These are interesting studies, and the conclusions drawn by the authors, though based on a relatively low "n" (nine-15 subjects per group) and a short duration of treatment (four weeks), provide food for thought.

Numerous studies have shown (1) that a high-fat diet is proinflammatory in nature, whereas a low-fat diet reduces inflammation (lowers blood inflammatory markers). Thus, decreased inflammation is likely to be the basis of improvement in delayed visual memory for both the healthy control and aMCI groups that received the low diet. This would be consistent with the findings (2) of Holmes and Perry, which showed that increased inflammation in MCI patients resulted in a rapid decline of cognitive performance. It will be helpful to measure the levels of inflammatory markers (IL-6, TNF-α, MCP-1, leukotrienes, etc.) in the blood and CSF of all four groups.

One way of interpreting the observation that low diet improves the memory score in both the control and aMCI groups, whereas it increases CSF Aβ42 in aMCI and decreases it in controls, is that there is...  Read more

These are interesting studies, and the conclusions drawn by the authors, though based on a relatively low "n" (nine-15 subjects per group) and a short duration of treatment (four weeks), provide food for thought.

Numerous studies have shown (1) that a high-fat diet is proinflammatory in nature, whereas a low-fat diet reduces inflammation (lowers blood inflammatory markers). Thus, decreased inflammation is likely to be the basis of improvement in delayed visual memory for both the healthy control and aMCI groups that received the low diet. This would be consistent with the findings (2) of Holmes and Perry, which showed that increased inflammation in MCI patients resulted in a rapid decline of cognitive performance. It will be helpful to measure the levels of inflammatory markers (IL-6, TNF-α, MCP-1, leukotrienes, etc.) in the blood and CSF of all four groups.

One way of interpreting the observation that low diet improves the memory score in both the control and aMCI groups, whereas it increases CSF Aβ42 in aMCI and decreases it in controls, is that there is no correlation between CSF Aβ42 levels and memory improvement. After all, the authors also find no changes in CSF tau or phospho-tau levels, despite the improvement in memory score. Comparison of Figures 2A, 2D, and 2E shows that the levels of F2-isoprostanes, markers for free radical injury, are better indicators of memory improvement than Aβ42 levels.

The argument that CSF Aβ42 levels in the control and aMCI groups move in opposite directions due to the onset of plaque deposition is relatively weak. The mean age of healthy subjects in this study is 69.7 years, suggesting that there is a strong possibility that at least a third of them are already PIB-positive. Inclusion of PIB scans would have made these studies significantly more powerful.

If we are serious about controlling AD, then changes in lifestyle factors such as diet and exercise are probably the most effective option currently available. Even metabolic disorders such diabetes, hypercholesterolemia, and cardiovascular diseases, against which we do have effective drugs, still require lifestyle changes to maintain the benefits from the drugs.

References:
1. Bulló M, Casas-Agustench P, Amigó-Correig P, Aranceta J, Salas-Salvadó J. Inflammation, obesity and comorbidities: the role of diet. Public Health Nutr. 2007 Oct;10(10A):1164-72. Abstract

2. Holmes C, Cunningham C, Zotova E, Woolford J, Dean C, Kerr S, Culliford D, Perry VH. Systemic inflammation and disease progression in Alzheimer disease. Neurology. 2009 Sep 8;73(10):768-74. Abstract

View all comments by Sanjay W. Pimplikar