimer's, mixed dementia generally refers to the co-occurrence of Alzheimer's and vascular dementia.

Risk factors

In general, unsurprisingly, vascular dementia has the same risk factors as cerebrovascular disease.

A study1 of 173 people from the Scottish Mental Survey of 1932 who have developed dementia has found that, compared to matched controls, those with vascular dementia were 40% more likely to have low IQ scores when they were children than the people who did not develop dementia. Because this was not true for those with Alzheimer's disease, it suggests that low childhood IQ may act as a risk factor for vascular dementia through vascular risks rather than the "cognitive reserve" theory.

Prevention

The exciting thing about vascular dementia is that it is far more preventable than other forms of dementia. As with risk, as a general rule, the same things that help you protect you from heart attacks and stroke will help protect you from vascular dementia. This means diet, and it means exercise.

A four-year study2 involving 749 older adults has found that the top one-third of participants who exerted the most energy in moderate activities such as walking were significantly less likely to develop vascular dementia than those people in the bottom one-third of the group.

Treatment

Apart from normal medical treatment for cerebrovascular problems, there are a couple of interesting Chinese studies that have looked specifically at vascular dementia.

The herb gastrodine has been used in China for centuries to treat disorders such as dizziness, headache and even ischemic stroke. A 12-week, randomized, double-blind trial3 involving 120 stroke patients who were diagnosed with mild to moderate vascular dementia has found that  gastrodine and Duxil® (a drug used to treat stroke patients in China) produced similar overall levels of cognitive improvement -- although more patients showed 'much improvement' with gastrodine (23% vs 14%).

A Chinese pilot study4 involving 25 patients with mild to moderate vascular dementia found that ginseng compound significantly improved their average memory function after 12 weeks, but more research (larger samples, placebo-controls) is needed before this finding can be confirmed. Five years on I have still not seen such a study.

References: 

  1. McGurn, B., Deary, I.J. & Starr, J.M. 2008. Childhood cognitive ability and risk of late-onset Alzheimer and vascular dementia. Neurology, first published on June 25, 2008 as doi: doi:10.1212/01.wnl.0000319692.20283.10
  2. Ravaglia, G. et al. 2007. Physical activity and dementia risk in the elderly. Findings from a prospective Italian study. Neurology, published online ahead of print December 19.
  3. Tian, J.Z. et al. 2003. A double-blind, randomized controlled clinical trial of compound of Gastrodine in treatment of mild and moderate vascular dementia in Beijing, China. Presented at the American Heart Association's Second Asia Pacific Scientific Forum in Honolulu on June 10.
  4. Tian, J.Z. et al. 2003. Presented at the American Stroke Association's 28th International Stroke Conference on February 14 in Phoenix. Press release

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Different kinds of physical activity improve brain volume & cut Alzheimer's risk

  • A large long-running study adds to growing evidence that higher levels of physical activity reduce brain atrophy and Alzheimer's risk, and shows that many types of aerobic activity are beneficial.

Data from 876 patients (average age 78) in the 30-year Cardiovascular Health Study show that virtually any type of aerobic physical activity can improve brain volume and reduce Alzheimer's risk.

A higher level of physical activity was associated with larger brain volumes in the frontal, temporal, and parietal lobes including the hippocampus, thalamus and basal ganglia. Among those with MCI or Alzheimer's (25% of the participants), higher levels of physical activity were also associated with less brain atrophy. An increase in physical activity was also associated with larger grey matter volumes in the left inferior orbitofrontal cortex and the left precuneus.

Further analysis of 326 of the participants found that those with the highest energy expenditure were half as likely to have developed Alzheimer's disease five years later.

Physical activity was assessed using the Minnesota Leisure-Time Activities questionnaire, which calculates kilocalories/week using frequency and duration of time spent in 15 different leisure-time activities: swimming, hiking, aerobics, jogging, tennis, racquetball, walking, gardening, mowing, raking, golfing, bicycling, dancing, calisthenics, and riding an exercise cycle.

