Deans' stroke musings: Abstract 23: BDNF val66met Genotype is Associated With Greater Brain Atrophy After Stroke

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.

Monday, January 29, 2018

Abstract 23: BDNF val66met Genotype is Associated With Greater Brain Atrophy After Stroke

So what is your doctor going to do about this problem? ANYTHING AT ALL?

Abstract 23: BDNF val66met Genotype is Associated With Greater Brain Atrophy After Stroke

Steven C CRAMER, Brent J Liu, Matthew A Edwardson, Jill See, Ximing Wang, Shlomit Radom-Aizik, Babak Shahbaba, Steven L Wolf, Alexander Dromerick, Carolee Winstein

Stroke. 49:A23

Abstract

met and ApoE e4, controlling for the 3 covariates employed in ICARE: motor deficits, enrollment site, and time post-stroke at study entry.

Results:

There were 61 MRI and 66 CT scans. These were acquired 5±11 days post-stroke, which did not vary according to either genotype. Median ventricle volume=26.1 cc; brain volume=1,163 cc; and VBR=0.024. The BDNF val⁶⁶met genotype was present in 23 subjects; ApoE e4, in 41; both were in HW equilibrium. Presence of the BDNF val⁶⁶met genotype was associated with greater atrophy: median VBR increased 1.97-fold when this genotype was present vs. absent (p=0.01), controlling for above covariates; and remained significant (p=0.04) when also controlling for age. This BDNF gene-imaging correlate did not extend to gene-behavioral findings. The ApoE e4 genotype was not related to VBR (p=0.88).

Conclusions:

Median degree of brain atrophy is 97% greater in patients with stroke when the BDNF val⁶⁶met genotype is present, at least for the mild-moderately impaired subjects enrolled in ICARE. Understanding the biology of inter-subject differences in brain anatomy after stroke can provide insights into patient heterogeneity and inform efforts to individualize stroke recovery therapies.