Diffusion-weighted imaging (DWI) had a higher predictive value than fluid-attenuated inversion recovery (FLAIR) MRI for detecting patients within the recommended time window for thrombolysis, according to a study that was published in the November issue of Lancet Neurology. Researchers analyzed the clinical and MRI data from patients with acute stroke who had undergone DWI and FLAIR imaging within 12 hours of symptom onset, and they determined that patients with an acute ischemic lesion detected with DWI but not with FLAIR imaging are likely to be within a time window for which thrombolysis is safe and effective. “DWI-FLAIR mismatch identified patients within four to five hours of symptom onset with 62% sensitivity, 78% specificity, 83% positive predictive value, and 54% negative predictive value,” the investigators stated. “These findings lend support to the use of DWI-FLAIR mismatch for selection of patients in a future randomized trial of thrombolysis in patients with unknown time of symptom onset.”
Older adults who were taking statins before sustaining moderate or severe head injury had improved survival and functional outcomes, according to the results of a study that was published in the October issue of the Journal of Trauma. “Of 523 eligible individuals, 117 (22%) used statins at the time of injury,” the investigators wrote. “Statin use was associated with a 76% lower adjusted risk of in-hospital death.” Patients who took the cholesterol-lowering drugs were also 13% more likely to have a good recovery at 12 months postinjury, compared with patients who did not use statins. However, individuals with cardiovascular comorbidities lose this benefit, the investigators noted. “Statins, as possible protective agents in head trauma, warrant further study,” the study authors concluded.
A neuron’s inability to secrete beta-amyloid (Aß) plays a major role in the pathogenesis of Alzheimer’s disease, a finding that contradicts the dominant theory in Alzheimer’s disease pathology, according to a study in the October 26 Journal of Neuroscience. By studying neurons in Alzheimer’s disease–transgenic and wild-type mice, the investigators found that an increase in intracellular Aß occurred early in the beginning stages of the disease, and that this accumulation of Aß inside the neuron was caused by the neuron’s inability to properly secrete Aß. “We demonstrate that synaptic activity promotes an increase in the Aß-degrading protease neprilysin at the cell surface and a concomitant increase in colocalization with Aß42,” the investigators stated. “Remarkably, Alzheimer’s disease–transgenic but not wild-type neurons show reduced levels of neprilysin with time in culture. This impaired ability to secrete Ab and reduce intraneuronal Aß has important implications for the pathogenesis and treatment of Alzheimer’s disease.”
Long-term estrogen deprivation in aging rats is associated with a decrease in estrogen receptors in the brain, and with a loss of the hormone’s neuroprotective effects, according to a study that was published in the August 30 issue of the Proceedings of the National Academy of Sciences. Researchers studied estrogen levels in middle-aged rats that had undergone long periods of estrogen deprivation and observed an enhanced interaction between estrogen receptors and the CHIP enzyme (a carboxyl terminus of Hsc70-interacting protein), which contributed to the decrease of estrogen receptors in the hippocampus. They also found that administration of 17b-estradiol (E2) replacement therapy shortly before, but not after, the drop in hormone levels prevented degradation of estrogen receptors in the brain, and preserved estrogen’s neuroprotective effects. “As a whole, the study provides support for a ‘critical period’ for E2 neuroprotection of the hippocampus and provides important insight into the mechanism underlying the critical period,” the researchers concluded.