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.

Sunday, June 25, 2017

Multivariate Analyses of Peripheral Blood Leukocyte Transcripts Distinguish Alzheimer’s, Parkinson’s, Control and Those at Risk for Developing Alzheimer’s

You'll want your doctor to follow this up with for your risk of getting dementia/Alzheimers
http://www.neurobiologyofaging.org/article/S0197-4580(17)30167-7/fulltext



Highlights

  • Peripheral blood leukocyte transcripts can be used as a prognostic marker of progression to the clinical stages of Alzheimer’s disease in unimpaired older adults.
  • Peripheral blood leukocyte transcripts distinguish Parkinson’s disease from Alzheimer’s disease.
  • Peripheral blood leukocyte transcripts distinguish cognitively resilient apoe4 homozygotes.
  • The same peripheral blood leukocyte transcripts used to distinguish probable Alzheimer’s disease in blood samples were also able to distinguish neuropathologically confirmed Alzheimer’s disease in brain samples.

Abstract

The need for a reliable, simple and inexpensive blood test for Alzheimer’s disease (AD) suitable for use in a primary care setting is widely recognized. This has led to a large number of publications describing blood tests for AD, which have, for the most part, not been replicable. We have chosen to examine transcripts expressed by the cellular, leukocyte compartment of blood. We have used hypothesis based cDNA arrays and quantitative PCR to quantify expression of selected sets of genes followed by multivariate analyses in multiple independent samples. Rather than one study with no replicates we chose an experimental design in which there were multiple replicates using different platforms and different sample populations. We have divided 177 blood and 27 brain samples into multiple replicates to demonstrate the ability to distinguish early clinical AD (CDR 0.5), Parkinson’s disease (PD), and cognitively unimpaired APOE4 homozygotes, as well as to determine persons at risk for future cognitive impairment with significant accuracy. We assess our methods in a training/test set and also show that the variables we use distinguish AD, PD and control brain. Importantly, we describe variability of the weights assigned to individual transcripts in multivariate analyses in repeated studies and suggest that the variability we describe may be the cause of inability to repeat many prior studies. Our data constitute a proof of principle that multivariate analysis of the transcriptome related to cell stress and inflammation of peripheral blood leukocytes has significant potential as a minimally invasive and inexpensive diagnostic tool for diagnosis and early detection of risk for AD.

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