Mercury from Seafood Consumption Not Linked to Alzheimer's Pathology

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Mercury from Seafood Consumption Not Linked to Alzheimer's Pathology
Mercury from Seafood Consumption Not Linked to Alzheimer's Pathology

Moderate accumulation of mercury as a result of seafood consumption does not directly correlate with Alzheimer's disease (AD) neuropathology, according to a study published in JAMA. Higher levels of seafood consumption was associated with higher accumulations of mercury in the brain; however, this did not directly correspond to increased neuropathology.

Seafood consumption has been associated with lower levels of AD neuropathology in a number of previous studies, leading to presumptions that diets higher in fish and seafood may be neuroprotective against the development of AD. This potential benefit has been overshadowed by concerns over increased simultaneous consumption of mercury, a neurotoxin that impairs cognitive development.

Martha Clare Morris, ScD, Director, Section of Nutrition & Nutritional Epidemiology at Rush University Medical Center in Chicago, IL, led a study to evaluate the impact of mercury levels in consumed fish on brain neuropathology.  “To our knowledge,” she reported, “this is the first study to report on the relationship between brain concentrations of mercury and brain neuropathology or diet.”

CLINICAL CHART: Alzheimer's Dementia Treatments

Dr Morris and colleagues identified a cohort of 286 participants (mean age 89.9 years) from the Memory and Aging Project (MAP) study who had died during the period between November 2004 and November 2014, had completed at least 1 dietary assessment prior to death, and on whom a brain autopsy was performed. Of those patient cases analyzed, 125 (43.7%) had completed 1 questionnaire, 58 (20.3%) had completed 2, and 103 (36%) had answered 3 or more, with a mean response of 2.4 years prior to death.

Neuropathology among individuals who were positive for apolipoprotein E (APOE ε4) who had consumed at least one seafood meal weekly (or higher intake of n-3 fatty acids) was lower in comparison to people who reported lower consumption. This correlation did not exist in people who were APOE ε4  negative.

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