Deans' stroke musings: Retinoic acid induces neurogenesis by activating both retinoic acid receptors (RAR) and peroxisome proliferator-activated receptor β/δ (PPARβ/δ)

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, October 29, 2012

Retinoic acid induces neurogenesis by activating both retinoic acid receptors (RAR) and peroxisome proliferator-activated receptor β/δ (PPARβ/δ)

You have to ask your doctor how this can be translated into a therapy protocol.
http://www.jbc.org/content/early/2012/10/26/jbc.M112.410381.short

Abstract

Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARβ/δ and their respective cognate lipid binding proteins CRABP-II and FABP5. RA induces neuronal differentiation but the contributions of the two transcriptional pathways of the hormone to the process are unknown. Here we show that RA-induced commitment of P19 stem cells to neuronal progenitors is mediated by the CRABP-II/RAR path and that the FABP5/PPARβ/δ path can inhibit the process through induction of the RAR repressors SIRT1 and Ajuba. In contrast with its inhibitory activity in early steps of neurogenesis, the FABP5/PPARβ/δ path promotes differentiation of neuronal progenitors to mature neurons, an activity mediated in part by the PPARβ/δ target gene PDK1. Hence, RA-induced neuronal differentiation is mediated through RAR in early stages and through PPARβ/δ in late stages of the process. The switch in RA signaling is accomplished by a transient upregulation of RARβ concomitantly with a transient increase in the CRABP-II/FABP5 ratio at early stages of differentiation. In accordance with these conclusions, hippocampi of FABP5-null mice display excess accumulation of neuronal progenitor cells and a deficit in mature neurons vs. wild-type animals.