Alzheimers prevention

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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Estrogen for Alzheimer's

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

For women over 65, Combined Hormone Therapy increases risk of dementia

Much to the researchers’ surprise and disappointment, a four-year experiment involving 4,532 women at 39 medical centers, has found that combined hormone therapy (involving both estrogen and progestin) doubles the risk of Alzheimer's disease and other types of dementia in women who began the treatment at age 65 or older, although the risk is still small : for every 10,000 women 65 and older who take hormones, 23 of the predicted 45 cases of dementia a year, will be attributable to the hormones. The study also found that the combined hormone therapy produced no improvement in general cognitive function, and in fact had adverse effects on cognition among some women. This supports an earlier study suggesting that, while estrogen is helpful to cognitive function in postmenopausal women, the benefits can be cancelled out by progestin / progesterone. The study also confirmed previous research showing that the combination therapy increased the risk of stroke - previous research has indicated that risk factors for stroke are also risk factors for cognitive decline.

Shumaker, S.A., Legault, C., Rapp, S.R., Thal, L., Wallace, R.B., Ockene, J.K., Hendrix, S.L., Jones, B.N. III, Assaf, A.R., Jackson, R.D., Kotchen, J.M., Wassertheil-Smoller, S. & Wactawski-Wende, J. 2003. Estrogen Plus Progestin and the Incidence of Dementia and Mild Cognitive Impairment in Postmenopausal Women: The Women's Health Initiative Memory Study: A Randomized Controlled Trial. JAMA, 289, 2651-2662.

Rapp, S.R., Espeland, M.A., Shumaker, S.A., Henderson, V.W., Brunner, R.L., Manson, J.E., Gass, M.L.S., Stefanick, M.L., Lane, D.S., Hays, J., Johnson, K.C., Coker, L.H., Dailey, M. & Bowen, D. 2003. Effect of Estrogen Plus Progestin on Global Cognitive Function in Postmenopausal Women: The Women's Health Initiative Memory Study: A Randomized Controlled Trial. JAMA, 289, 2663-2672.

Wassertheil-Smoller, S., Hendrix, S., Limacher, M., Heiss, G., Kooperberg, C., Baird, A., Kotchen, T., Curb, J.D., Black, H., Rossouw, J.E., Aragaki, A., Safford, M., Stein, E., Laowattana, S. & Mysiw, W.J. 2003. Effect of Estrogen Plus Progestin on Stroke in Postmenopausal Women: The Women's Health Initiative: A Randomized Trial. JAMA, 289, 2673-2684.

http://www.eurekalert.org/pub_releases/2003-05/wfub-chr052203.php

Animal studies suggest why estrogen can't help after dementia has developed

Research with rats suggests that nerve cells in the brain called cholinergic neurons are needed for estrogen to help learning and memory. This suggests why starting estrogen after dementia has developed is ineffective.

Gibbs, R.B. 2002. Basal Forebrain Cholinergic Neurons Are Necessary for Estrogen to Enhance Acquisition of a Delayed Matching-to-Position T-Maze Task, Hormones and Behavior, 42(3), 245-257.

http://www.eurekalert.org/pub_releases/2002-11/uopm-asp110502.php

Long-term ERT in postmenopausal women with Alzheimer's may worsen memory

A study using female rats investigated the interaction of two conditions known to exist within the brains of female Alzheimer's patients: 1) the presence of chronic neuroinflammation, and 2) having too much or not enough estrogen. They found that rats who had their ovaries removed (to model the condition of post-menopausal women) performed more poorly on a water maze task when they had chronic brain inflammation OR long-term estrogen replacement therapy. Most significantly, those who had both conditions performed much more poorly – beyond what would be expected by either condition alone. That such results extend to postmenopausal women is supported by a 2000 study involving a long term, placebo-controlled study that examined the effects of estrogen replacement therapy on cognitive function in women with mild to moderate Alzheimer's. The effects of ERT were initially beneficial, but the performance of women receiving sustained ERT declined more than that of women receiving the placebo treatment. The results of these studies suggest that postmenopausal women with Alzheimer's disease who undergo long-term estrogen replacement therapy may make their memory loss worse.

