Aβ42 in molecular mechanism of combines Parkinson's and Alzherimer's disease, Authors: I. F. Tsigelny, Y. Sharikov, E. Masliah: © Argonne National Laboratory Every month more studies are published that demonstrate that if there is
to be successful avoidance of, or limitation to, the ravages of
Alzheimer's disease, intervention needs to begin as early as possible.
Several suggest that treatments begin before Alzheimer's symptoms
appear. One study, published online just yesterday in the Archives of
Neurology, shows the benefits of doing such.
Longitudinal Change of Biomarkers in Cognitive Decline, was conducted at 59 sites of the Alzheimer's Disease Neuroimaging Initiative, with 819 participants 55 to 90 years old. The study measured levels of amyloid beta peptide Aβ42 in cerebrospinal fluid (CSF), fludeoxyglucose F18 (FDG), and hippocampal volume, all known biomarkers of Alzheimer's disease. The researchers compared the development of these biomarkers with their subjects' cognitive changes at different ages and stages of Alzheimer's disease.
Findings reveal that the depth of the tracks left by the biomarkers become more and more prominent as the symptoms of Alzheimer's appear, but that the levels of CSF Aβ42, in particular, decline prior to cognitive loss. This information strongly calls for an intervention as soon as the CSF Aβ42 marker begins to decline, thus very possibly altering the course of the disease.
Roger N. Rosenberg, MD and editor of the Archives, cites the above study as well as others in his editorial published June 13, 2011 online edition of the Archives, in which he argues for the treatment of Alzheimer's before it is diagnosed. But, he writes, "In our research to develop a DNA anti-Aβ42 vaccine as preventive
therapy for AD, we have encountered the idea that it
should be clinically tested only after the diagnosis of AD has
"It is incumbent on the AD research community," Rosenberg continues, "to educate our
colleagues, the public, and regulatory agencies to accept that
it is necessary to treat AD before it is symptomatic. Alzheimer's
disease therapies must be allowed to be given in rigorous, phase-1
clinical trials to individuals who have progressive memory loss
or mild cognitive impairment, before they are diagnosed with
dementia due to AD, when preventive therapy has a chance to
Low fat, low glycemic index diet appears to help memoryIn an unrelated study, also published in the Archives of Neurology, researchers from the Veterans Administration Medical Center in Seattle compared levels of CSF Aβ42 in healthy adults and adults with mild cognitive impairment before and after a 4-week diet. Two diets, one a high fat, high glycemic index diet, and the second a low fat, low glycemic index diet, were randomly assigned to the groups.
After four weeks, CSF testing showed that the healthy group on the low fat diet reduced their CSF biomarkers for the disease, and they also performed better on memory tests than they did prior to the diet. Healthy persons on the high fat diet increased their biomarkers for Alzheimer's disease, characteristic of "a pre-symptomatic state of Alzheimer's Disease."
The early stage Alzheimer's subjects, those with mild cognitive impairments, did not experience a reduction in CSF biomarkers after the 4 week low fat diet, unfortunately. But the study certainly does force the issue of early intervention. Whether it's drugs or diet, these conclusions regarding the timing of Alzheimer's intervention should not be ignored.
sources: Archives of Neurology, Longitudinal Cahnge of Biomarkers in Cognitive Decline, Archives of Neurology, Treat Alzheimer Disease Before It Is Symptomatic. Archives of Neurology, Diet Intervention and Cerebrospinal Fluid Biomarkers in Amnestic Mild Cognitive Impairment via The Telegraph.