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.

Wednesday, January 5, 2022

Genetic evidence supporting a causal role of depression on Alzheimer’s disease

 It is your doctor's responsibility to prevent stroke depression, not just treat it. And the prevention method is EXACT STROKE PROTOCOLS LEADING TO 100% RECOVERY. Your survivor will be too busy exercising and counting to get depressed because the end result will be recovery.

Genetic evidence supporting a causal role of depression on Alzheimer’s disease

Published:December 16, 2021DOI:https://doi.org/10.1016/j.biopsych.2021.11.025

Abstract

Background

Depression is associated with higher risk for Alzheimer’s disease (AD) in several prospective studies; however, mechanisms underlying this association remain unclear.

Methods

We examined genetic correlation between depression and AD using LDSC regression. We then tested for evidence of causality between depression and AD using Mendelian randomization and genome-wide association study (GWAS) results. Subsequently, cis and trans quantitative trait locus (QTL) analyses for the depression-GWAS signals were performed to resolve the genetic signals to specific DNA-methylation sites, brain transcripts, and proteins. These transcripts and proteins were then examined for associations with AD and its endophenotypes. Lastly, associations between depression polygenic risk score (PRS) and AD endophenotypes were examined.

Results

We detected a significant genetic correlation between depression and AD suggesting that they have a shared genetic basis. Furthermore, we found that depression has a causal role in AD through Mendelian randomization but did not find evidence for a causal role of AD on depression. Moreover, we identified 75 brain transcripts and 28 brain proteins regulated by the depression GWAS signals through QTL analyses. Among these, 46 transcripts and 7 proteins were associated with rates of cognitive decline over time, AD pathologies, and AD diagnosis in two separate cohorts, implicating them in AD. Additionally, we found that higher depression PRS was associated with faster decline of episodic memory over time.

Conclusions

Depression appears to have a causal role in AD, and this causal relationship is likely driven, in part, by the 53 brain transcripts and proteins identified in this study.

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