The study participants were 34 amyloid-beta (A?)-positive individuals with mild cognitive impairment or early Alzheimer's disease (prodromal/early Alzheimer's disease) and 55 A?-negative cognitively normal (CN) subjects. The links between nutritional status (body mass index, fat-free mass index, fat mass index, waist to height ratio) and brain changes have been mapped by multiple analysis using statistical parametric mapping.
“These results suggest that hypometabolism in the medial prefrontal areas is specifically associated with Alzheimer's disease-related weight loss, and decrease in fat mass may have a key role. However, this cross-sectional study provides preliminary results, so we need further longitudinal investigation considering the fat tissue metabolism including adipokines to deepen our understanding of Alzheimer's disease-related weight loss,” says Dr. Takashi Sakurai, head of the Memory Clinic at NCGG and a corresponding author of the study.
In the prodromal/early Alzheimer's disease group, nutritional status has been significantly positively linked with regional cerebral glucose metabolism (rCGM) in the medial prefrontal cortices, while varying topographical associations have been observed in the CN group.
Sub-analysis in the prodromal/early Alzheimer's disease group shows that fat mass index, but not fat-free mass index, has been positively linked with rCGM in the medial prefrontal areas.
This study is the first to show the associations of nutritional status with Alzheimer's disease-related brain changes by utilizing multi-imaging modalities such as amyloid-beta (A?)-positron emission topography (PET), 18-F-fluorodeoxyglucose (FDG)-PET and structural magnetic resonance imaging.
The findings of reduced glucose metabolism in the medial prefrontal areas of A?-positive individuals may give answer to the mechanism of weight loss in Alzheimer's disease.
How Alzheimer's disease spreads
Researchers from the Perelman School of Medicine at the University of Pennsylvania have found out that A? begins the interaction plaques and abnormal tau protein, causing the spread of mutated tau proteins in the neurons, which instigates the descent of long-term Alzheimer's disease.
The researchers have been able to come up with this finding by injecting human Alzheimer's disease brain extracts of pathological tau protein (from postmortem donated tissue) into mice with varying amounts of A? plaques in their brains.
“Making an Alzheimer's disease mouse model that incorporates both A? and tau pathologies in a more Alzheimer's disease-relevant context has been greatly sought after but difficult to accomplish. This study is a big step for Alzheimer's disease research, which will allow us to test new therapies in a more realistic context,” says senior author Virginia Lee, Ph.D., director of the Center for Neurodegenerative Disease Research at Penn.
Tau stabilizes microtubules in axons that have the task of transporting material inside neurons. The removal of tau protein from microtubules as a result of its clumping in nerve cells causes the affected neurons to lose their ability to properly function, leading to their degeneration, and ultimately, to Alzheimer's disease.
“For the first time we could see and study the tau clumps in dystrophic axons surrounding A? plaques in a mouse model, just like we see in a human brain with Alzheimer's disease,” says first author Zhuohao He, Ph.D., a postdoctoral fellow in Lee's lab.
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