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Dietary composition modulates brain mass and solubilizable Abeta levels in a mouse model of aggressive Alzheimer's amyloid pathology. Pedrini S, Thomas C, Brautigam H, Schmeidler J, Ho L, Fraser P, Westaway D, Hyslop PS, Martins RN, Buxbaum JD, Pasinetti GM, Dickstein DL, Hof PR, Ehrlich ME, Gandy S. Mol Neurodegener. 2009 Oct 21;4:40. PMID: 19845940 doi:10.1186/1750-1326-4-40 INTERPRETATION: Dissociation of Abeta changes from brain mass changes raises the possibility that diet plays a role not only in modulating amyloidosis but also in modulating neuronal vulnerability. However, in the absence of a study of the effects of a high protein/low carbohydrate diet on nontransgenic mice, one cannot be certain how much, if any, of the loss of brain mass exhibited by high protein/low carbohydrate diet-fed TgCRND8 mice was due to an interaction between cerebral amyloidosis and diet. Given the recent evidence that certain factors favor the maintenance of cognitive function in the face of substantial structural neuropathology, we propose that there might also exist factors that sensitize brain neurons to some forms of neurotoxicity, including, perhaps, amyloid neurotoxicity. Identification of these factors could help reconcile the poor clinicopathological correlation between cognitive status and structural neuropathology, including amyloid pathology.

Amyloid-degrading ability of nattokinase from Bacillus subtilis natto. Hsu RL, Lee KT, Wang JH, Lee LY, Chen RP. J Agric Food Chem. 2009 Jan 28;57(2):503-8. PMID: 19117402 DOI: 10.1021/jf803072r\n

A multi-institutional team of researchers led by Emory University has defined for the first time how metal ions bind to amyloid fibrils in the brain in a way that appears toxic to neurons. Amyloid fibrils are linked to the development of neurodegenerative

Marambaud P, Zhao H, Davies P. Resveratrol promotes clearance of Alzheimer's disease amyloid-beta peptides. J Biol Chem. 2005 Nov 11;280(45):37377-82. Epub 2005 Sep 14. PMID: 16162502 [PubMed - indexed for MEDLINE]

A ketogenic diet reduces amyloid beta 40 and 42 in a mouse model of Alzheimer's disease. Van der Auwera I, Wera S, Van Leuven F, Henderson ST. Nutr Metab (Lond). 2005 Oct 17;2:28. PMID: 16229744 doi:10.1186/1743-7075-2-28 CONCLUSION: Previous studies have suggested that diets rich in cholesterol and saturated fats increased the deposition of Abeta and the risk of developing AD. Here we demonstrate that a diet rich in saturated fats and low in carbohydrates can actually reduce levels of Abeta. Therefore, dietary strategies aimed at reducing Abeta levels should take into account interactions of dietary components and the metabolic outcomes, in particular, levels of carbohydrates, total calories, and presence of ketone bodies should be considered.

People in Asia have been eating fermented foods for more than 1,000 years. One vegan fermented food, renowned in Asia for its ability to protect against heart attacks, was recently shown to have a powerful ability in lab experiments to prevent formation of the clumps of tangled protein involved in Alzheimer's disease. if this works as well in the human brain as scientists expect, it will be a great addition to the tables of anyone who is concerned about this terrible disease

View Michael Mullan's professional profile on LinkedIn. Dr Michael Mullan, CEO and President of the Roskamp Institute, Sarasota, FL. He research to cure Alzheimer's Disease. He discovered Swedish Mutation in the Amyloid Precursor Protein gene that is widely used in Alzheimer's research today.

Michael Mullan, CEO and President of the Roskamp Institute, Sarasota, FL. He is a biomedical researcher of the beta amyloid protein and its relation to Alzheime.

Michael Mullan, CEO and President of the Roskamp Institute, Sarasota, FL. He research to cure Alzheimer's Disease. He discovered Swedish Mutation in the Amyloid Precursor Protein gene that is widely used in Alzheimer's research today. Michael Mullan is a leading expert in Alzheimers Research and other neurodegnerative disorder.