Marriott, L.K., Hauss-Wegrzyniak, B., Benton, R.S., Vraniak, P.D. & Wenk, G.L. 2002. Long-Term Estrogen Therapy Worsens the Behavioral and Neuropathological Consequences of Chronic Brain Inflammation. Behavioral Neuroscience, 116 (5), 902-11.

http://www.eurekalert.org/pub_releases/2002-10/apa-lei102202.php

Estrogen patch may improve memory for women with Alzheimer's

A new study suggests that an estrogen skin patch given to women with mild to moderate Alzheimer's disease can improve their memory and attention skills. The study involved only 20 women for eight weeks, and the results will need to be confirmed by a larger-scale study. Research to date has been equivocal about the effects of estrogen on women with Alzheimer's, with some finding a memory-enhancing effect, and others finding no effect. It is speculated that the type of estrogen might be critical. The present study used estradiol, a type of estrogen that has been shown to have an effect on the brain.

Asthana, S., Baker, L. D., Craft, S., Stanczyk, F. Z., Veith, R. C., Raskind, M. A., & Plymate, S. R. (2001). High-dose estradiol improves cognition for women with AD Results of a randomized study. Neurology, 57(4), 605–612. doi:10.1212/WNL.57.4.605

http://www.eurekalert.org/pub_releases/2001-08/aaon-epm082001.php

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Importance of vascular factors in Alzheimer's disease

Analysis of 5715 cases from the National Alzheimer's Coordinating Center (NACC) database has found that nearly 80% of more than 4600 Alzheimer's disease patients showed some degree of vascular pathology, compared with 67% of the controls, and 66% in the Parkinson's group. The link was especially strong for younger patients with Alzheimer’s.

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Walking to work cuts risk of diabetes and high blood pressure

Data from a survey of 20,000 people across the UK has found that people who cycle, walk, or take public transport to work had a lower risk of being overweight than those who drove or took a taxi. People who walked to work were 40% less likely to have diabetes than those who drove and 17% less likely to have high blood pressure. Cyclists were around half as likely to have diabetes as drivers.

http://www.eurekalert.org/pub_releases/2013-08/icl-wtw080513.php

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Gardening as good as exercise in cutting heart attack risk

A Swedish study of some 4,000 60-year-olds has found that regular “non-exercise” physical activity such as gardening or DIY significantly reduced risk of heart attack or stroke, with those who were most active on a daily basis having a 27% lower risk of a heart attack or stroke and a 30% reduced risk of death from all causes. This was so regardless of how much regular formal exercise was taken.

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Exercise improves heart function via mitochondria

A mouse study has found that long-term physical activity increased levels of two proteins in the mitochondria of their heart. It’s thought this might help explain why regular exercise improves cardiovascular health.

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Why dark chocolate is good for your heart

A study involving 44 middle-aged overweight men who consumed 70 grams of dark chocolate per day over two periods of four weeks, has found that dark chocolate helps restore flexibility to arteries while also preventing white blood cells from sticking to the walls of blood vessels. Both arterial stiffness and white blood cell adhesion are known factors that play a significant role in atherosclerosis.

http://www.eurekalert.org/pub_releases/2014-02/foas-wdc022714.php

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Increased intake of fish can boost good cholesterol levels

A Finnish study has found that people who increased their intake of fatty fish to a minimum of 3–4 weekly meals had more large HDL cholesterol in their blood than people who were less frequent eaters of fish. Large HDL particles are believed to protect against cardiovascular diseases.

http://www.eurekalert.org/pub_releases/2014-03/uoef-iio030314.php

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Mediterranean diet may lower risk of diabetes

A review of 19 studies involving over 162,000 people has found that adherence to the Mediterranean diet was associated with a 21% reduced risk of diabetes, with a greater effect (27%) for those at high risk for cardiovascular disease. The association was found in both European and non-European groups.

The research was presented at the American College of Cardiology's 63rd Annual Scientific Session.

http://www.eurekalert.org/pub_releases/2014-03/acoc-mdm032614.php

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