Unlocking the Mind’s Backup Battery to Fight Alzheimer’s

Published on August 10, 2022

Imagine your brain as a car battery, powering your cognitive abilities. In a fascinating study, scientists explored the concept of ‘cognitive reserve’—your brain’s backup power source. They wanted to see how this reserve affects the progression of amnestic mild cognitive impairment (MCI) due to Alzheimer’s disease. To investigate, they analyzed cognitive tests and brain scans of patients with MCI. The results were eye-opening! They found that patients with higher levels of cognitive reserve—those who had received more education—showed more severe hypometabolism in certain brain regions. This means their brain cells were not receiving enough glucose, leading to faster cognitive decline. On the other hand, patients with lower cognitive reserve experienced less severe hypometabolism. Intriguingly, the study also found that cognitive decline was more rapid in patients with higher cognitive reserve during the 3-year follow-up period. These findings suggest that having a strong cognitive reserve may not always be beneficial in MCI due to Alzheimer’s disease. Want to dive deeper into this research? Check out the full article!

This study aimed to investigate the effect of cognitive reserve (CR) on the rate of cognitive decline and cerebral glucose metabolism in amnestic mild cognitive impairment (MCI) using the Study on Diagnosis of Early Alzheimer’s Disease-Japan (SEAD-J) dataset. The patients in SEAD-J underwent cognitive tests and fluorodeoxyglucose-positron emission tomography (FDG-PET). MCI to be studied was classified as amnestic MCI due to Alzheimer’s disease (AD) with neurodegeneration. A total of 57 patients were visually interpreted as having an AD pattern (P1 pattern, Silverman’s classification). The 57 individuals showing the P1 pattern were divided into a high-education group (years of school education ≥13, N = 18) and a low-education group (years of school education ≤12, N = 39). Voxel-based statistical parametric mapping revealed more severe hypometabolism in the high-education group than in the low-education group. Glucose metabolism in the hippocampus and temporoparietal area was inversely associated with the years of school education in the high- and low-education groups (N = 57). General linear mixed model analyses demonstrated that cognitive decline was more rapid in the high-education group during 3-year follow-up. These results suggest that the cerebral glucose metabolism is lower and cognitive function declines faster in patients with high CR of amnestic MCI due to AD defined by FDG-PET.

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