Researchers determined that MRI imaging may predict which persons with cognitive impairment will progress to Alzheimer’s disease in a report published in the April 6 online Radiology. Baseline MRI was obtained for 164 individuals with late-onset Alzheimer’s disease, 317 with mild cognitive impairment, and 203 healthy controls. The investigators then used MRI to measure the thickness and amount of atrophy in the cerebral cortex. “Individualized risk estimates from baseline MRI examinations indicated that the one-year risk of conversion to Alzheimer’s disease ranged from 3% to 40%,” the researchers reported. “Relative to the risk of conversion to Alzheimer’s disease conferred by the clinical diagnosis of mild cognitive impairment alone, MRI measures yield substantially more informative patient-specific risk estimates. Such predictive prognostic information will be critical if disease-modifying therapies become available.”
Cotinine, a compound derived from tobacco, reduced brain plaques associated with dementia and memory loss, according to a study published in the online February 14 Journal of Alzheimer’s Disease. A group of investigators studied the effects of cotinine on b-amyloid plaque aggregation in the brains of mice with Alzheimer’s disease. Mice treated with the compound performed better than untreated mice on tasks measuring working memory and thinking skills; long-term treatment also appeared to prevent spatial memory impairment. Overall, the treated mice showed a 26% reduction in amyloid plaque deposits. “Cotinine, the main metabolite of nicotine, has a long half-life and does not have cardiovascular or addictive side effects in humans,” the authors wrote. “The good safety profile in humans and its beneficial effects suggest that cotinine may be an excellent therapeutic candidate for the treatment of Alzheimer’s disease.”
A study published in the April 13 online Neurology provides evidence that treating certain vascular risk factors helps lower the risk for conversion from mild cognitive impairment to Alzheimer’s disease. Investigators assessed memory and thinking skills of 837 patients with mild cognitive impairment and then reassessed them five years later; 414 participants had at least one vascular risk factor at baseline. “At the end of follow-up 298 subjects converted to Alzheimer’s disease dementia, while 352 remained with mild cognitive impairment,” the investigators reported. “Treatment of individual vascular risk factors including hypertension, diabetes, and hypercholesterolemia was associated with the reduced risk of Alzheimer’s disease conversion.” The findings of the study are observational, the authors concluded, but they suggest that active intervention and treatment of certain risk factors might reduce progression to Alzheimer’s disease.
Researchers have identified mutations of the synapsin 1 gene as a possible common genetic cause for both epilepsy and autism. Their study, published online in the April 12 Human Molecular Genetics, involved members of a large French-Canadian family who had autism spectrum disorders or epilepsy. The severe Q555X mutation appeared in all family members with epilepsy, and in all those who had an autism spectrum disorder. In addition, other mutations in synapsin 1 (A51G, A550T, and T567A) were found in 1% and 3.5% of a separate cohort of French-Canadian individuals with autism and epilepsy, respectively. “These results demonstrate that [synapsin 1] is a novel predisposing gene to [autism spectrum disorders], in addition to epilepsy,” the authors concluded. “[The results also] strengthen the hypothesis that a disturbance of synaptic homeostasis underlies the pathogenesis of both diseases.”
Men who reported chronic ecstasy (MDMA) use were more likely to develop structural brain damage than those who did not use ecstasy, according to a study that was published in the March 28 online Journal of Neurology, Neurosurgery and Psychiatry. Using MRI, researchers measured the hippocampal volume of 10 male ecstasy users (average age, 21.3), compared with seven age- and gender-matched subjects who did not use ecstasy. The hippocampal volume of ecstasy users was 10.5% smaller than those of nonusing peers; the overall proportion of gray matter was 4.6% smaller, suggesting that the drug’s effects are not limited to the hippocampus. “These data provide preliminary evidence that ecstasy users may be prone to incurring hippocampal damage,” the authors wrote, adding: “Hippocampal atrophy is a hallmark for disease of progressive cognitive impairment in older patients, such as Alzheimer’s disease.”
In a study published in the March 28 online Journal of Neurology, Neurosurgery and Psychiatry, researchers reported that epileptic seizures carry a subsequent risk for brain tumor. “Our study suggests that tumor as an underlying cause for epilepsy may not become apparent for several years after onset, and indicates a need for ongoing vigilance,” the authors stated. In the retrospective cohort study, the investigators examined data regarding individuals with first-time epilepsy admissions and determined that, compared with patients admitted for other common and minor disorders, patients with epilepsy were almost 20 times more likely to develop cerebral tumor. The risk for developing malignant tumors was more than twice the risk for developing benign tumors. “The risk was highest for those aged 15 to 44 years at initial admission for epilepsy,” the authors reported. “The risk of cerebral tumor was still raised several years after initial admission for epilepsy.”