Atrophy in the hippocampus may be a biomarker of initial cognitive decline in patients with Parkinson’s disease, according to a study published in the December 2011 Archives of Neurology. Researchers analyzed brain MRIs of 84 patients with Parkinson’s disease and 23 healthy control subjects, finding that patients with Parkinson’s disease and mild cognitive impairment (MCI) showed greater hippocampal atrophy than patients with Parkinson’s disease and normal cognition. Furthermore, patients with Parkinson’s disease and normal cognition did not exhibit significant brain atrophy compared with healthy control patients, and patients with Parkinson’s disease and dementia-level deficits showed both hippocampal and medial temporal lobe atrophy. “Use of a pattern classification approach may allow identification of diffuse regions of cortical gray and white matter atrophy early in the course of cognitive decline,” the authors concluded.
Patients with traumatic brain injury (TBI) who also experience spreading mass neuronal depolarization have worse neurologic outcomes, researchers reported in the December 2011 Lancet Neurology. Investigators conducted a prospective, multicenter study that included 109 adults who required neurosurgery for acute TBI. Of the 109 patients, 58 (56%) experienced a total of 1,328 spreading depolarizations, which were further classified as either cortical spreading depression or isoelectric spreading depolarization. After controlling for conventional prognostic variables, the researchers found that spreading depolarization was linked with an unfavorable neurologic outcome in patients. “The possibility that spreading depolarizations have adverse effects on the traumatically injured brain, and therefore might be a target in the treatment of TBI, deserves further research,” the researchers wrote.
Cognitively normal people with a thinner cortex, as measured by an MRI, are more likely to experience the cognitive decline seen in preclinical Alzheimer’s disease, according to research published in the online December 21, 2011, Neurology. Researchers used MRI to measure cortical thickness in 159 cognitively normal participants, classifying 19 subjects as having a high risk for developing Alzheimer’s disease based on their cortical thickness, 116 as having an average risk, and 24 as having a low risk. A three-year follow-up showed that 21% of the high-risk group experienced cognitive decline, compared with 7% of those with an average risk and 0% of those with a low risk. The biomarker identification practiced in the study may provide future investigators with a cognitively normal population that has a high likelihood of developing early Alzheimer’s disease, the researchers concluded.
Researchers have synthesized a new molecule, J147, that prevents cognitive decline in mice with Alzheimer’s disease and may soon be tested in humans, investigators reported in the December 14, 2011, PLoS One. Most drug research focuses solely on the amyloid beta peptide (Ab) and has not been successful in clinical trials. The investigators tried a different approach, testing new synthetic compounds on living neurons grown in laboratory dishes and examining whether the compounds effectively protected brain cells from pathologies related to aging. The researchers altered the lead compound to maximize effectiveness and eventually created J147, a more potent, neurotrophic molecule that they found prevented cognitive decline in rodents with Alzheimer’s disease and caused the animals to produce more brain-derived neurotrophic factor.
The FDA has approved the Infrascanner Model 1000, a hand-held device that can help detect an intracranial hematoma and allow physicians to determine whether patients with critical head injury need immediate brain imaging such as a CT scan. The device uses near-infrared light to detect differences in the optical density of intracranial hematomas and other parts of the brain, with results transmitted wirelessly to a hand-held monitor display. A review of data from 383 adults who had undergone a CT scan and an Infrascanner showed that the scanner found nearly 75% of the hematomas detected by CT scan and identified no hematoma in 82% of the cases with no hematoma identified by CT scan. The Infrascanner 1000 may help to determine whether further diagnostic procedures are necessary in patients presenting with critical head injuries.
Alzheimer’s disease patterns of atrophy may serve as biomarkers of future cognitive decline in cognitively normal patients with Parkinson’s disease, according to a study published in the online November 21, 2011, Brain. Using MRI, researchers assessed 84 patients with Parkinson’s disease, including those with dementia, mild cognitive impairment (MCI), and no dementia. Patients’ scans were quantified with an Alzheimer’s disease spatial pattern of brain atrophy, and higher Alzheimer’s disease pattern of atrophy scores were associated with worse global cognitive performance across all groups. Furthermore, in 59 patients with Parkinson’s disease and normal cognition at baseline, higher Alzheimer’s disease pattern scores predicted cognitive decline during the two-year follow-up period. “An Alzheimer’s disease pattern of brain atrophy may be a preclinical biomarker of cognitive decline in Parkinson’s disease,” the study authors stated.
A two-week course of continuous theta-burst stimulation may help patients with hemispatial neglect resulting from subacute ischemic stroke recover more quickly, according to a study published in the online December 13, 2011, issue of Neurology. In a randomized, double-blind study, researchers evaluated the safety and efficacy of two weeks of continuous theta-burst stimulation compared with a course of sham treatment. Patients who received real treatment showed a 16.3% increase in Behavioral Inattention Test (BIT) scores after two weeks and a 22.6% score increase at one-month follow-up. Furthermore, real treatment decreased hyperexcitability in left hemisphere parieto–frontal circuits while sham treatment did not. According to the researchers, these findings suggest that continuous theta-burst stimulation “may be a potential effective strategy in accelerating recovery from visospatial neglect in subacute stroke patients.”
Performing a bilateral cardiac sympathetic denervation (BCSD) on patients with incessant ventricular arrhythmias may help to suppress these arrhythmias when other treatments have not been effective, researchers reported in the January 3 issue of the Journal of the American College of Cardiology. The investigators reviewed records from patients who presented with incessant ventricular arrhythmia and were poor candidates for a heart transplant. After these patients had unsuccessfully undergone other treatments, they received surgery to snip the cardiac sympathetic nerves reaching both sides of the heart. Following the surgery, four of the six total patients had no more arrhythmias, one patient had a partial response, and one did not respond at all. The investigators plan further research to assess the role of the procedure in stopping arrhythmias in a larger patient population.
Caloric restriction in mice may activate the CREB1 molecule, which may, in turn, activate genes linked to longevity and brain health, according to research published in the online December 21, 2011, Proceedings of the National Academy of Sciences. The calorie-restricted mice ate only 70% of the food they would normally consume, and investigators found that such a diet turns on CREB1, a molecule that keeps the brain young by activating the sirtuin group of molecules and regulating memory, learning, and anxiety. The study shows that CREB1 is necessary for caloric restriction to work on the brain. Mice without CREB1 do not experience improved memory and other benefits, and they also exhibit brain disabilities similar to those of obese or old animals. Future research may lead to a drug-based way to activate CREB1 and mitigate the effects of the aging process.
Overexpression of Sirt1, a type of sirtuin enzyme, may have a neuroprotective effect in mice with Huntington’s disease, according to two separate studies published in the December 18, 2011, online Nature Medicine. Researchers knocked out Sirt1 expression in the brains of mice with Huntington’s disease, which increased the pathology characterizing the disease. However, mice with overexpressed Sirt1 showed less neurodegeneration, greater lifespan, and more brain-derived neurotrophic factor (BDNF). In addition, experiments demonstrated that Sirt1 directly targets neurons to protect them from the mutant huntingtin protein (HTT), which causes Huntington’s disease. “Mutant HTT interferes with the transcription coactivator 1-CREB interaction to repress BDNF transcription, and Sirt1 rescues this defect in vitro and in vivo,” one team of authors stated. The researchers hope that the Sirt1 findings contribute to the development of new, neuroprotective therapies for Huntington’s disease.