Atrophy, Infarcts Independently Drive Memory Loss

Susan Jeffrey

December 28, 2011

December 28, 2011 — A new study shows that hippocampal volume and brain infarcts independently contribute to memory loss in elderly people without dementia.

"We found that brain infarcts are associated with a smaller hippocampus, and that both infarcts and hippocampal volume are independently associated with global memory functioning," the researchers, with senior author Adam M. Brickman, PhD, from the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University Medical Center in New York, New York, conclude. "Furthermore, infarcts and hippocampal volume are associated with specific aspects of memory functioning, which are overlapping but unique."

Vascular dementia has been primarily considered a decline in nonmemory domains of cognition, particularly executive function and perceptual speed, they note, with any significant memory decline generally attributed to coexisting Alzheimer's disease (AD) with its associated hippocampal atrophy.

"Although the current study did not examine individuals with dementia per se, the implication of our data is significant in that they suggest that history of brain infarcts can lead to a phenotype that is typically thought of as prodromal AD — that is, infarcts are associated with poorer memory, and smaller hippocampus, not just poorer performance in nonmemory domains," the authors conclude.

Their report is published in the January 3 print issue of Neurology; the embargo was released early. It is the first study, to their knowledge, to examine whether memory is associated with the presence of prior infarcts independent of hippocampal atrophy, they write.

Brain Infarcts and Volumes

For this report, the researchers used data from high-resolution structural magnetic resonance imaging (MRI) of 658 community-dwelling elderly people aged 65 years and older, and free of dementia at baseline, participating in the Washington Heights-Inwood Columbia Aging Project. Brain images were used to calculate hippocampal and relative brain volumes, as well as assessing cortical and subcortical brain infarcts.

All also underwent neuropsychological testing, with summary scores reflecting performance on tasks of memory, language, processing speed, and visuospatial function, the authors note. "We used multiple regression analyses to relate cortical and subcortical infarcts, hippocampal and relative brain volume, to measures of cognitive performance in domains of memory, language, processing speed, and visuospatial ability."

They found that the presence of brain infarcts was associated with a smaller hippocampus, and a smaller hippocampal volume was associated specifically with poorer memory. "Brain infarcts were associated with poorer memory and cognitive performance in all other domains, which was independent of hippocampus volume," the authors write.

The observation that brain infarcts affect memory and other cognitive domains independent of changes in the hippocampus suggests a "critical need for stroke prevention," they add.

"Multiple Hits"

In a previous prospective sample of elderly persons, they note, more than 50% of those with dementia had multiple pathologies at autopsy, while more than 80% of nondemented people had single or no pathology.

"This observation suggests that dementia is a cumulative effect of 'multiple hits' that most often include AD, Parkinson/Lewy body pathology, and brain infarcts; focusing on prevention of one of the 'hits' may decrease the incidence of dementia."

Brain infarcts are a largely preventable brain injury, with clearly identified risk factors and prevention programs, they conclude. "A public health push toward emphasizing stroke prevention may significantly decrease incidence of dementia."

The study was supported by the National Institutes of Health (NIH) and the Charles and Ann Lee Saunders Fellowship. Dr. Brickman serves on the editorial boards of the Journal of the International Neuropsychological Society and Neuropsychology Review; serves as a consultant for ProPhase LLC; and receives research support from the NIH and the Alzheimer's Association. Disclosures for coauthors are found in the paper.

Neurology. 2012;78:38-46. Abstract