The study does not look at whether some types of physical activity are better than others, unfortunately, but its message that overall physical activity, regardless of type, helps in the fight against cognitive impairment is encouraging.

http://www.eurekalert.org/pub_releases/2016-03/ip-dko030916.php

http://www.eurekalert.org/pub_releases/2016-03/uops-bmc031016.php

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Fish reduces Alzheimer's risk for those with APOE gene

  • A new study finds that seafood consumption reduces Alzheimer's pathology, but only in those with the Alzheimer's gene APOEe4. While fish oil didn't appear to affect brain health, the omega-3 acid found in flaxseed did.

I've spoken before about how the presence or absence of the “Alzheimer's gene” may affect which lifestyle changes are beneficial for you. A new study has added to that idea with a finding that seafood consumption was associated with fewer signs of Alzheimer's-related pathology, but only among those with the APOEe4 gene.

Seafood consumption was also associated with increased mercury levels in the brain, with levels rising the more seafood was consumed. However, higher levels of mercury were not correlated with any neuropathologies.

Fish oil supplementation was not associated with any differences in neuropathology. However, higher levels of alpha-linolenic acid (an omega-3 fatty acid found in flaxseed, chia seeds, walnuts, etc) were associated with a reduced chance of cerebral infarctions.

The study involved 554 deceased participants (average age 89.9 years) from the long-running Memory and Aging Project (MAP) conducted by Rush University Medical Center. The participants had completed annual dietary questionnaires over a number of years. The brains of 286 participants were autopsied, to assess neuropathologies and mercury levels.

The average educational attainment of the participants was 14.6 years; 67% were women.

The finding tempers the evidence from many studies that eating fish reduces Alzheimer's risk. However, it is consistent with what I believe is becoming apparent: that there are different paths to Alzheimer's, and thus different factors involved in preventing it, depending on your own particular gene-environment attributes.

http://www.eurekalert.org/pub_releases/2016-02/nioe-scm020116.php

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Alzheimer's disease consists of 3 distinct subtypes

  • A very small study points to three subtypes of Alzheimer's disease, each of which seems to be associated with:
    • different physiological abnormalities
    • different causes and risk factors
    • different symptoms / progression
    • different age-onsets.
  • This suggests that effective treatments need to be tailored to the subtype.

A two-year study which involved metabolic testing of 50 people, suggests that Alzheimer's disease consists of three distinct subtypes, each one of which may need to be treated differently. The finding may help explain why it has been so hard to find effective treatments for the disease.

The subtypes are:

  • Inflammatory, in which markers such as C-reactive protein and serum albumin to globulin ratios are increased.
  • Non-inflammatory, in which these markers are not increased but other metabolic abnormalities (such as insulin resistance, hypovitaminosis D, and hyper-homocysteinemia) are present. This tends to affect slightly older individuals than the first subtype: 80s rather than 70s.
  • Cortical, which affects relatively young individuals (typically 50s- early 70s) and appears more widely distributed across the brain than the other subtypes, showing widespread cortical atrophy rather than marked hippocampal atrophy. It typically presents with language and number difficulties first, rather than memory loss. Typically, there is an impaired ability to hold onto a train of thought. It is often misdiagnosed, typically affects people without a family history of Alzheimer's, who do not have an Alzheimer's-related gene, and is associated with a significant zinc deficiency (Zinc is implicated in multiple Alzheimer's-related metabolic processes, such as insulin resistance, chronic inflammation, ADAM10 proteolytic activity, and hormonal signaling. Zinc deficiency is relatively common, and associated with increasing age.).

The cortical subtype appears to be fundamentally a different condition than the other two.

I note a study I reported on last year, that found different molecular structures of amyloid-beta fibrils in the brains of Alzheimer's patients with different clinical histories and degrees of brain damage. That was a very small study, indicative only. However, I do wonder if there's any connection between these two findings. At the least, I think this approach a promising one.

The idea that there are different types of Alzheimer's disease is of course consistent with the research showing a variety of genetic risk factors, and an earlier study indicating at least two pathways to Alzheimer's.

