Keeping you up to date on recent headlines in neurology.

Alzheimer's and diabetes study results surprising ... Researchers from France and the UK who set out to investigate whether people with Alzheimer's disease (AD) and diabetes have more rapid memory loss were surprised to find not only that they did not, but that their memory loss was actually slower than that of AD patients without diabetes. Speculating on the reasons, they suggested it could be the effect of diabetes drugs, or that AD patients with diabetes have different kinds of lesions in the brain. The study is published in the October 27 print issue of Neurology. The researchers found that after applying a "mixed model" to take into account "sex, age, educational level, dementia severity, cholinesterase inhibitor use, and vascular factors (hypertension, atrial fibrillation, coronary heart disease, and hypercholesterolemia)", the results showed that: At the start of the study period, both groups (Alzheimer's patients with and without diabetes) had the same average MMSE scores of 20; Over each six-month testing period, the overall group score went down by an average of 1.24 points; However, those without diabetes declined by 0.38 points more per six-month period than those with diabetes. The researchers concluded that "In a cohort of community-dwelling patients with AD, the presence of diabetes mellitus was associated with a lower rate of cognitive decline."

Brain cell transplants help repair neural damage ... A Swiss research team has found that using an animal's own brain cells (autologous transplant) to replace degenerated neurons in select brain areas of donor primates with simulated but asymptomatic Parkinson's disease and previously in a motor cortex lesion model, provides a degree of brain protection and may be useful in repairing brain lesions and restoring function. "We aimed at determining whether autografted cells derived from cortical gray matter, cultured for one month and re-implanted in the caudate nucleus of dopamine depleted primates, effectively survived and migrated," said Jean-Francoise Brunet, MD, who published the study in Cell Transplantation. "The autologous, re-implanted cells survived at an impressively high rate of 50% for four months post-implantation," he said. While the use of neural grafts to restore function after lesions or degeneration of the central nervous system has been widely reported, the objective of this study was to replace depleted neurons to a restricted brain area and to avoid both the ethical controversies accompanying fetal cell transplants as well as immune rejection. Researchers found that the cultured cells migrated, re-implanted into the right caudate nucleus, and migrated through the corpus callosum to the contralateral striatum. Most of the cells were found in the most dopamine depleted region of the caudate nucleus. This study replicated in primates the success the research team had previously reported using laboratory mice.

Possible new cause of MS to be focus of new study ... Neurologists at the University at Buffalo (UB; Buffalo, New York) are beginning a research study that could overturn the prevailing wisdom on the cause of multiple sclerosis (MS). The researchers will test the possibility that the symptoms of MS result from narrowing of the primary veins outside the skull, a condition called "chronic cerebrospinal venous insufficiency," or CCSVI. "If we can prove our hypothesis, that cerebrospinal venous insufficiency is the underlying cause of MS," said Robert Zivadinov, MD, PhD, UB associate professor of neurology, director of the Buffalo Neuroimaging Analysis Center and principal investigator on the study, "it is going to change the face of how we understand MS." The preliminary findings were based on a pilot study which showed that several abnormalities affecting the predominant pathways that return venous blood from the brain to the heart occurred more frequently in MS patients than in controls. The new study will involve 1,600 adults and 100 children. The cohort will be comprised of 1,100 patients who were diagnosed with possible or definite MS, 300 age-and-sex matched normal controls, and 300 patients with other autoimmune and neurodegenerative diseases.

Deep brain stimulation and Tourette syndrome... Deep brain stimulation may be a safe and effective treatment for Tourette syndrome, according to research published in the Oct. 27, 2009, print issue of Neurology. "Our findings hold promise for helping people with severe Tourette syndrome, who are in need of new treatment options to improve their quality of life," said study author Andrea Cavanna, MD, of the University of Birmingham (UK). The participants were followed and tested for two years after deep brain stimulation, which involves a surgically implanted brain pacemaker that sends electrical impulses to certain parts of the brain. The study found that the participants experienced 52% fewer tics on average and a 26% to 33% improvement in the symptoms of OCD, depression and anxiety two years after deep brain stimulation began. Deep brain stimulation had no significant effect on thinking abilities in the study. "The results showed that all 15 people who were assessed after two years' treatment experienced improvements in disabling tics and neurological problems, which is encouraging. Unfortunately three patients from the original group of 18 were no longer part of the study at follow up and this limits the ability to generalize our findings. More research needs to be done to confirm that deep brain stimulation is a safe and effective treatment for Tourette syndrome," said Cavanna.

Epilepsy drugs could treat Alzheimer's and Parkinson's ... Researchers have discovered a potential new function for anti-epileptic drugs in treating neurodegenerative disorders such as Alzheimer's and Parkinson's disease. The study, published in Molecular Neurodegeneration, found that neurons in the brain were protected after treatment with T-type calcium-channel blockers, which are commonly used to treat epilepsy. Calcium signaling pathways play a vital role in the survival of neurons in the brain. As age increases, calcium homeostasis can be disrupted in the brain, which may lead to cognitive and functional decline. It therefore raises the possibility that chemicals able to modulate calcium homeostasis could protect neurons. Scientists from Washington University (St. Louis) explored the possible protective effects of blockers for T-type calcium channels. The mechanisms for neuroprotection by these antiepileptic drugs were previously unknown. The team established cell culture models to directly test whether these drugs could preserve neurons in long- and short-term cultures in vitro. They found that neurons showed an increase in viability after treatment with either L-type or T-type calcium channel inhibitors. Furthermore, neurons in the long-term and short-term cultures were protected, respectively, by L-type and T-type calcium channel blockers, suggesting that more than one calcium-signaling mechanism exists to regulate long- and short-term neuron survival.

— compiled by Rob Kimball, MDD