A new study examining the effect of diet on Alzheimer disease (AD) development has reportedly linked diets high in saturated fat to increased levels of lipid-depleted β-amyloid peptides (LD Aβ) in the brain. Angela Hanson, et al., “Effect of Apolipoprotein E Genotype and Diet on Apolipoprotein E Lipidation and Amyloid Peptides,” JAMA Neurology, June 2013. According to the study, which notes that the Aβ peptides partly responsible for AD “can be bound to lipids or to lipid carrier proteins, such as apolipoprotein E (ApoE), or be free in solution,” “levels of LD Aβ are higher in the plasma of adults with AD, but less is known about these peptides in the cerebrospinal fluid (CSF).” The researchers thus measured the levels of LD Aβ42, LD Aβ40 and ApoE in the CSF of 20 older adults with normal cognition and 27 older adults with mild cognitive impairment (MCI), with randomized members of both groups placed on either a diet high in saturated fat content with a high glycemic index or a diet low in saturated fat content with a low glycemic index.

The results apparently suggested that compared to participants with normal cognition, those with MCI had higher CSF LD Aβ levels, especially if they also had a specific APOE genotype linked to AD risk. At the same time, however, the study’s authors reported that “the diet low in saturated fat tended to decrease LD Aβ levels, whereas the diet high in saturated fat increased these fractions.”

“These findings have implications not only for cognitively normal older adults but also for cognitively normal adults who have risk factors for AD,” they concluded. “We also show that changes in LD Aβ peptide levels induced by diet moved in the opposite direction from [central nervous system] insulin levels, which may be one of the mechanisms for how diets impart AD risk or protection. Overall, these results suggest that the lipidation states of apolipoproteins and amyloid peptides might play a role in AD pathological process and are influenced by APOE genotype and diet.” See JAMA Neurology Press Release, June 17, 2013.