It's also worth noting that the present study built on an earlier study, which showed that a program of lifestyle, exercise and diet changes designed to improve the body's metabolism reversed cognitive decline within 3-6 months in nine out of 10 patients with early Alzheimer's disease or its precursors. Note that this was a very small pilot program, and needs a proper clinical trial. Nevertheless, it is certainly very interesting.

http://www.eurekalert.org/pub_releases/2015-09/uoc--adc091615.php

Reference: 

Bredesen, D.E. 2015. Metabolic profiling distinguishes three subtypes of Alzheimer's disease. AGING, 7 (8), 595-600. Full text at http://www.impactaging.com/papers/v7/n8/full/100801.html

Bredesen, D.E. 2014. Reversal of cognitive decline: A novel therapeutic program. AGING, Vol 6, No 9 , pp 707-717. Full text at http://www.impactaging.com/papers/v6/n9/full/100690.html

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Limited benefit of physical activity for preventing cognitive decline

  • A large study of older adults (70+) found no cognitive benefit from a regular exercise program, compared to another social & mental intervention.
  • However, a subset of participants (those over 80, and those with poor physical function at the beginning of the study) did show improvement in executive function.
  • Participants in both programs showed no cognitive decline over the two-year period, suggesting both interventions were helpful.

A large, two-year study challenges the evidence that regular exercise helps prevent age-related cognitive decline.

The study involved 1,635 older adults (70-89) who were enrolled in the Lifestyle Interventions and Independence for Elders (LIFE) study. They were sedentary adults who were at risk for mobility disability but able to walk about a quarter mile. Participants had no significant cognitive impairment (as measured by the MMSE) at the beginning of the study. Around 90% (1476) made it to the end of the study, and were included in the analysis.

Half the participants were randomly assigned to a structured, moderate-intensity physical activity program that included walking, resistance training, and flexibility exercises, and the other half to a health education program of educational workshops and upper-extremity stretching.

In the physical activity condition, participants were expected to attend 2 center-based visits per week and perform home-based activity 3 to 4 times per week. The sessions progressed toward a goal of 30 minutes of walking at moderate intensity, 10 minutes of primarily lower-extremity strength training with ankle weights, and 10 minutes of balance training and large muscle group flexibility exercises.

The health education group attended weekly health education workshops during the first 26 weeks of the intervention and at least monthly sessions thereafter. Sessions lasted 60 to 90 minutes and consisted of interactive and didactic presentations, facilitator demonstrations, guest speakers, or field trips. Sessions included approximately 10 minutes of group discussion and interaction and 5 to 10 minutes of upper-extremity stretching and flexibility exercises.

Cognitive assessments were made at the beginning of the study and at 24 months, as well as a computerized assessment at either 18 or 30 months.

At the end of the study, there was no significant difference in cognitive score, or incidence of MCI or dementia, between the two groups. However, those in the exercise group who were 80 years or older ( 307) and those with poorer baseline physical performance ( 328) did show significantly better performance in executive function.

Executive function is not only a critical function in retaining the ability to live independently, research has also shown that it is the most sensitive cognitive domain to physical exercise.

Note also that there was no absolute control group — that is, people who received no intervention. Both groups showed remarkably stable cognitive scores over the two years, suggesting that both interventions were in fact effective in “holding the line”.

While this finding is disappointing and a little surprising, it is not entirely inconsistent with the research. Studies into the benefits of physical exercise for fighting age-related cognitive decline and dementia have produced mixed results. It does seem clear that the relationship is not a simple one, and what's needed is a better understanding of the complexities of the relationship. For example, elements of exercise that are critical, and the types of people (genes; health; previous social, physical, and cognitive attributes) that may benefit.

http://www.eurekalert.org/pub_releases/2015-08/tjnj-eop082115.php

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These 5 healthy habits reduce dementia risk

There are five healthy behaviors that appear to significantly reduce the risk of dementia,

A 35-year study that monitored the healthy behaviors of 2,235 Welsh men aged 45 to 59 at the beginning of the study has found that those who consistently followed at least four of these five healthy behaviors — regular exercise, no smoking, acceptable BMI, high fruit and vegetable intake, and low/moderate alcohol intake — experienced a 60% reduction in dementia and cognitive decline compared with people who followed none. They also had 70% fewer instances of diabetes, heart disease, and stroke,.

Exercise was the most important of these factors.

