Keeping you up to date on recent headlines in neurology.

Amyloid plaques removed from live animals with AD ... A breakthrough discovery by scientists from the Mayo Clinic (Jacksonville, Florida) may lead to a new treatment for Alzheimer's disease (AD) that actually removes amyloid plaques - considered a hallmark of the disease - from patients' brains. This discovery, published online in The FASEB Journal, is based on the unexpected finding that when the brain's immune cells (microglia) are activated by the interleukin-6 protein (IL-6), they actually remove plaques instead of causing them or making them worse. The research was performed in a model of AD established in mice. "Our study highlights the notion that manipulating the brain's immune response could be translated into clinically tolerated regimens for the treatment of neurodegenerative diseases," said Pritam Das, co-author of the study. Das and colleagues made this unexpected discovery when they initially set out to prove that the activation of microgila trigger inflammation, making the disease worse. Their hypothesis was that microglia would attempt to remove the plaques, but would be unable to do so, and in the process cause excessive inflammation. To the surprise of the researchers, when microglia were activated by IL-6, they cleared the plaques from the brains. This research suggests that manipulating the brain's own immune cells through inflammatory mediators could lead to new therapeutic approaches for the treatment of neurodegenerative diseases, particularly AD.

Report lists neuroscience hot spots ... In a new study published by NeuroInsights and the Neurotechnology Industry Organization (both San Francisco), nine metropolitan regions around the world are leading the way in innovating treatments for the largest unmet medical market, brain-related illness. By developing the necessary infrastructure to discover and develop neurotechnology drugs, medical devices, biologics, cell-based therapeutics, and diagnostics for the brain and nervous system, these regions are helping spur local economies while fighting many of the most vexing medical problems of modern times, such as Alzheimer's disease, depression, obesity, stroke, epilepsy and chronic pain. The San Francisco Bay Area and Greater Boston top the list, followed closely by New York/New Jersey, Greater London, San Diego and Los Angeles/Irvine, according to the new study "Neurotech Clusters 2010: Mapping the Business of Neuroscience," which was released ahead of the Society for Neuroscience (Washington) 39th Annual Meeting in Chicago. According to NeuroInsights and NIO, the top nine neurotech regions with composite scores are: 1. San Francisco Bay Area (100), 2. Greater Boston (98), 3. New York/New Jersey (91), 4. London, UK (84), 5. San Diego (83), 6. Los Angeles/Irvine (81), 7. Baltimore (69), 8. Greater Philadelphia (66), 9. Minneapolis (53).

Other cognitive abilities may decline before onset of AD ... Cognitive abilities other than memory, including visuospatial skills needed to perceive relationships between objects, may decline years prior to a clinical diagnosis in patients with Alzheimer's disease, according to a report in the October issue of Archives of Neurology. "Recent studies have focused on identifying the beginning of the transition from healthy aging to dementia," the authors write as background information in the article. "As new interventions become available, it will become important to identify the disease as early as possible." Loss of episodic memory remembering events in one's life that can be explicitly stated is commonly linked to Alzheimer's disease, but it is not the only aspect of cognition (thinking, learning and memory) that is affected. David Johnson, PhD, of the University of Kansas (Lawrence), assessed 444 individuals who did not have dementia when they were enrolled in the study, between 1979 and 2006. Upon enrolling, each participant underwent a clinical evaluation and a psychometric assessment including tests of four cognitive factors: global cognition, verbal memory, visuospatial skill and working memory. The authors conclude that "In summary, converging longitudinal evidence suggests that after a sharp departure from the relatively flat course of normal aging there is a preclinical period in Alzheimer's disease with insufficient cognitive decline to warrant clinical diagnosis using conventional criteria but that can be seen with longitudinal data from multiple domains of cognition and not just memory."

Urate in blood and spinal fluid may predict slower decline in Parkinson's ... Higher concentration of urate (an antioxidant) in the blood and spinal fluid of patients with early Parkinson's disease (PD) is associated with slower rates of clinical decline, according to a report posted online today that will appear in the December print issue of Archives of Neurology. Urate is an antioxidant that occurs naturally in the blood as an end product of normal metabolism. Antioxidants counteract oxygen-related cell damage, thought to contribute to the neurodegenerative process in PD, according to background information in the article. Therefore, urate and similar substances may provide a defense against the development and progression of PD. Alberto Ascherio, MD, of Harvard School of Public Health and Harvard Medical School (both Boston), and colleagues studied 800 individuals with early PD enrolled in a clinical trial of two medications for the condition. At the beginning of the study, urate levels were measured in the blood of 774 participants. Cerebrospinal fluid also was collected from 713 of them and then after twenty years of freezer storage was analyzed for urate. After two years of follow-up, 48% of patients with blood urate measurements became disabled enough to begin therapy with levodopa a medication used to treat symptoms of PD. The one-fifth of patients with the highest levels of blood urate had a 36% reduced risk of disease progression to this point when compared with the one-fifth who had the lowest levels.

Dysfunctional protein dynamics behind neurological disease ... Researchers at Lund University (Sweden) have taken a snapshot of proteins changing shape, sticking together and creating structures that are believed to trigger deadly processes in the nervous system. The discovery opens the possibility of designing drugs for the neurological disease, amyotrophic lateral sclerosis (ALS). Research indicates that ALS, in common with other neurological disorders, such as Alzheimer's and Parkinson's disease, is caused by our own proteins, which form aberrant aggregates that are fatally toxic to our nerve cells. However, it has not been known what causes these proteins to aggregate. The researchers have now revealed what happens with proteins during the very first, critical step towards forming larger aggregates. It turns out that the protein superoxide dismutase interchanges between its normal structure and a misfolded form. During a brief moment the structure becomes partially misfolded to expose sticky patches that normally are hidden in the interior. These patches cause two or several protein molecules to stick together, thereby forming the cornerstone of the larger structures that are believed to underlie ALS.

— Compiled by Rob Kimball, MDD