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Obesity differentially effects the somatosensory cortex and striatum of TgF344-AD rats
Minhal Ahmed1,2, Aaron Y Lai1, Mary E Hill1
1Biological Sciences, Sunnybrook Research Institute, Toronto, ON, M4N 3M5, Canada.
Scientific Reports
|March 28, 2024
Summary
Obesity in late-life Alzheimer's disease (AD) may paradoxically reduce AD risk by altering brain myelination. This study in TgF344-AD rats suggests diet impacts brain regions differently, potentially explaining the obesity paradox in AD.
Area of Science:
- Neuroscience
- Metabolic Disorders
- Aging Research
Background:
- Mid-life obesity, hypertension, and diabetes increase late-life Alzheimer's disease (AD) risk.
- Paradoxically, late-life obesity appears to reduce AD risk and slow disease progression.
Purpose of the Study:
- To investigate the mechanisms behind the obesity paradox in Alzheimer's disease (AD).
- To examine how a high-carbohydrate, high-fat (HCHF) diet affects brain regions with differing white and gray matter densities in an AD rat model.
Main Methods:
- TgF344-AD rats were fed a HCHF diet from 9 to 12 months of age to induce obesity and model AD.
- Brain regions, specifically the somatosensory cortex (gray matter) and striatum (white matter), were analyzed for changes in myelination, inflammation, and neuronal integrity.
Main Results:
- HCHF diet induced obesity and AD pathology without neuronal loss in the somatosensory cortex.
- Increased myelin and oligodendrocytes were observed in the somatosensory cortex, alongside decreased inflammation despite AD pathology.
- The striatum showed fewer changes compared to the somatosensory cortex.
Conclusions:
- Diet-induced obesity impacts brain myelination in an AD model in a region-specific manner.
- Gray matter-rich regions (like the somatosensory cortex) may be preferentially affected, offering a mechanistic explanation for the late-life obesity paradox in Alzheimer's disease.
