Alzheimer's & other dementias
More evidence that excess abdominal fat, independent of your overall BMI, places otherwise healthy, middle-aged people at greater risk for dementia later in life.
A study involving 733 participants from the Framingham Heart Study Offspring Cohort (average age 60) provides more evidence that excess abdominal fat places otherwise healthy, middle-aged people at greater risk for dementia later in life. The study also confirms that a higher BMI (body mass index) is associated with lower brain volumes in both older and middle-aged adults. However the association between visceral fat and total brain volume was independent of BMI. Visceral fat differs from subcutaneous fat in that it is buried deeper, beneath the muscles, around the organs. While it can only be seen by CT imaging, a pot belly or thick waist suggests its presence. For women (who become particularly vulnerable to this after menopause), a waistline above 88 cm is regarded as signaling a dangerous amount of visceral fat. Regular vigorous exercise, and consumption of polyunsaturated fats rather than saturated fats, is recommended.
 Debette, S., Beiser A., Hoffmann U., DeCarli C., O'Donnell C. J., Massaro J. M., et al.
(2010). Visceral fat is associated with lower brain volume in healthy middle-aged adults.
Annals of Neurology. 9999(9999), NA - NA.
A long-running study has revealed that caring for a spouse with dementia is as strong a risk factor for developing Alzheimer's as having the 'Alzheimer's gene'.
A 12-year study involving 1,221 married couples ages 65 or older (part of the Cache County (Utah) Memory Study) has revealed that husbands or wives who care for spouses with dementia are six times more likely to develop Alzheimer’s themselves than those whose spouses don't have it. The increased risk is of comparable size to having the ‘Alzheimer's gene’. The researchers speculate that the great stress of caregiving might be responsible for the increased dementia risk, emphasizing the need for greater caregiver support.
 Norton, M. C., Smith K. R., Østbye T., Tschanz JA. T., Corcoran C., Schwartz S., et al.
(2010). Greater Risk of Dementia When Spouse Has Dementia? The Cache County Study.
Journal of the American Geriatrics Society. 58(5), 895 - 900.
A new study reveals that having the 'Alzheimer's gene' doesn't simply increase your risk of developing Alzheimer's, but affects how the brain is damaged.
A comprehensive study reveals how the ‘Alzheimer's gene’ (APOE ε4) affects the nature of the disease. It is not simply that those with the gene variant tend to be more impaired (in terms of both memory loss and brain damage) than those without. Different parts of the brain (and thus different functions) tend to be differentially affected, depending on whether the individual is a carrier of the gene or not. Carriers displayed significantly greater impairment on tests of memory retention, while noncarriers were more impaired on tests of working memory, executive control, and lexical access. Consistent with this, carriers showed greater atrophy in the mediotemporal lobe, and noncarriers greater atrophy in the frontoparietal area. The findings have implications both for diagnosis and treatment.
 Wolk, D. A., & Dickerson B. C.
(2010). Apolipoprotein E (APOE) genotype has dissociable effects on memory and attentional–executive network function in Alzheimer’s disease.
Proceedings of the National Academy of Sciences. 107(22), 10256 - 10261.
Mouse studies suggest a way to reverse both normal age-related memory loss, and dementia.
Although research has so far been confined to mouse studies, researchers are optimistic about the promise of histone deacetylase inhibitors in reversing age-related memory loss — both normal decline, and the far more dramatic loss produced by Alzheimer’s. The latest study reveals that memory impairment in the aging mouse is associated with altered hippocampal chromatin plasticity, specifically with the failure of histone H4 lysine 12 acetylation, leading to a failure to initiate the gene expression program associated with memory consolidation. Restoring this acetylation leads to the recovery of cognitive abilities.
 Peleg, S., Sananbenesi F., Zovoilis A., Burkhardt S., Bahari-Javan S., Agis-Balboa R C., et al.
(2010). Altered Histone Acetylation Is Associated with Age-Dependent Memory Impairment in Mice.
Science. 328(5979), 753 - 756.
A preliminary study suggests that a regime of high doses of folic acid, B12 and B6 reduces levels of homocysteine in people with mild to moderate Alzheimer’s. A larger study, recruiting 400 participants from all over the U.S., is to be undertaken to assess whether such a vitamin regime can slow the progression of Alzheimer's disease. In the meantime, it is not advised that people take high doses of these vitamins, as there are possible side-effects, including peripheral nerve damage.
 Bell, K., Sano M., Aisen P. S., Egelko S., Andrews H., Diaz-Arrastia R., et al.
(2003). A pilot study of vitamins to lower plasma homocysteine levels in Alzheimer disease.
The American Journal of Geriatric Psychiatry: Official Journal of the American Association for Geriatric Psychiatry. 11(2), 246 - 249.
A study involving 4,740 elderly (65 years or older) found the greatest reduction in both prevalence and incidence of Alzheimer's in those who used individual vitamin E and C supplements in combination, with or without an additional multivitamin. There was no significant benefit in using vitamin C alone, vitamin E alone, or vitamin C and multivitamins in combination.
Zandi, P.P., Anthony, J.C., Khachaturian, A.S., Stone, S.V., Gustafson, D., Tschanz, J.T., Norton, M.C., Welsh-Bohmer, K.A. & Breitner, J.C.S. 2004. Reduced Risk of Alzheimer Disease in Users of Antioxidant Vitamin Supplements: The Cache County Study. Archives of Neurology, 61, 82-88.
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