Findings of HHS Funded Report Preventing Alzheimer’s Disease and Cognitive Decline


The Agency for Healthcare Research and Quality under The Department of Health and Human Services used our tax dollars to have the Duke University, Evidence-based Practice Center (EPC) conduct research for a report “Preventing Alzheimer’s Disease and Cognitive Decline”. The failure of these researchers to find only one one study fitting their criteria linking mercury to Alzheimer’s disease is incredibly as there is over 20 years worth of publish studies showing a relationship between mercury and Alzheimer’s disease.



The Agency for Healthcare Research and Quality (AHRQ), through its Evidence-Based Practice Centers (EPCs), sponsors the development of evidence reports and technology assessments to assist public- and private-sector organizations in their efforts to improve the quality of health care in the United States. The National Institutes of Health (NIH) Office of Medical Applications of Research (OMAR) requested and provided funding for this report.

The reports and assessments provide organizations with comprehensive, science-based information on common, costly medical conditions and new health care technologies. The EPCs systematically review the relevant scientific literature on topics assigned to them by AHRQ and conduct additional analyses when appropriate prior to developing their reports and assessments. 

To bring the broadest range of experts into the development of evidence reports and health technology assessments, AHRQ encourages the EPCs to form partnerships and enter into collaborations with other medical and research organizations. The EPCs work with these partner organizations to ensure that the evidence reports and technology assessments they produce will become building blocks for health care quality improvement projects throughout the Nation.

The reports undergo peer review prior to their release. 

AHRQ expects that the EPC evidence reports and technology assessments will inform individual health plans, providers, and purchasers as well as the health care system as a whole by providing important information to help improve health care quality.

We welcome comments on this evidence report. They may be sent by mail to the Task Order Officer named below at: Agency for Healthcare Research and Quality, 540 Gaither Road, Rockville, MD 20850, or by e-mail to

Structured Abstract

Objectives: To assess whether previous research on purported risk or protective factors for Alzheimer’s disease (AD) and cognitive decline is of sufficient strength to warrant specific recommendations for behavioral, lifestyle, or pharmaceutical interventions/modifications targeted to these endpoints.

Data Sources: MEDLINE® and the Cochrane Database of Systematic Reviews. Additional studies were identified from reference lists and technical experts.

Review Methods: A group of experts in the field developed the list of factors to be evaluated in preparation for an upcoming National Institutes of Health (NIH) Office of Medical Applications of Research (OMAR) State-of-the-Science Conference addressing the prevention of AD and cognitive decline.

We grouped the factors into the following categories:

  • nutritional factors, 
  • medical conditions
  • prescription and non-prescription medications
  • social/economic/behavioral factors
  • toxic environmental factors
  • genetics.

Outcomes of interest were the development of AD or cognitive decline.

Both observational and intervention studies were evaluated.

Studies were evaluated for eligibility and quality, and data were abstracted on study design, demographics, intervention or predictor factor, and cognitive outcomes.

Results: A total of 25 systematic reviews and 250 primary research studies were included. Only a few factors showed a consistent association with AD or cognitive decline across multiple studies, including both observational studies and randomized controlled trials (when available).

Such factors associated with increased risk of AD and cognitive decline were: diabetes, epsilon 4 allele of the apolipoprotein E gene (APOE e4), smoking, and depression. Factors showing a fairly consistent association with decreased risk of AD and cognitive decline were: cognitive engagement and physical activities. A consistent association does not imply that findings were robust, as the data were often limited, and the quality of evidence was typically low.

In addition, the modification of risk for reported associations was typically small to moderate for AD, and small for cognitive decline. Some of the factors that did not show an association with AD or cognitive decline in this review may still play an influential role in late-life cognition, but there was not sufficient evidence to draw this conclusion. Many of the factors evaluated are not amenable to randomization, so rigorous observational studies are required to assess their effect on AD and cognitive decline.

Conclusions: The current research on the list of putative risk or protective factors is largely inadequate to confidently assess their association with AD or cognitive decline. Further research that addresses the limitations of existing studies is needed prior to be able to make recommendations on interventions.


Our problem with this report is quite obvious. The researchers limited their search criteria that excluded over 20 years worth of published studies linking mercury to Alzheimer’s disease as found in this comprehensive overview

Toxic Environmental Exposures, page 13

Our search identified two additional studies on the exposures of interest, one evaluating aluminum exposure and one evaluating blood mercury levels. 

Using a subgroup from the Canadian Study of Health and Aging (15 percent of the cohort), Kroger et al.81 used a nested case-control design to evaluate the association between blood mercury levels and AD. After a median of 4.9 years, individuals in the 3rd (OR 0.41; 95 percent CI 0.23 to 0.74) and 4th quartiles of exposure (OR 0.56, 0.32 to0.99) were at lower risk for AD. However, the relatively low participation rate may have introduced significant selection bias. 

In summary, few cohort studies have examined the association between toxic-environmental exposures and risk of AD. Most case-control studies have important methodological limitations that may bias the results.

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