Only 5% of the men were living a healthy lifestyle (i.e., following at least 4 of these healthy behaviors). Just under half of the 2235 men were non-smokers (46%), and around a third (35%) had an acceptable BMI. Only 15 men ate their “5+” daily (!!), so the requirement was reduced to only three or more portions of fruit and vegetables, enabling 18% to reach it. 39% exercised regularly and 59% reported alcohol intake within the guidelines. Only two men managed five healthy behaviors, and 109 managed four; 19% managed three; 36% two; 31% one; 8% couldn’t manage any.

http://www.futurity.org/five-healthy-behaviors-can-reduce-dementia-risk/

http://www.eurekalert.org/pub_releases/2013-12/cu-3ys120913.php

Reference: 

Elwood, P., Galante, J., Pickering, J., Palmer, S., Bayer, A., Ben-Shlomo, Y., … Gallacher, J. (2013). Healthy Lifestyles Reduce the Incidence of Chronic Diseases and Dementia: Evidence from the Caerphilly Cohort Study. PLoS ONE, 8(12), e81877. doi:10.1371/journal.pone.0081877

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Exercise helps MCI

A pilot study involving 17 older adults with mild cognitive impairment and 18 controls (aged 60-88; average age 78) has found that a 12-week exercise program significantly improved performance on a semantic memory task, and also significantly improved brain efficiency, for both groups.

The program involved treadmill walking at a moderate intensity. The semantic memory tasks involved correctly recognizing names of celebrities well known to adults born in the 1930s and 40s (difficulty in remembering familiar names is one of the first tasks affected in Alzheimer’s), and recalling words presented in a list. Brain efficiency was demonstrated by a decrease in the activation intensity in the 11 brain regions involved in the memory task. The brain regions with improved efficiency corresponded to those involved in Alzheimer's disease, including the precuneus region, the temporal lobe, and the parahippocampal gyrus.

Participants also improved their cardiovascular fitness, by about 10%.

http://www.eurekalert.org/pub_releases/2013-07/uom-emb073013.php

Reference: 

Smith, J.C. et al. 2013. Semantic Memory Functional MRI and Cognitive Function After Exercise Intervention in Mild Cognitive Impairment. Journal of Alzheimer’s Disease, 37 (1), 197-215.

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Healthy midlife diet may prevent dementia later

Data from the population-based Finnish Cardiovascular Risk Factors, Aging and Incidence of Dementia (CAIDE) study has revealed that healthy dietary choices in midlife may prevent dementia in later years. Out of 2,000 participants, 1,449 took part in the follow-up. The participants were 39 to 64 years old at baseline and 65 to 75 years old at follow-up.

Those who ate the healthiest diet at around age 50 had an almost 90% lower risk of dementia in a 14-year follow-up study than those whose diet was the least healthy.

Healthy foods included vegetables, berries and fruits, fish and unsaturated fats from milk products and spreads; unhealthy foods included sausages, eggs, sweets, sugary drinks, salty fish and saturated fats from milk products and spreads.

Consistent with other research, a high intake of saturated fats was also linked to poorer cognition and an increased risk of mild cognitive impairment 21 years later. A higher saturated fat intake was also associated with an increased risk of dementia among those carrying the “Alzheimer's gene”, ApoE4.

Those consuming 3 to 5 cups of coffee daily had a smaller risk of dementia than those consuming less or more.

http://www.eurekalert.org/pub_releases/2014-03/uoef-hmd031014.php

Reference: 

Eskelinen, Marjo: The effects of midlife diet on late-life cognition: an epidemiological approach. Publications of the University of Eastern Finland. Dissertations in Health Sciences., no 220. http://epublications.uef.fi/pub/urn_isbn_978-952-61-1394-4/

Eskelinen MH, Ngandu T, Helkala E-L, Tuomilehto J, Nissinen A, Soininen H, Kivipelto M. Fat intake at midlife and cognitive impairment later in life: a population-based CAIDE study. Int J Geriatr Psychiatry 23(7): 741, 2008.

Laitinen MH, Ngandu T, Rovio S, Helkala E-L, Uusitalo U, Viitanen M, Nissinen A, Tuomilehto J, Soininen H, Kivipelto M. Fat Intake at Midlife and Risk of Dementia and Alzheimer's Disease: A Population-Based Study. Dement Geriatr Cogn Disord 22(1): 99, 2006.

