Caption: Exposure to ambient air pollution, such as car exhaust, has been linked to a higher risk of developing dementia; genetics can heighten the risk (source: IQAir)
Co-lead authors Carol E. Franz, PhD and William S. Kremen, PhD, professors of psychiatry and co-directors of the Center for Behavior Genetics of Aging at UC San Diego School of Medicine, and colleagues examined baseline cognitive assessments of approximately 1,100 men participating in the ongoing Vietnam Era Twin Study of Aging. Average baseline age was 56, with 12 years of follow up.
They additionally looked at measures of exposure to particular matter (PM2.5) in the air and nitrogen dioxide (NO2), which is created when fossil fuels are burned, and assessments of episodic memory, executive function, verbal fluency, brain processing speed and APOE genotype.
APOE is a gene that provides instructions for making a protein crucial to the transport of cholesterol and other fats in the bloodstream. One version or allele of APOE called APOE-4 has been identified as a strong risk factor gene for Alzheimer’s disease.
The researchers found that participants with higher levels of exposure to PM2.5 and NO2 in their 40s and 50s displayed worse cognitive functioning in verbal fluency from age 56 to 68. And persons with the APOE-4 allele appeared even more sensitive, with those exposed to higher PM2.5 levels showing worse outcomes for executive function and those with higher NO2 exposure showing better outcomes involving episodic memory.
Executive function refers to higher-level cognitive skills used to plan, control and coordinate mental behaviors and acts. Episodic memory is the ability to recall and re-experience distinct, specific past events.
“The 2020 Lancet report concluded that modifying 12 risk factors, which include others like education and depression at midlife, could reduce dementia incidence by as much as 40%,” said Franz.
“That report placed ambient air pollution as a greater risk for Alzheimer’s and related dementias than diabetes, physical activity, hypertension, alcohol consumption and obesity. Our findings underscore the importance of identifying modifiable risk factors as early in life as possible — and that the processes by which air pollution affects risk for later-life cognitive decline begins earlier than previous studies suggest.”
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NOTES FOR EDITORS
Media contact
Nicole Mlynaryk, 858-249-0419, npmlynaryk@health.ucsd.edu
Full study
"Associations Between Ambient Air Pollution and Cognitive Abilities from Midlife to Early Old Age: Modification by APOE Genotype", https://doi.org/10.3233/jad-221054
Co-authors include: Daniel E. Gustavson, University of Colorado Boulder; Jeremy A. Elman, Christine Fennema-Notestine, Donald J. Hagler, Jr., Xin M. Tu, Tsung-Chin Wu and Nathan Whitsel, all at UC San Diego; Aaron Baraff, VA Puget Sound Health Care, Seattle; Jaden DeAnda, UC San Diego and San Diego State University; Asad Beck and Joel D. Kaufman, University of Washington; Caleb E. Finch and Jiu-Chiuan Chen, University of Southern California; and Michael J. Lyons, Boston University.
Funding for this research came, in part, from the National Institute on Aging at the National Institutes of Health (grants PO1 AG055367 AND R01S AG050595, AG022381, AG076838, AG037985 AND AG064955.
About the Journal of Alzheimer’s Disease
Now in its 26th year of publication, the Journal of Alzheimer’s Disease (JAD) is an international multidisciplinary journal to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment, and psychology of Alzheimer’s disease. The journal publishes research reports, reviews, short communications, book reviews, and letters-to-the-editor. Groundbreaking research that has appeared in the journal includes novel therapeutic targets, mechanisms of disease, and clinical trial outcomes. JAD has a Journal Impact Factor of 4.160 according to Journal Citation Reports (Clarivate, 2022). The journal is published by IOS Press. j-alz.com
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