ArticleChronic stress (Thousand Oaks, Calif.)
Post-Stroke PTSD: The Protective Role of CCR5-Δ32 Polymorphism.
Article in Chronic stress (Thousand Oaks, Calif.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Up to 25% of stroke survivors develop post-traumatic stress disorder (PTSD) symptoms, yet the predisposing factors remain largely unknown. The C-C-Chemokine receptor-5 gene (CCR5) loss-of-function mutation (LOFM, CCR5-Δ32) has been identified as a protective factor against post-stroke depression. This study investigates whether CCR5-Δ32 also confers protection against post-stroke PTSD, in conjunction with two additional polymorphisms: the 5-HTTLPR in the serotonin transporter gene and the BDNF Val66Met variant. Methods: We conducted a prospective analysis of 432 survivors of first-ever mild-to-moderate ischemic stroke, assessing PTSD symptomatology at 6, 12, and 24 months post-stroke. Genetic screening for CCR5-Δ32 status and PTSD symptom data were available for these participants. Results: PTSD was diagnosed in 48 participants (11%) within the first year post-stroke. CCR5-Δ32 carriers exhibited significantly fewer PTSD symptoms at 6, 12, and 24 months compared to non-carriers ( Conclusions: Our findings suggest that CCR5-Δ32 carriers are less likely to develop PTSD symptoms following stroke, including individuals with pre-existing maladaptive coping styles. These results highlight a potential genetic target for future intervention strategies, with CCR5 blockade emerging as a promising therapeutic avenue for post-stroke PTSD prevention.
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