Eskelinen MH, Ngandu T, Tuomilehto J, Soininen H, Kivipelto M. Midlife Coffee and Tea Drinking and the Risk of Late-Life Dementia: A Population-based CAIDE Study. J Alzheimers Dis 16(1): 85-91, 2009.

Eskelinen MH, Ngandu T, Tuomilehto J, Soininen H, Kivipelto M. Midlife Healthy Diet Index and Late-Life Dementia and Alzheimer's Disease. Dement Geriatr Cogn Disord Extra 1(1): 103-112, 2011.

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Vaccines

Older news items (pre-2010) brought over from the old website

Immunization with AB42 does not prevent dementia despite clearing associated brain plaques

Disappointingly, analysis of 80 Alzheimer's patients who had been involved in trialing immunisation against amyloid-β in September 2000, has found that, despite a lower level of amyloid-β plaques, there was no improved survival or increased time to severe dementia in those who were immunised.

Holmes, C. et al. 2008. Long-term effects of AB42 immunisation in Alzheimer's disease: follow-up of a randomised, placebo-controlled phase I trial. The Lancet, 372 (9634), 216-223.

http://www.eurekalert.org/pub_releases/2008-07/l-iwa071608.php

Vaccine prevents Alzheimer's

A vaccine has successfully prevented the development of amyloid plaques and tau tangles in the brains of genetically engineered mice. The vaccinated mice also demonstrated normal learning skills and functioning memory. There were no major side-effects. Human trials are still a few years off.

Frazer, M.E. et al. 2008. Reduced Pathology and Improved Behavioral Performance in Alzheimer's Disease Mice Vaccinated With HSV Amplicons Expressing Amyloid-β and Interleukin-4. Molecular Therapy, 16, 845-853.

http://www.eurekalert.org/pub_releases/2008-05/uorm-vti051908.php

Alzheimer's vaccine clears plaque but doesn't improve memory

A two-year canine study has revealed that although a promising vaccine being tested for Alzheimer's disease clears beta-amyloid plaques from the brain, it doesn’t seem to help restore lost learning and memory abilities. Autopsies showed that although plaques had been cleared from multiple brain regions, damaged neurons remained. The findings suggest that simply treating beta-amyloid plaques may have only limited clinical benefit if started after there is significant plaque growth, and a combination of vaccination with other therapies aimed at repairing damaged neurons may be best.

Head, E. et al. 2008. A Two-Year Study with Fibrillar β-Amyloid (Aβ) Immunization in Aged Canines: Effects on Cognitive Function and Brain Aβ. Journal of Neuroscience, 28, 3555-3566.

http://www.eurekalert.org/pub_releases/2008-04/uoc--avc040408.php

Transdermal vaccine effective in treating Alzheimer's disease in mice

Previous research on an Alzheimer's vaccine proven safe and effective in an animal model was suspended when the initial clinical trial caused brain inflammation and death in a small percentage of patients. A new mouse study has now had success with a transdermal method of delivery (a skin patch), that doesn’t appear to trigger the toxic reaction of past immunization strategies. Further research is needed to assess whether the transdermal vaccine can curb memory loss as well as reduce Ab plaque.

Nikolic, W.V. et al. 2007. Transcutaneous -amyloid deposits without T cell infiltration and microhemorrhage. Proceedings of the National Academy of Sciences, 104 (7), 2507-2512.

http://www.eurekalert.org/pub_releases/2007-01/uosf-tve011807.php

Hopeful results from interrupted Alzheimer's vaccine study

Phase 2 of a human clinical trial vaccinating patients with beta-amyloid was halted in 2002 when some participants developed brain inflammation. Participants continued to be monitored, however, and results show that participants whose immune systems mounted a response against beta amyloid performed significantly better on a series of memory tests than those who received a placebo injection (but not on 5 tests often used to diagnose dementia). There were also signs of reduced levels of tau protein (a protein considered a sign of cell death) in those who had an immune response. As a result, new trials are underway, this time using humanized antibodies rather than beta amyloid itself. The antibodies should help trigger the immune system to attack beta amyloid, but will be cleared by the body soon after injection.

