Deans' stroke musings: The influence of obesity on structure, biochemistry and function of brain regions involved in cognition

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, February 23, 2013

The influence of obesity on structure, biochemistry and function of brain regions involved in cognition

Are your cognition problems due to this latest obesity one rather than your stroke. Your doctor had better know the answer.
http://scholar.google.com/scholar_url?hl=en&q=http://dataspace.princeton.edu/jspui/bitstream/88435/dsp015t34sj614/1/Bocarsly_princeton_0181D_10489.pdf&sa=X&scisig=AAGBfm3_VU255HF84XRDv0wJv03uUxfBxA&oi=scholaralrt
Short Abstract
Obesity is a major public health problem, affecting more than one-third of the U.S. population. Several studies suggest deficits in cognition in obese people and several neuroimaging studies indicate reduced volume of certain brain regions, including the hippocampus and prefrontal cortex. These brain regions are important for cognition and anxiety regulation, and thus structural change in them may contribute to alterations in cognition and mood reported in overweight people. No studies have investigated the effects of weight gain on brain structure and function at a level of analysis that would permit identification of cellular mechanisms, which could lead to
future treatment options. This dissertation uses a rat model of diet-induced obesity (DIO) to explore behavioral, structural and biochemical changes in three brain regions important in cognition: the medial prefrontal cortex (mPFC), perirhinal cortex (PRC), and hippocampus (HIP).
Obese rats performed poorly on cognitive tasks specific to the mPFC and PRC, but not the HIP, compared to normal weight controls. In order to begin to characterize the behavioral differences observed, the influence of obesity on brain volume, dendritic architecture and spine density, as well as on associated pre- and post-synaptic markers in the mPFC, PRC and HIP were determined. Deficits in mPFC and PRC-related tasks were accompanied by decreased dendritic spine density and decreased pre- and postsynaptic markers in the mPFC and PRC. Finally, to identify potential mechanisms that might be driving these results, hormones that have previously been linked to changes in brain structure, and/or metabolism and obesity, were surveyed. While there was no difference in testosterone, glucose or insulin levels between groups, leptin was increased in the DIO model, providing a potential mechanism leading to changes in neurological structure and function. Further, obese rats had decreased peripheral corticosterone levels, a condition previously linked to decreased dendritic architecture, suggesting another potential involved mechanism. The DIO animal model of obesity has allowed us to look into the cellular changes that underlie alterations in brain structure and function, and provided us with foundational research needed to identify mechanisms for future intervention.