You can help your brain, especially as it ages, by eating and drinking right
Two new animal studies offer hope for a drug treatment for traumatic brain injury and stroke.
Following indications that the curry spice curcumin (the active ingredient in turmeric) may help protect brain cells from damage, two new studies have been testing a compound called CNB-001, derived from curcumin.
The first (rabbit) study found that CNB-001 is at least as effective as the only existing drug used to treat stroke (TPA), without the unwanted side-effect of reducing clotting in the blood vessels of the brain.
The second study found that CNB-001 dramatically reversed the behavioral deficits in both locomotion and memory in brain-injured rats. As with stroke, CNB-001 was again found to maintain the critical signaling pathways required for nerve cell survival, as well as the connections between nerve cells that are lost with the injury.
At present, there is no treatment for TBI, and only one FDA-approved drug for ischemic stroke
 Lapchak, P. A., Schubert D. R., & Maher P. A.
(2011). Delayed treatment with a novel neurotrophic compound reduces behavioral deficits in rabbit ischemic stroke.
Journal of Neurochemistry. 116(1), 122 - 131.
More evidence that vascular disease plays a crucial role in age-related cognitive impairment and Alzheimer’s comes from data from participants in the Alzheimer's Disease Neuroimaging Initiative.
The study involved more than 800 older adults (55-90), including around 200 cognitively normal individuals, around 400 people with mild cognitive impairment, and 200 people with Alzheimer's disease. The first two groups were followed for 3 years, and the Alzheimer’s patients for two. The study found that the extent of white matter hyperintensities (areas of damaged brain tissue typically caused by cardiovascular disease) was an important predictor of cognitive decline.
Participants whose white matter hyperintensities were significantly above average at the beginning of the study lost more points each year in cognitive testing than those whose white matter hyperintensities were average at baseline. Those with mild cognitive impairment or Alzheimer's disease at baseline had additional declines on their cognitive testing each year, meaning that the presence of white matter hyperintensities and MCI or Alzheimer's disease together added up to even faster and steeper cognitive decline.
The crucial point is that this was happening in the absence of major cardiovascular events such as heart attacks, indicating that it’s not enough to just reduce your cardiovascular risk factors to a moderate level — every little bit of vascular damage counts.
 Carmichael, O., Schwarz C., Drucker D., Fletcher E., Harvey D., Beckett L., et al.
(2010). Longitudinal Changes in White Matter Disease and Cognition in the First Year of the Alzheimer Disease Neuroimaging Initiative.
Arch Neurol. 67(11), 1370 - 1378.
A new study suggests that the link between midlife obesity and cognitive impairment and dementia in old age may be explained by poorer insulin sensitivity.
Previous research has indicated that obesity in middle-age is linked to higher risk of cognitive decline and dementia in old age. Now a study of 32 middle-aged adults (40-60) has revealed that although obese, overweight and normal-weight participants all performed equally well on a difficult cognitive task (a working memory task called the 2-Back task), obese individuals displayed significantly lower activation in the right inferior parietal cortex. They also had lower insulin sensitivity than their normal weight and overweight peers (poor insulin sensitivity may ultimately lead to diabetes). Analysis pointed to the impaired insulin sensitivity mediating the relationship between task-related activation in that region and BMI.
This suggests that it is insulin sensitivity that is responsible for the higher risk of cognitive impairment later in life. The good news is that insulin sensitivity is able to be modified through exercise and diet.
A follow-up study to determine if a 12-week exercise intervention can reverse the differences is planned.
 Gonzales, M. M., Tarumi T., Miles S. C., Tanaka H., Shah F., & Haley A. P.
(2010). Insulin Sensitivity as a Mediator of the Relationship Between BMI and Working Memory-Related Brain Activation.
Obesity. 18(11), 2131 - 2137.
Another study adds to growing evidence that diabetes, or poor glycaemic control, has serious implications for brain function.
A small study comparing 18 obese adolescents with type 2 diabetes and equally obese adolescents without diabetes or pre-diabetes has found that those with diabetes had significantly impaired cognitive performance, as well as clear abnormalities in the integrity of their white matter (specifically, reduced white matter volume, especially in the frontal lobe, as well as impaired integrity in both white and grey matter). Similar abnormalities have previously been found in adults with type 2 diabetes, but the subjects were elderly and, after many years of diabetes, generally had significant vascular disease. One study involving middle-aged diabetics found a reduction in the volume of the hippocampus, which was directly associated with poor glycaemic control.
It remains to be seen whether such changes can be reversed by exercise and diet interventions. While those with diabetes performed worse in all cognitive tasks tested, the differences were only significant for intellectual functioning, verbal memory and psychomotor efficiency.
 Yau, P. L., Javier D. C., Ryan C. M., Tsui W. H., Ardekani B. A., Ten S., et al.
(2010). Preliminary evidence for brain complications in obese adolescents with type 2 diabetes mellitus.
 Gold, S. M., Dziobek I., Sweat V., Tirsi A., Rogers K., Bruehl H., et al.
(2007). Hippocampal damage and memory impairments as possible early brain complications of type 2 diabetes.
Diabetologia. 50(4), 711 - 719.