Gilman, S., Koller, M., Black, R.S., Jenkins, L., Griffith, S.G., Fox, N.C., Eisner, L., Kirby, L., Boada Rovira, M., Forette, F. & Orgogozo, J-M. for the AN1792(QS-21)-201 Study Team. 2005. Clinical effects of Aß immunization (AN1792) in patients with AD in an interrupted trial. Neurology, 64, 1553-1562.

Fox, N.C., Black, R.S., Gilman, S., Rossor, M.N., Griffith, S.G., Jenkins, L. & Koller, M. for the AN1792(QS-21)-201 Study Team. Effects of Aß immunization (AN1792) on MRI measures of cerebral volume in Alzheimer disease. Neurology, 64, 1563-1572.

http://www.eurekalert.org/pub_releases/2005-05/uomh-hrf050505.php

Progress on Alzheimer's vaccine

Efforts to create a vaccine for Alzheimer’s have been hindered by potential side effects — some human participants in an earlier trial developed severe inflammation in the brain. A mouse study has now substantially increased the safety of the vaccine by including a tetanus toxin to alter the immune response. Future studies are planned using the herpes virus.

Bowers, W.J., Mastrangelo, M.A., Stanley, H.A., Casey, A.E., Milo, L.J.Jr. & Federoff, H.J. 2004. HSV amplicon-mediated Ab vaccination in Tg2576 mice: differential antigen-specific immune responses. Neurobiology of Aging, available online 25 June 2004.

http://www.eurekalert.org/pub_releases/2004-06/uorm-hta062904.php

Mice immunized against Alzheimer's

Using a new vaccine, NYU School of Medicine researchers have prevented the development of Alzheimer's disease in mice genetically engineered with the human gene for the disease. The researchers are optimistic that this new vaccine is safer than one already being tested in early human clinical trials. The new vaccine, modeled on a fragment of a protein called amyloid, which is most frequently implicated in causing Alzheimer's, reduced the amount of amyloid plaque in the brains of mice by 89 percent. At the same time, the vaccine reduced the amount of soluble amyloid beta in the brain by 57 percent. Early clinical trials of the new vaccine could begin within one year.

Sigurdsson, E. M., Scholtzova, H., Mehta, P. D., Frangione, B., & Wisniewski, T. (2001). Immunization with a Nontoxic/Nonfibrillar Amyloid-β Homologous Peptide Reduces Alzheimer’s Disease-Associated Pathology in Transgenic Mice. The American Journal of Pathology, 159(2), 439–447. doi:10.1016/S0002-9440(10)61715-4

http://www.eurekalert.org/pub_releases/2001-08/nyum-nrs080101.php

A vaccine for Alzheimer's

A vaccine may help prevent and treat the disabling memory loss and cognitive impairment of Alzheimer's disease. Alzheimer's occurs when amyloid-beta peptides accumulate in the brain, forming plaque. While previous studies have shown that vaccinating mutated mice with this amyloid-beta peptide could remove the plaque deposits, there was never any evidence of improvement in brain function, until now. The researchers also believe this study provides the final element of proof that Alzheimer's is initiated by amyloid-beta peptides. The researchers believe clinical trials could begin on human subjects within the year.

Johnson, J. D., McDuff, S. G. R., Rugg, M. D., & Norman, K. A. (2009). Recollection, Familiarity, and Cortical Reinstatement: A Multivoxel Pattern Analysis. Neuron, 63(5), 697–708. doi:10.1016/j.neuron.2009.08.011

http://www.eurekalert.org/pub_releases/2000-12/UoT-UoTr-1912100.php

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Diet & supplements for Alzheimer's

Older news items (pre-2010) brought over from the old website

Caffeine reverses memory impairment in Alzheimer's mice

Consistent with earlier indications that moderate caffeine consumption may protect against memory decline, a study of genetically engineered mice has found that when the old mice began to show memory impairment, those given caffeine for 2 months performed as well as normal aged mice on cognitive tests, while those given plain drinking water continued to do poorly. The Alzheimer's mice received the equivalent of five 8-oz. cups of regular coffee a day (or two cups of Starbucks coffee, or 14 cups of tea). Moreover, the brains of the caffeinated mice showed nearly a 50% reduction in levels of beta amyloid. The effect appears to be through suppression of both β-secretase and presenilin 1 /g-secretase expression. Caffeine had this effect only on those with Alzheimer’s; normal mice given caffeine through adulthood showed no cognitive benefit.

