Mercury may not thwart seafood brain benefits

By Eleanor McDermid, Senior medwireNews Reporter

Accumulation of mercury in the brain from eating seafood does not appear to lead to Alzheimer’s disease (AD) neuropathology, shows research published in JAMA.

The autopsy study showed that seafood consumption was associated with reduced AD pathology in carriers of the APOE ε4 allele. And while it was also associated with increased mercury levels, this did not appear to counteract its positive effects.

“This latter finding is reassuring because ingested mercury accumulates in the body over decades and brain levels hence result from exposure, which likely precedes any Alzheimer disease or dementia development”, said Edeltraut Kröger and Robert Laforce, from Université Laval in Québec City, Canada, in a linked editorial.

They say the results suggest “that seafood can be consumed without substantial concern of mercury contamination diminishing its possible cognitive benefit in older adults.”

Researcher Martha Clare Morris (Rush University Medical Center, Chicago, Illinois, USA) and team autopsied the brains of 286 deceased participants of the Rush Memory and Aging Project who had completed at least one dietary assessment before they died, when aged an average of 89.9 years.

Average brain tissue mercury levels, assessed in 203 brains, ranged from 0.25 µg/g in the inferior temporal region to 0.87 µg/g in the cerebellum and correlated significantly with the participants’ weekly consumption of seafood.

However, mercury levels did not correlate with AD or dementia pathology; in fact, global AD pathology, neuritic plaque density and neurofibrillary tangle severity tended to be less in participants in the higher versus the lowest mercury tertiles. Likewise, macroinfarcts and Lewy bodies tended to be less frequent in the higher versus the lowest tertiles and microinfarcts were significantly less so.

Among APOE ε4 carriers, significantly less severe AD pathology was observed among those who ate seafood at least once a week and those who had sources of long-chain n-3 fatty acids in their diets versus those who did not. But there was no such effect among people without the risk allele.

In the overall cohort, higher consumption of α-linoleic acid was associated with a significantly reduced likelihood of macroinfarcts and microinfarcts, but long-chain n-3 fatty acids did not have this effect, which Kröger and Laforce say confirms “current understanding of the cardiovascular benefits of α-linoleic acid.”

They add that the “differences in the correlations between fish or n-3 fatty acids and Alzheimer disease or dementia brain pathology ,according to APOE ε4 status, underscore the present limits in understanding Alzheimer disease and other dementias resulting from neurodegenerative processes.”

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