Deans' stroke musings: Brain-derived neurotrophic factor protects against neurodegeneration in a mouse model of human tauopathy

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.

Tuesday, December 6, 2016

Brain-derived neurotrophic factor protects against neurodegeneration in a mouse model of human tauopathy

What is your doctor doing to make sure your BDNF is high enough to prevent neurodegeneration? Or is s/he waiting for decades for human research to be done? Thus dooming you to dementia/Alzheimers. If you won't go down without a fight you will need to start screaming at your doctors for help in solving this problem. Now, not 50 years from now.
https://espace.library.uq.edu.au/view/UQ:413018
Jiao, S.-S., Shen, L.-L., Zhu, C., Bu, X.-L., Liu, Y.-H., Liu, C.-H., Yao, X.-Q., Zhang, L.-L., Zhou, H.-D., Walker, D. G., Tan, J., Götz, J., Zhou, X.-F. and Wang, Y.-J. (2016) Brain-derived neurotrophic factor protects against neurodegeneration in a mouse model of human tauopathy. Translational Psychiatry, 6 10: . doi:10.1038/tp.2016.186
Abstract Collection year 2017 Language

Author	Jiao, S.-S. Shen, L.-L. Zhu, C. Bu, X.-L. Liu, Y.-H. Liu, C.-H. Yao, X.-Q. Zhang, L.-L. Zhou, H.-D. Walker, D. G. Tan, J. Götz, J. Zhou, X.-F. Wang, Y.-J.
Title	Brain-derived neurotrophic factor protects against neurodegeneration in a mouse model of human tauopathy
Journal name	Translational Psychiatry Check publisher's open access policy
ISSN	2158-3188
Publication date	2016-10-04
Sub-type	Article (original research)
DOI	10.1038/tp.2016.186
Open Access Status	DOI
Volume	6
Issue	10
Total pages	11
Place of publication	London, United Kingdom
Publisher	Nature Publishing Group
eng
Reduced expression of brain-derived neurotrophic factor (BDNF) has a crucial role in the pathogenesis of Alzheimer’s disease (AD), which is characterized with the formation of neuritic plaques consisting of amyloid-beta (Aβ) and neurofibrillary tangles composed of hyperphosphorylated tau protein. A growing body of evidence indicates a potential protective effect of BDNF against Aβ-induced neurotoxicity in AD mouse models. However, the direct therapeutic effect of BDNF supplement on tauopathy in AD remains to be established. Here, we found that the BDNF level was reduced in the serum and brain of AD patients and P301L transgenic mice (a mouse model of tauopathy). Intralateral ventricle injection of adeno-associated virus carrying the gene encoding human BDNF (AAV-BDNF) achieved stable expression of BDNF gene and restored the BDNF level in the brains of P301L mice. Restoration of the BDNF level attenuated behavioral deficits, prevented neuron loss, alleviated synaptic degeneration and reduced neuronal abnormality, but did not affect tau hyperphosphorylation level in the brains of P301L mice. Long-term expression of AAV-BDNF in the brain was well tolerated by the mice. These findings suggest that the gene delivery of BDNF is a promising treatment for tau-related neurodegeneration for AD and other neurodegenerative disorders with tauopathy.