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 14, 2015

Treadmill Running Reverses Cognitive Declines due to Alzheimer's Disease

How many times will exercise be found as helpful in preventing/delaying dementia before your doctor sets up a stroke protocol to address this problem?
http://www.ncbi.nlm.nih.gov/pubmed/25574797

Abstract

PURPOSE:

This study investigated the effect of treadmill running on cognitive declines in the early and advanced stages of Alzheimer's disease (AD) in 3xTg-AD mice.

METHODS:

At 4 months of age, 3xTg-AD mice (N=24) were assigned to control (AD+CON, n=12) or exercise (AD+EX, n=12) group. At 24 months of age, 3xTg-AD mice (N=16) were assigned to AD+CON (n=8) or AD+EX (n=8) group. The AD+EX mice were subjected to treadmill running for 12-week. At each pathologic stage, the background strain mice were included as wild type control (WT+CON, n=8-12).

RESULTS:

At the early stage of AD, 3xTg-AD mice had impaired short- and long-term memory based on Morris water maze along with higher cortical Aβ deposition, higher hippocampal and cortical tau pathology, and lower hippocampal and cortical PSD-95 and synaptophysin. A 12-week treadmill running reversed the impaired cognitive declines and significantly improved the tau pathology along with suppression of the decreased PSD-95 and synaptophysin in the hippocampus and cortex. At the advanced stage of AD, 3xTg-AD mice had impaired short- and long-term memory along with higher levels of Aβ deposition, soluble Aβ1-40 and Aβ1-42, tau pathology, and lower levels of BDNF, PSD-95 and synaptophysin in the hippocampus and cortex. A 12-week treadmill running reversed the impaired cognitive declines and significantly improved the Aβ and tau pathology along with suppression of the decreased synaptic proteins and BDNF in the hippocampus and cortex.

CONCLUSION:

The current findings suggest that treadmill running provides a non-pharmacologic means to combat cognitive declines due to AD pathology.

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