Arendash, G.W. et al. 2009. Caffeine Reverses Cognitive Impairment and Decreases Brain Amyloid-β Levels in Aged Alzheimer's Disease Mice. Journal of Alzheimer's Disease, 17 (3), 661-680.

Cao, C. et al. 2009. Caffeine Suppresses Amyloid-β Levels in Plasma and Brain of Alzheimer's Disease Transgenic Mice. Journal of Alzheimer's Disease, 17 (3), 681-697.

http://www.eurekalert.org/pub_releases/2009-07/uosf-crm070109.php

Vitamin B3 reduces Alzheimer's symptoms, lesions

High doses of nicotinamide, a form of vitamin B3, has been found to dramatically lower levels of tau protein in mice with Alzheimer's disease. The vitamin also increased proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. Not only did the vitamin prevent memory loss in Alzheimer’s mice, it also slightly improved cognitive performance in normal mice. Nicotinamide is a water-soluble vitamin sold in health food stores. It generally is safe but can be toxic in very high doses. Clinical trials have shown it benefits people with diabetes complications and has anti-inflammatory properties that may help people with skin conditions. Clinical trials with Alzheimer’s patients are now underway.

Green, K.N. et al. 2008. Nicotinamide Restores Cognition in Alzheimer's Disease Transgenic Mice via a Mechanism Involving Sirtuin Inhibition and Selective Reduction of Thr231-Phosphotau. Journal of Neuroscience, 28, 11500-11510.

http://www.eurekalert.org/pub_releases/2008-11/uoc--vbr103008.php

Vitamin E may help Alzheimer's patients live longer

A study of 847 Alzheimer's patients has found that those who took 1,000 international units of vitamin E twice a day, were 26% less likely to die over a five-year period than people who didn't take vitamin E.  It also appears that taking vitamin E plus a cholinesterase inhibitor may be more beneficial than taking either agent alone.

The research was presented at the American Academy of Neurology Annual Meeting in Chicago, April 12 – April 19.

http://www.eurekalert.org/pub_releases/2008-04/aaon-vem040208.php

Omega-3 fatty acids may slow cognitive decline in some patients with very mild Alzheimer's disease

Several studies have shown that eating fish, which is high in omega-3 fatty acids, may protect against Alzheimer's disease. A Swedish study has now tested whether supplements could have similar effects. Patients with mild-to-moderate Alzheimer’s who took 1.7 grams of DHA and .6g of EPA showed the same rate of cognitive decline as those taking a placebo, however, among a subgroup of 32 patients with very mild cognitive impairment, those who took the fatty acids experienced less decline in six months compared with those who took placebo. It may be that anti-inflammatory effects are an important reason for the benefit, potentially explaining why effects were seen only in those with very early-stage disease, when levels of inflammation seem to be higher.

Freund-Levi;, Y. et al. 2006. w-3 Fatty Acid Treatment in 174 Patients With Mild to Moderate Alzheimer Disease: OmegAD Study: A Randomized Double-blind Trial. Archives of Neurology, 63, 1402-1408.

http://www.eurekalert.org/pub_releases/2006-10/jaaj-ofa100506.php

Dietary supplements offer new hope for Alzheimer's patients

A "cocktail" of dietary supplements (omega-3 fatty acids, uridine and choline) has been found to dramatically increase the amount of membranes that form brain cell synapses in gerbils. The treatment is now in human clinical trials. It is hoped that such treatment may significantly delay Alzheimer's disease. The treatment offers a different approach from the traditional tactic of targeting amyloid plaques and tangles. Choline can be found in meats, nuts and eggs, and omega-3 fatty acids are found in a variety of sources, including fish, eggs, flaxseed and meat from grass-fed animals. Uridine, which is found in RNA and produced by the liver and kidney, is not obtained from the diet, although it is found in human breast milk.

