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.

Thursday, June 4, 2015

‘O’ blood type is associated with larger grey-matter volumes in the cerebellum

I'm sure there is no one in the world that I can ask whether my blood type of O negative is enough to offset my 33% dementia chance post-stroke from an Australian study.
This is what is so bad with stroke knowledge today, there is no one in the world any survivor can ask ANY SIMPLE QUESTION and expect any answer other than the f*ckingly stupid response of
'All strokes are different, all stroke recoveries are different' .
http://www.sciencedirect.com/science/article/pii/S0361923015000805

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Highlights

‘O’ blood type adults have increased volumes in the posterior cerebellum.
‘O’ blood type might be protective against dementia.
Biological explanations include possible fostering of endothelial dysfunction.

Abstract

Recent evidence indicated higher incidence of cognitive deficits in ABO blood-type system ‘AB’ individuals. Since this statistical difference might originate from the lack of protective effects exerted by ‘O’ alleles on the brain via vascular or non-vascular routes, this study investigated volumetric differences in grey matter between ‘O’ and non-‘O’ adults to explore the possibility of a structural endophenotype visible in ‘O’ adults without cognitive impairment or neurodegeneration.
A large sample of cognitively healthy adults who had previously undergone structural MRI for research purposes were contacted telephonically and enquired about their ABO blood type. Out of the 189 individuals who were able to retrieve and communicate this information, ‘O’ (n = 76) and ‘A’ adults (n = 65) were included in Model 1. In Model 2, all non-‘O’ (n = 113) were instead collapsed in a single group. Voxel-Based Morphometry analyses were carried out on three-dimensional T1-weighted scans, and between-sample t tests were run to compare the maps of grey-matter volumes of the subgroups of interest, controlling for major nuisance variables.
In Model 1, ‘O’ adults had larger grey-matter volumes in two symmetrical clusters within the posterior ventral portion of the cerebellum. This was confirmed in Model 2. Additionally, non-‘O’ adults showed lower volume values in temporal and limbic regions, including the left hippocampus.
The cerebellar clusters were located in regions previously found to be part of a network responsible for sensorimotor integration. It is speculated that the structural reductions seen in non-‘O’ adults might result in a susceptibility to down-regulation of this network. This occurrence is likely to intensify along the ageing process and may contribute to foster cognitive decline. Although Model 2 seems to suggest that having a ‘O’ blood type might play a role in protection against those conditions in which temporal and mediotemporal volumetric loss is observed (Alzheimer's disease), additional supporting evidence is needed.
A number of potential biological processes might sustain these between-group differences, including sensorimotor ontogenesis, hormonal function, and a regional impact of cerebral amyloid angiopathy. These findings identify the cerebellar tissue as a candidate for further studying ABO function, and support a general association between ABO blood type and variance in the development of the nervous system.

Graphical abstract

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