The new study, published in JAMA Neurology, examined whether modifications to the lipidation states in certain proteins related to the development of Alzheimer's disease (AD) are modified by dietary interventions - finding that the lipidation states beta-amyloid peptides in the brain are related to the development of AD and appear to differ depending by genotype and diet.
“Overall, these results suggest that the lipidation states of apolipoproteins and amyloid peptides might play a role in AD pathological processes and are influenced by APOE genotype and diet,” explained the study authors - led by Dr Angela Hanson from the University of Washington, USA.
"Concentrations can be modulated by diet," explained the research team. "These findings may provide insight into the mechanisms through which apolipoprotein E4 and unhealthy diets impart risk for developing AD."
Hanson added that their data from this small pilot study now needs to be replicated in a larger sample size before any firm conclusions can be drawn.
Writing in an accompanying editorial, Dr Deborah Blacker from the Massachusetts General Hospital and Harvard Medical School, USA, suggested that the findings of the new study may underlie some of the mechanisms behind recent epidemiologic findings regarding diabetes and other cardiovascular risk factors and risk for AD.
"The specifics of their model may not capture the real underlying biological effect of these diets, and it is unclear whether the observed changes in the intermediate outcomes would lead to beneficial changes in oligomers or plaque burden, much less to decreased brain atrophy or improved cognition,” she said.
“At some level, however, the details of the biological model are not critical; the important lesson from the study is that dietary intervention can change brain amyloid chemistry in largely consistent and apparently meaningful ways – in a short period of time."
Hanson and her colleagues noted that the lipidation states - or modifications - of certain proteins in the brain that are related to the development of Alzheimer disease appear to differ depending on genotype and diet. Such proteins, they added, can be bound to lipids or lipid carrier proteins - like apolipoprotein E (ApoE) - or can be free in solution (lipid-depleted [LD] beta-amyloid).
While it is known that levels of LD beta-amyloid are higher in the plasma of adults with AD, less is known about these peptides in the cerebrospinal fluid (CSF), they added.
As part of the new study, Hanson and her team studied 20 older adults with normal cognition (average age 69 years) and 27 older adults with amnestic mild cognitive impairment (average age 67 years).
Participants were randomised to consume a diet high in saturated fat content (45% energy from fat, with more than 25% from saturated fat) and with a high glycemic index, or a diet low in saturated fat content (25% energy from fat with less than 7% sat fat) and a low glycemic index.
The main outcomes the researchers measured were lipid depleted (LD) beta-amyloid 42 and, beta-amyloid 40, and ApoE in cerebrospinal fluid.
Hanson's results showed that baseline levels of LD beta-amyloid were greater for adults with mild cognitive impairment compared with adults with normal cognition.
Results indicated that a diet low in saturated fat tended to decrease LD beta-amyloid levels, whilst a diet high in saturated fat increased their levels.
The team also noted that their findings were more apparent in adults with mild cognitive impairment and the epsilon4 allele (a risk factor for AD), who had higher LD apolipoprotein E levels irrespective of cognitive diagnosis
Source: JAMA Neurology
Published online ahead of print, doi: 10.1001/jamaneurol.2013.396
"Effect of Apolipoprotein E Genotype and Diet on Apolipoprotein E Lipidation and Amyloid PeptidesRandomized Clinical Trial"
Authors: Angela J. Hanson, Jennifer L. Bayer-Carter, et al