But didn't your competent? doctor immediately prescribe statins to help in your recovery?
Or don't you have a functioning stroke doctor who incompetently missed this research from 2011?
1. Statins.
tested in rats from 2003
http://Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke
Simvastatin Attenuates Stroke-induced Splenic Atrophy and Lung Susceptibility to Spontaneous Bacterial Infection in Mice
Or,
Simvastatin attenuates axonal injury after experimental traumatic brain injury and promotes neurite outgrowth of primary cortical neurons
October 2012
tested in humans, March, 2011
http://www.medwirenews.com/39/91658/Stroke/Acute_statin_therapy_improves_survival_after_ischemic_stroke.html
And now lost even to the Wayback Machine
So I think this below is the actual research;
Association Between Acute Statin Therapy, Survival, and Improved Functional Outcome After Ischemic Stroke April 2011
The latest here:
Statin Initiation and Risk of Incident Alzheimer Disease and Cognitive Decline in Genetically Susceptible Older Adults
Abstract
Background and Objectives
The association of statin initiation with incident Alzheimer disease (AD) dementia and cognitive decline by the APOE
ε4 allele is unknown. Our objective was to examine whether the
association of statin initiation with incident AD dementia and cognitive
decline differs by the APOE ε4 allele.
Methods
This
population-based longitudinal cohort study was conducted in 4 urban
communities in Chicago, IL, United States, consisting of 4,807
participants. Statin initiation is based on the inspection of
medications during home assessments. Clinical diagnosis for incident AD
used the NINCDS-ADRDA criteria, and longitudinal measurements of global
cognition consisted of episodic memory, perceptual speed, and the
Mini-Mental State Examination tests.
Results
The
study participants had a mean age of 72 years, consisting of 63% female
individuals and 61% non-Hispanic Black individuals. During the study
period, 1,470 (31%) participants reported statin initiation. In a
covariate-adjusted competing risk model, statin initiation was
associated with a reduced risk of incident clinical AD [hazard ratio
(HR) 0.81 (95% CI 0.70–0.94)] compared with nonusers. This association
was statistically significantly lower (p interaction = 0.015) among participants with the APOE ε4 allele [HR 0.60 (95% CI 0.49–0.74)] compared with those without the APOE
ε4 allele [HR 0.96 (95% CI 0.82–1.12)]. The annual decline in global
cognition (β = 0.021, 95% CI 0.007–0.034) and episodic memory (β =
0.020, 95% CI 0.007–0.033) was also substantially slower among
participants with the APOE ε4 allele after statin initiation
compared with nonusers. However, the association of statin initiation
with cognitive decline was not significant among those without the APOE ε4 allele.
Discussion
Our findings suggest that statins might be associated with a lower risk of incident AD among individuals with the APOE
ε4 allele. The benefits of statin therapy need further consideration in
randomized clinical trials, especially among those with the APOE ε4 allele.
Classification of Evidence
This
study provides Class II evidence that among those aged 65 years or
older, statin initiation was associated with a reduced risk of Alzheimer
disease, especially in the presence of an APOE-e4 allele.
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