Are omega-3 fatty acids options for prevention and treatment of cognitive decline and dementia? Cederholm T, Palmblad J. Curr Opin Clin Nutr Metab Care. 2009 Dec 16. [Epub ahead of print] PMID: 20019606 PURPOSE OF REVIEW: To report recent data on the potential role of omega-3 fatty acids (n-3 FA) found in oily fish, especially docosahexaenoic acid (DHA), to prevent and treat cognitive decline and Alzheimer's disease. RECENT FINDINGS: Observational studies still provide conflicting results, in which the majority indicate beneficial effects on cognition, both when assessed as a continuous variable or as incident dementia, mainly Alzheimer's disease. Experimental studies have demonstrated potentially ameliorating effects of eicosapentaenoic acid (EPA) and DHA on amyloid fragment formation, signal transduction including upregulation of the apolipoprotein receptor SorLA, as well as on angiogenesis. The role of EPA and DHA metabolites on Alzheimer's disease pathology is under investigation. Recently, three randomized intervention studies, with duration up to 6 months have been reported. In contrast to a small study from Taiwan, no positive overall effects were reported from the Swedish OmegAD Study or from a Dutch study, although post hoc analyses indicate that selected individuals with mild forms of Alzheimer's disease or cognitive decline may respond to treatment. SUMMARY: No firm conclusions can be drawn. Based on epidemiological data, fish including oily fish could be advised as part of a balanced diet for public health purpose, although the evidence for better cognition is only fairly consistent. It is unlikely that n-3 FA will emerge as a treatment option in general for improving cognitive function in patients with Alzheimer's disease. n-3 FA, especially DHA, may turn out as an adjuvant therapy in selected cases. Further long-term intervention studies on individuals with mild cognitive reductions are awaite"

Biochemical effects of consumption of eggs containing omega-3 polyunsaturated fatty acids. Ohman M, Akerfeldt T, Nilsson I, Rosen C, Hansson LO, Carlsson M, Larsson A. Ups J Med Sci. 2008;113(3):315-23.P MID: 18991244 Today, eggs with an increased content of -3 fatty acids are available but there are few publications on the effects of consumption of such eggs on the lipoproteins and acute phase markers in humans. The aim of the present study was to evaluate the effects of consumption of standard eggs and -3 enriched eggs on lipoproteins, glucose and inflammation markers. Nineteen healthy volunteers consumed one extra egg per day of either standard eggs or omega-3 enriched eggs in a double-blind, cross-over study. The duration of each period was 1 month. The effects of the different egg diets on apolipoprotein A1 and B (Apo A1 and B), lipoprotein (a), creatinine, cystatin C, C-reactive protein, serum amyloid protein A, interleukin 6, triglycerides, glucose, total-, high-density lipoprotein and low-density lipo-protein cholesterol concentrations were analyzed. Addition of one regular egg per day to the normal diet had no negative impact on blood lipids or inflammation markers. Consumption of omega-3 enriched eggs resulted in higher levels of ApoA1, lower ApoB/ApoA1 ratio and lower plasma glucose. These effects have been associated in previous studies with a reduced risk for cardiovascular mortality and diabetes.

ScienceDaily (Feb. 20, 2009) - A vegan food renowned in Asia for its ability to protect against heart attacks also shows a powerful ability in lab experiments to prevent formation of the clumps of tangled protein involved in Alzheimer's disease, scientists in Taiwan are reporting. \n\nRita P. Y. Chen and colleagues point out that people in Asia have been eating natto - a fermented food made from boiled soybeans -for more than 1,000 years. Natto contains an enzyme, nattokinase, that has effects similar to clot-busting drugs used in heart disease.Nattokinase is sold a dietary supplement to impro 

Eating a curry once or twice a week could help prevent the onset of Alzheimer's disease and dementia, a US researcher suggests. The key ingredient is curcumin, a component of the spice turmeric.

Ginkgo has many alleged nootropic properties, and is mainly used as memory[25] and concentration enhancer, and anti-vertigo agent. However, studies differ about its efficacy. The largest and longest independent clinical trial to assess ginkgo biloba's ability to prevent memory loss has found that the supplement does not prevent or delay dementia or Alzheimer's disease.[26] Some controversy has arisen over the conclusions drawn by some studies that were allegedly funded by a firm which marketed Ginkgo.[27] In 2002, a long-anticipated paper appeared in JAMA (Journal of the American Medical Association) titled "Ginkgo for memory enhancement: a randomized controlled trial." This Williams College study, sponsored by the National Institute on Aging rather than Schwabe, examined the effects of ginkgo consumption on healthy volunteers older than 60. The conclusion, now cited in the National Institutes of Health's ginkgo fact sheet, said: "When taken following the manufacturer's instructions, ginkgo provides no measurable benefit in memory or related cognitive function to adults with healthy cognitive function." ... The impact of this seemingly damning assessment, however, was ameliorated by the almost simultaneous publication of a Schwabe-sponsored study in the less prestigious Human Psychopharmacology. This rival study, conducted at Jerry Falwell's Liberty University, was rejected by JAMA, and came to a very different-if not exactly sweeping-conclusion: There was ample evidence to support "the potential efficacy of Ginkgo biloba EGb 761 in enhancing certain neuropsychological/memory processes of cognitively intact older adults, 60 years of age and over." According to some studies, in a few cases, Ginkgo can significantly improve attention in healthy individuals.[28][29] Allegedly, the effect is almost immediate and reaches its peak in 2.5 hours after the intake.[30] [edit] In dementia A 2004 conference paper[31] summarizes how various trials indicate that Gi