Low BMI Is Associated With Biomarkers for Alzheimer’s Disease
In cognitively normal people and among patients with mild cognitive impairment, lower BMI is associated with the presence of biomarkers indicative of Alzheimer’s disease, researchers reported in the November 22 issue of Neurology. Eric Vidoni, PhD, of the Department of Neurology at the University of Kansas Medical Center in Kansas City, and colleagues studied data from 506 participants enrolled in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database. The researchers examined the relationship between biomarkers and the progression of Alzheimer’s disease, using in vivo measures that assess cerebral amyloid burden (CSF amyloid β 1–42 [Aβ] and PET imaging with Pittsburgh Compound B) and neurofibrillary tangles (CSF tau). Participants were followed for two years and included people with no dementia, those with mild cognitive impairment, and those with Alzheimer’s disease.
After controlling for age and sex, the investigators found an association between BMI and CSF amyloid β (β = 0.181), tau (β = – 0.179), tau/AB ratio (β = – 0.180), and global Pittsburgh Compound B uptake (β = – 0.272). They also found biomarkers of increased Alzheimer’s disease burden in people with lower BMI (BMI less than 25 kg/m2). This relationship was observed in the overall, combined sample. The researchers also explored the presence of biomarkers in normal weight compared with those who were overweight (BMI greater than 25 kg/m2) participants, finding that fewer overweight people had a high prevalence of biomarkers indicating Alzheimer’s disease.
In addition, the study showed that the relationship between low BMI and Alzheimer’s disease biomarkers was greatest in participants with mild cognitive impairment. Thus, normal or low-weight people with mild cognitive impairment may have a higher level of amyloid-based cognitive impairment than those who are overweight.
According to Dr. Vidoni’s group, “This relationship of higher Alzheimer’s disease pathophysiology with lower BMI was most strongly evident in those without major cognitive or functional change. These results provide further support that Alzheimer’s disease has systemic manifestations that may be the result of longstanding neuropathologic change or lifestyle patterns. Further, cognitive impairment in those who are overweight may be more likely to be the result of heterogeneous pathophysiology.”
Vidoni ED, Townley RA, Honea RA, et al. Alzheimer disease biomarkers are associated with body mass index. Neurology. 2011;77(21):1913-1920.
Long-Term Follow-Up Shows Statin Therapy Is Safe and Effective
Prolonged use of statin treatment produces larger reductions in vascular events, and the benefits persist for at least five years after treatment is stopped, researchers reported in the November 23 online issue of Lancet.
To address questions about the long-term efficacy and safety of statin treatment, Rory Collins, MD, of the University of Oxford, United Kingdom, and principal investigator of the Heart Protection Study Collaborative Group (HPS), and colleagues followed up with patients enrolled in the original HPS study, which used minimized randomization to study 20,536 men and women ages 40 to 80 who were at high risk of vascular and nonvascular outcomes. The patients were allocated either 40 mg simvastatin daily or placebo.
The mean follow-up was 5.3 years, while the mean, post-trial follow-up of the surviving 17,519 patients was 11.0 years. The study’s primary end point for prolonged follow-up was the first major vascular event that occurred postrandomization, which was defined as nonfatal myocardial infarction or coronary death, fatal or nonfatal stroke, and coronary or noncoronary revascularization.
Analysis of the in-trial period showed that patients allocated to receive simvastatin had an average reduction in LDL cholesterol of 1.0 mmol/L, as well as a 23% proportional decrease in major vascular events. Although the investigators found no significant difference in major vascular events during the first year of the trial, significant divergence—with reductions of about one quarter—occurred during each subsequent in-trial year.
The researchers also examined the post-trial period, when statin use and lipid concentrations were similar in both allocation groups, and they noted no additional significant reductions in either major vascular events (risk ratio [RR], 0.95) or vascular mortality (RR, 0.98). Furthermore, during the trial period as well as afterward, all the study sites recorded no significant difference in cancer occurrence (RR, 0.98), and none of the individual sites documented significant differences in cancer occurrence or in mortality attributed to cancer (RR, 1.01) or to nonvascular causes (RR, 0.96).
These results may reassure both prescribers and patients about the long-term benefits of lowering LDL cholesterol through statin therapy, the researchers concluded. They stated, “These findings provide further support for the prompt initiation and long-term continuation of statin treatment in people at increased risk of vascular events.”
Heart Protection Study Collaborative Group. Effects on 11-year mortality and morbidity of lowering LDL cholesterol with simvastatin for about 5 years in 20,536 high-risk individuals: a randomized controlled trial. Lancet. 2011 Nov 23; [Epub ahead of print].