Genetic Factors, Brain Atrophy, and Response to Rehabilitation Therapy After Stroke.
Steven C Cramer, Jill See, Brent Liu and 8 others
PMID 34933635WHAT IT FOUND
BDNF val 66 met and ApoE ε4 did not predict 12-month arm motor recovery after stroke.
BDNF val 66 met was linked to greater brain atrophy, but not to that recovery outcome.
Key findings
01Neither BDNF val 66 met nor ApoE ε4 carrier status was associated with the primary 12-month change in arm motor function.
02BDNF val 66 met carriers had greater cerebral atrophy, reported as a 1.34-greater ventricle-brain ratio, driven by larger ventricles.
03ApoE ε4 carriers were 4.6 years younger at stroke onset.
STILL TO COME
How it was doneWhat they foundWhat it means for OTs
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What it does not show
Only 216 of the 361 ICARE patients joined the genetics substudy, and complete genotype data were available for 206, so the genetic analysis did not include the full trial sample. The genetics substudy group had slightly milder strokes and earlier randomization than the group not studied genetically. Neuroimaging was available in 127 of the genetics substudy participants, and scans were a mix of CT and MRI acquired 5±11 days post-stroke. Ventricle-brain ratio is a global measure and did not provide regional brain atrophy measures. Because the three ICARE treatment groups did not differ in the primary endpoint, the 12-month change may reflect spontaneous recovery as well as response to therapy. Entry criteria required stroke 14 to 106 days earlier and a specific level of upper limb weakness, so results may not apply to all stroke patients.
Declared interests
The paper lists NIH extramural research support. Dr Cramer reports consulting relationships with commercial companies named in the declaration.
The easy way to misread this
Do not read the BDNF brain atrophy finding as evidence that BDNF val 66 met predicts poor response in the trial's upper limb rehabilitation groups. The primary 12-month arm motor outcome showed no association with either BDNF val 66 met or ApoE ε4.