Pozytonowa tomografia emisyjna białka translokatorowego jako wskaźnik epilepsji pourazowej i zaburzeń zachowania po urazie mózgu
Translocator protein positron emission tomography as a biomarker for posttraumatic epilepsy and behavioral comorbidities following traumatic brain injury
W skrócie
Badanie pokazuje, że specjalny rodzaj skanowania mózgu (PET) może przewidzieć, czy pacjent po urazie głowy rozwinie epilepsję i zaburzenia pamięci. Naukowcy obserwowali szczury z urazami mózgu i odkryli, że zmierzone w mózgu działanie pewnego białka pozwala na wcześniejsze rozpoznanie, które zwierzęta będą miały problemy z pamięcią i który rozwinie epilepsję. Ta metoda może w przyszłości pomóc lekarzom w lepszym prognozowaniu powikłań po poważnych urazach głowy.
Oryginalny abstract (angielski)
OBJECTIVE: Traumatic brain injury (TBI) induces widespread and persistent neuroinflammation, which is increasingly recognized as a key contributor to chronic sequelae including posttraumatic epilepsy (PTE), cognitive deficits, and neuropsychiatric disturbances. However, reliable biomarkers for identifying individuals at risk for these long-term outcomes remain limited. In this study, we evaluated in vivo positron emission tomography (PET) imaging of the 18-kDa translocator protein (TSPO) as a predictive biomarker of epileptogenesis and neurobehavioral dysfunction in a rat model of moderate-severe TBI. METHODS: Adult rats received lateral fluid percussion injury (n = 61) or sham surgery (n = 14). TSPO PET was performed using [F]-PBR06 at 1 and 4 weeks postinjury. Long-term behavioral outcomes were assessed at 5-6 months post-TBI, followed by continuous 4-week video-electroencephalographic monitoring during 7 month to identify epileptic rats. RESULTS: TBI rats demonstrated robust and sustained increases in TSPO binding across multiple brain regions at both time points compared with sham animals (p < .001). At 4 weeks postinjury, however, TSPO binding in the cortex, hippocampus, and thalamus was significantly lower in rats that later developed epilepsy (PTE) than in those that did not (PTE; p < .05), with receiver operating characteristic (ROC) analysis showing good predictive performance (area under the curve [AUC] = .76, p < .01). Behavioral testing identified deficits in spatial learning, memory, and open-field activity in TBI rats (p < .05). Data-driven stratification identified behaviorally impaired (TBI-BI) and unimpaired (TBI-BI) subgroups, with cortical TSPO moderately distinguishing impaired animals (AUC ≈ .7). Among impaired rats, those with multidomain behavioral deficits (n = 33) showed elevated thalamic TSPO compared to those with a single impairment (p = .032), with ROC analysis confirming discrimination (AUC = .72, p = .018). SIGNIFICANCE: Our findings support TSPO PET imaging as a promising early biomarker for predicting PTE and neurobehavioral outcomes following TBI.