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 21, 2015

Sitagliptin, a DPP-4 inhibitor, improves recognition memory, oxidative stress, hippocampal neurogenesis and up-regulates key genes involved in cognitive decline

This is only in mice so don't expect any use to come from this for 50 years.
http://www.ncbi.nlm.nih.gov/pubmed/25580570
Gault VA1, Lennox R, Flatt PR.

Author information

Abstract

AIM:

Increasing evidence suggests an important link between diabetes and cognitive decline with insulin resistance and oxidative stress as possible common factors. In this study, we examined whether prolonged DPP-4 inhibition could reverse learning and memory impairment in high-fat fed mice.

METHODS:

High-fat fed mice received sitagliptin (50 mg/kg bw) orally (po) once-daily or saline vehicle over 21 days. An additional group of mice on standard chow received saline vehicle. Energy intake, body weight, glucose and insulin concentrations were measured at regular intervals. Glucose tolerance, insulin sensitivity, novel object recognition, DPP-4 activity, hormone analysis, hippocampal gene expression and histology were performed.

RESULTS:

Sitagliptin decreased circulating DPP-4 activity and improved glucose tolerance, glucose-stimulated insulin secretion, insulin sensitivity and reduced plasma triglycerides and cholesterol levels. DPP-4 inhibition improved recognition memory (1.2-fold increase) without affecting hypermoteric activity or anxiety levels. Improvement in memory and learning was linked to reduced immunostaining for 8-oxoguanine and increased doublecortin (DCX) staining in the hippocampus indicative of reduced brain oxidative stress and increased hippocampal neurogenesis, respectively. These effects were associated with significant up-regulation of hippocampal gene expression of GLP-1R, GIPR, Synaptophysin, SIRT1, GSK-3β, SOD2, Nrf2, and VEGF. Total plasma and brain GLP-1 concentrations were significantly increased following sitagliptin therapy whereas DPP-4 activity in brain tissue was not altered.

CONCLUSION:

These studies demonstrate that sitagliptin can reverse memory impairment in high-fat fed mice in association with improved insulin sensitivity, enhanced hippocampal neurogenesis and reduced oxidative stress. Therefore, DPP-4 inhibitors may exhibit dual benefits by improving metabolic control and declining cognitive function.
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