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.

Thursday, August 19, 2021

Diabetes drugs slow cognitive decline in patients with Alzheimer’s disease

 

With your good chance of getting dementia ask your doctor EXACTLY WHAT PREVENTION PROTOCOLS have been setup. No protocols, fire that doctor. 


1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

Diabetes drugs slow cognitive decline in patients with Alzheimer’s disease

Dipeptidyl peptidase-4 inhibitor use in patients with diabetes and Alzheimer’s disease-related cognitive impairment correlated with lower amyloid burden and favorable long-term cognitive outcome, according to a study in Neurology.

“In the present study, we hypothesized that treatment with [dipeptidyl peptidase-4 inhibitors] may confer protective effects against [amyloid beta] retention in patients with [Alzheimer’s disease]-related cognitive impairment (ADCI),” Seong Ho Jeong, MD, from the department of neurology, Yonsei University College of Medicine in Seoul, South Korea, and colleagues wrote. “Therefore, we performed a comparative analysis of standardized uptake value ratios calculated from cerebral cortical areas by using 18F-florbetaben [amyloid beta] PET imaging and longitudinal changes in cognitive parameters in diabetic and non-diabetic patients with ADCI depending on prior treatment with [dipeptidyl peptidase-4 inhibitors].”

Jeong and colleagues retrospectively assessed data on 282 patients with ADCI who had a positive scan of 18F-florbetaben amyloid PET images. Patients were classified into the following three groups based on prior diagnosis of diabetes and dipeptidyl peptidase-4 inhibitor (DPP-4i) use: patients with diabetes treated with DPP-4i (ADCI-DPP-4i+, n=70), patients with diabetes treated without DPP-4i (ADCI-DPP-4i-, n=71) and patients without diabetes (n=141). Investigators conducted multiple linear regression analyses to determine inter-group differences in global and regional amyloid retention using standardized uptake value ratios calculated from cortical areas. Jeong and colleagues used a linear mixed model to evaluate longitudinal changes in Mini-Mental State Examination score.

After adjusting for age, sex, education, cognitive status and APOE e4 carrier status, Jeong and colleagues found the ADCI-DPP-4i+ group had higher global amyloid burden compared with the ADCI-DPP-4i group (beta = 0.075, SE = 0.024, P = .002) and the non-diabetic ADCI group (beta = 0.054, SE = 0.021, P = .010). Lower regional amyloid burden in temporo-parietal areas was noted in the ADCI-DPP-4i+ group compared with the ADCI-DPP-4i group and the non-diabetic ADCI group.

According to Jeong and colleagues, the ADCI-DPP-4i+ group compared with the ADCI-DPP-4i group demonstrated a slower decrease in Mini-Mental State Examination score (beta = 0.772, SE = 0.272, P = .005) and memory recall sub-score (beta = 0.291, SE = 0.116, P = .012).

“As sequential [amyloid beta] accumulation data were not available, the exact mechanism underlying the association between DPP-4i use and slow [Mini-Mental State Examination] score decline cannot be determined in this study,” Jeong and colleagues wrote. “Further randomized clinical trials are needed to clearly uncover the mechanisms of the beneficial effects of DPP-4i with respect to the progression of AD.”

 

No comments:

Post a Comment