How Fat May Hurt the Brain, and How Exercise May Help

Gretchen Reynolds at the New York Times writes about this here:
So does this mean that the first thing your doctor should be doing after your stroke is help your get rid of your fat(Lipectomy) and get some exercise?
http://well.blogs.nytimes.com/2014/03/05/how-fat-may-harm-the-brain-and-how-exercise-may-help/?_php=true&_type=blogs&_r=0

The research this is based upon:

Obesity Elicits Interleukin 1-Mediated Deficits in Hippocampal Synaptic Plasticity

1. Joanna R. Erion¹,*,
2. Marlena Wosiski-Kuhn¹,*,
3. Aditi Dey¹,
4. Shuai Hao¹,
5. Catherine L. Davis¹,²,
6. Norman K. Pollock², and
7. Alexis M. Stranahan¹

+Show Affiliations

1. Author contributions: J.R.E., M.W.-K., C.L.D., N.K.P., and A.M.S. designed research; J.R.E., M.W.-K., A.D., S.H., C.L.D., N.K.P., and A.M.S. performed research; J.R.E., M.W.-K., A.D., S.H., C.L.D., N.K.P., and A.M.S. analyzed data; J.R.E., M.W.-K., A.D., S.H., C.L.D., N.K.P., and A.M.S. wrote the paper.
2. ↵*J.R.E. and M.W.-K. contributed equally to this work.

1. The Journal of Neuroscience, 12 February 2014, 34(7): 2618-2631; doi: 10.1523/JNEUROSCI.4200-13.2014

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Abstract

Adipose tissue is a known source of proinflammatory cytokines in obese humans and animal models, including the db/db mouse, in which obesity arises as a result of leptin receptor insensitivity. Inflammatory cytokines induce cognitive deficits across numerous conditions, but no studies have determined whether obesity-induced inflammation mediates synaptic dysfunction. To address this question, we used a treadmill training paradigm in which mice were exposed to daily training sessions or an immobile belt, with motivation achieved by delivery of compressed air on noncompliance. Treadmill training prevented hippocampal microgliosis, abolished expression of microglial activation markers, and also blocked the functional sensitization observed in isolated cells after ex vivo exposure to lipopolysaccharide. Reduced microglial reactivity with exercise was associated with reinstatement of hippocampus-dependent memory, reversal of deficits in long-term potentiation, and normalization of hippocampal dendritic spine density. Because treadmill training evokes broad responses not limited to the immune system, we next assessed whether directly manipulating adiposity through lipectomy and fat transplantation influences inflammation, cognition, and synaptic plasticity. Lipectomy prevents and fat transplantation promotes systemic and central inflammation, with associated alterations in cognitive and synaptic function. Levels of interleukin 1β (IL1β) emerged as a correlate of adiposity and cognitive impairment across both the treadmill and lipectomy studies, so we manipulated hippocampal IL1 signaling using intrahippocampal delivery of IL1 receptor antagonist (IL1ra). Intrahippocampal IL1ra prevented synaptic dysfunction, proinflammatory priming, and cognitive impairment. This pattern supports a central role for IL1-mediated neuroinflammation as a mechanism for cognitive deficits in obesity and diabetes.