Wurtman, R.J., Ulus, I.H., Cansev, M., Watkins, C.J., Wang L. & Marzloff, G. 2006. Synaptic proteins and phospholipids are increased in gerbil brain by administering uridine plus docosahexaenoic acid orally. Brain Research, Available online ahead of print 21 April 2006.

http://www.eurekalert.org/pub_releases/2006-04/miot-mro042706.php

Compound in wine reduces levels of Alzheimer's disease-causing peptides

In cell studies, resveratrol has been found to lower levels of amyloid-beta peptides. Resveratrol is a natural compound occurring in abundance in grapes, berries and peanuts. The highest concentration has been reported in wines prepared from Pinot Noir grapes. The anti-amyloidogenic effect of resveratrol observed in cell cultures does not however necessarily mean that the beneficial effect can result simply from eating grapes or drinking wine. Further research aims to develop more active and more stable compounds.

Marambaud, P., Zhao, H. & Davies, P. 2005. Resveratrol Promotes Clearance of Alzheimer's Disease Amyloid- Peptides. Journal of Biological Chemistry, 280, 37377-37382.

http://www.eurekalert.org/pub_releases/2005-11/asfb-ciw110305.php

Clinical diagnosis of Alzheimer's may be delayed with donepezil

In a study of people with mild cognitive impairment, those who took the drug donepezil were at reduced risk of progressing to a diagnosis of Alzheimer's during the first years of the trial, but by the end of the 3-year study there was no benefit from the drug. Of the 769 participants, 212 developed possible or probable Alzheimer’s within the 3-year study period; the donepezil group's risk of progression to a diagnosis of Alzheimer’s was reduced by 58% one year into the study, and 36% at 2 years, but no risk reduction at the end of three years. Vitamin E was also tested in the study and was found to have no effect at any point in the study.

Petersen, R.C. et al. 2005. Vitamin E and Donepezil for the Treatment of Mild Cognitive Impairment. New England Journal of Medicine, 352 (23), 2379-2388.

http://www.eurekalert.org/pub_releases/2005-04/nioa-cdo041205.php
http://www.eurekalert.org/pub_releases/2005-04/mc-dia041105.php

Pilot study points to healing power of turmeric

A study using genetically engineered mice has found that those mice on a diet rich in curcumin (the yellow pigment in the curry spice turmeric) developed 85% few Alzheimer’s plaques then the control group. Curcumin has antioxidant, anti-inflammatory, and cholesterol lowering properties, and has long been used in India as treatment for a variety of ailments. A human trial involving 33 Alzheimer's patients will soon commence.

Yang, F., Lim, G.P., Begum, A.N., Ubeda, O.J., Simmons, M.R., Ambegaokar, S.S., Chen, P.P., Kayed, R., Glabe, C.G., Frautschy, S.A. & Cole, G.M. 2004. Curcumin inhibits formation of Abeta oligomers and fibrils and binds plaques and reduces amyloid in vivo. Journal of Biological Chemistry, published online ahead of print December 7, 2004
A copy of the full paper can be found on the Journal of Biological Chemistry Web site athttp://tinyurl.com/5bzbs

http://www.eurekalert.org/pub_releases/2004-12/potn-usn122804.php
http://www.sciencentral.com/articles/view.htm3?article_id=218392455

Dietary supplement helps Alzheimer’s

A three-month study of 55 elderly patients with mild or moderate Alzheimer’s found that those given EV-1, a dietary supplement containing, among other things, the putative antioxidant ingredient of red wine, showed no deterioration during the trial. The supplement is designed to interfere with a defective mitochondrial cycle thought to contribute to the metabolic disturbances associated with late onset Alzheimer’s. The Krebs tricarboxylic acid cycle is fuelled by glucose and regulates levels of reactive oxygen species in the body. EV-1 contains glucose, a compound called malate that primes or maintains the Krebs cycle, and resveratrol - the antioxidant component of red wine that is thought to soak up reactive oxygen species. More studies are needed to confirm this result.

The findings were presented in November at the annual meeting of the Society for Neuroscience (SFN) in New Orleans.

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