I have often spoken of the mantra: What’s good for your heart is good for your brain. The links between cardiovascular risk factors and cognitive decline gets more confirmation in this latest finding that people whose hearts pumped less blood had smaller brains than those whose hearts pumped more blood. The study involved 1,504 participants of the decades-long Framingham Offspring Cohort who did not have a history of stroke, transient ischemic attack or dementia. Participants were 34 to 84 years old.
Worryingly, it wasn’t simply those with the least amount of blood pumping from the heart who had significantly more brain atrophy (equivalent to almost two years more brain aging) than the people with the highest cardiac index. Those with levels at the bottom end of normal showed similar levels of brain atrophy. Moreover, although only 7% of the participants had heart disease, 30% had a low cardiac index.
 Jefferson, A. L., Himali J. J., Beiser A. S., Au R., Massaro J. M., Seshadri S., et al.
(2010). Cardiac Index Is Associated With Brain Aging: The Framingham Heart Study.
Circulation. 122(7), 690 - 697.
A mouse study demonstrates that the right diet can reverse Alzheimer’s damage in the early stages.
Following on from previous research with mice that demonstrated that a diet rich in methionine could increase the risk of developing Alzheimer's Disease through its effect on homocysteine levels, a new study has found that these effects were reversible if the mice then switched to a healthier diet. The mice, after five months on a methionine-rich diet, were divided into two groups, with one group continuing the diet and the second switching to the healthy diet for an additional two months. The cognitive impairment, and the build-up in amyloid plaques, was completely reversed after two months.
Methionine is an amino acid typically found in red meats, fish, beans, eggs, garlic, lentils, onions, yogurt and seeds. I note, however, that most of the items in this list are usually considered healthy! Fish, in particular, has been shown in a number of studies to reduce the risk of Alzheimer’s. The point is that methionine in itself is an essential amino acid and necessary for a healthy brain, but this indicates that, as with many foods, moderation is important. Clearly a balance is required; equally clearly, we still haven’t quite worked out the ‘perfect’ Alzheimer’s-prevention diet. Nevertheless, this study is welcome in demonstrating that diet can have such an effect on the brain, and adds to our knowledge of what makes a good diet for staving off dementia.
 Zhuo, J-M., & Pratico D.
(2010). Normalization of hyperhomocysteinemia improves cognitive deficits and ameliorates brain amyloidosis of a transgenic mouse model of Alzheimer's disease.
FASEB J.. fj.10-161828 - fj.10-161828.
Seniors who were most closely following a Mediterranean-like diet were 36% less likely to have brain infarcts than those least following the diet.
Following on from studies showing that a Mediterranean-like diet may be associated with a lower risk of Alzheimer's disease and may lengthen survival in people with Alzheimer's, a six-year study of 712 New Yorkers has revealed that those who were most closely following a Mediterranean-like diet were 36% less likely to have brain infarcts (small areas of dead tissue linked to thinking problems), compared to those who were least following the diet. Those moderately following the diet were 21% less likely to have brain damage. The association was comparable to the effects of high blood pressure — that is, not eating a Mediterranean-like diet was like having high blood pressure. The Mediterranean diet includes high intake of vegetables, legumes, fruits, cereals, fish and monounsaturated fatty acids such as olive oil; low intake of saturated fatty acids, dairy products, meat and poultry; and mild to moderate amounts of alcohol.
The study will be presented at the American Academy of Neurology's 62nd Annual Meeting in Toronto April 10 to April 17, 2010.
New analysis reveals the most important factors for predicting whether amnestic-MCI would develop into Alzheimer’s within 2 years were hyperglycemia, female gender and having the Alzheimer's gene.
An analysis technique using artificial neural networks has revealed that the most important factors for predicting whether amnestic mild cognitive impairment (MCI-A) would develop into Alzheimer’s within 2 years were hyperglycemia, female gender and having the APOE4 gene (in that order). These were followed by the scores on attentional and short memory tests.
Tabaton, M. et al. 2010. Artificial Neural Networks Identify the Predictive Values of Risk Factors on the Conversion of Amnestic Mild Cognitive Impairment. Journal of Alzheimer's Disease, 19 (3), 1035-1040.
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 variant of a gene called the fat mass and obesity associated (FTO) gene causes people to gain weight and puts them at risk for obesity. The gene variant is found in nearly half of all people in the U.S. with European ancestry, around one-quarter of U.S. Hispanics, 15 percent of African Americans and 15 percent of Asian Americans. A new study involving 206 healthy elderly subjects from around the U.S. now suggests that this gene variant is also associated with loss of brain tissue. It’s not clear why, but the gene is highly expressed in the brain. Those with the "bad" version of the FTO gene had an average of 8% less tissue in the frontal lobes, and 12% less in the occipital lobes. The brain differences could not be directly attributed to other obesity-related factors (cholesterol levels, hypertension, or the volume of white matter hyperintensities), which didn’t vary between carriers and non-carriers. But if you have this gene variant, your weight is associated with neuron loss, and if you don't, it isn’t. The finding emphasizes the need for those with the gene to fight weight gain (and brain loss) by exercising and eating healthily.
 Ho, A. J., Stein J. L., Hua X., Lee S., Hibar D. P., Leow A. D., et al.
(2010). A commonly carried allele of the obesity-related FTO gene is associated with reduced brain volume in the healthy elderly.
Proceedings of the National Academy of Sciences. 107(18), 8404 - 8409.
Full text is available at http://www.pnas.org/content/107/18/8404.abstract?sid=d95d84c7-f052-4d50-...
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