Surgery and Alzheimer's pathology
Research type
Research Study
Full title
Evaluating the influence of obesity on neuroinflammation and Alzheimer’s pathology
IRAS ID
149720
Contact name
Paul Edison
Contact email
Sponsor organisation
Faculty of Medicine, Imperial College, London
Duration of Study in the UK
1 years, 4 months, 16 days
Research summary
Obesity (a body mass index of more than 30) is associated with a significantly increased risk of dementia, ranging from 70% to three-fold. While there is significant evidence to suggest that metabolic syndrome (visceral (abdominal) obesity, dyslipidemia, high blood sugar and high blood pressure) increases the risk of Alzheimer’s disease (AD), the exact mechanisms by which metabolic syndrome and, in particular, obesity affects AD remain uncertain. It is suggested that visceral obesity and insulin resistance may arise from low-grade inflammation of the adipose (fat) tissue and that this subclinical inflammation of adipose tissue may interact with the impaired central inflammatory response, leading to neurodegeneration (degeneration of the nerve cells).
In this study we hypothesise that:
1. Obesity is associated with central (cortical) neuroinflammation in addition to inflammation in the hypothalamus in the brain, and this could be measured by [11C]PBR28 PET scanning.
2. Reducing peripheral fat content through bariatric (weight loss) surgery reduces cortical neuroinflammation by reducing the systemic inflammatory response induced by the adipose tissue, and this could be measured by reduction in [11C]PBR28 binding potential.This pilot study, leading to a much larger clinical and preclinical PET study, has the potential to answer the important question of the mechanism by which obesity and metabolic syndrome cause neurodegeneration, and therefore develop novel intervention strategies.
REC name
London - West London & GTAC Research Ethics Committee
REC reference
15/LO/0072
Date of REC Opinion
30 Mar 2015
REC opinion
Further Information Favourable Opinion