tag:blogger.com,1999:blog-82016552008-07-26T03:39:29.606-07:00BrainBlogAnthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comBlogger674125tag:blogger.com,1999:blog-8201655.post-50230440861680344962008-07-26T03:35:00.001-07:002008-07-26T03:39:29.615-07:00Current Event: International Conference on Alzheimer's Disease (ICAD) 2008, Chicago ILThe Alzheimer's Association ICAD 2008 conference begins today and continues through the 31st of July. The conference takes place in Chicago at McCormick Place.<br /><br />Details available at the conference website: <a href="http://www.alz.org/icad/">ICAD website</a>.Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-52549550444733978522008-07-11T19:19:00.000-07:002008-07-11T19:22:42.508-07:00Neuropsychology Abstract of the Day: Verbal Fluency and MCINutter-Upham KE, Saykin AJ, Rabin LA, Roth RM, Wishart HA, Pare N, Flashman LA. <b>Verbal fluency performance in amnestic MCI and older adults with cognitive complaints.</b> <i>Archives of Clinical Neuropsychology</i>. 2008 May; 23(3): 229-241.<br /><br />Neuropsychology Program, Department of Psychiatry, Dartmouth Medical School/DHMC, Lebanon, NH, USA.<br /><br />Verbal fluency tests are employed regularly during neuropsychological assessments of older adults, and deficits are a common finding in patients with Alzheimer's disease (AD). Little extant research, however, has investigated verbal fluency ability and subtypes in preclinical stages of neurodegenerative disease. We examined verbal fluency performance in 107 older adults with amnestic mild cognitive impairment (MCI, n=37), cognitive complaints (CC, n=37) despite intact neuropsychological functioning, and demographically matched healthy controls (HC, n=33). Participants completed fluency tasks with letter, semantic category, and semantic switching constraints. Both phonemic and semantic fluency were statistically (but not clinically) reduced in amnestic MCI relative to cognitively intact older adults, indicating subtle changes in the quality of the semantic store and retrieval slowing. Investigation of the underlying constructs of verbal fluency yielded two factors: Switching (including switching and shifting tasks) and Production (including letter, category, and action naming tasks), and both factors discriminated MCI from HC albeit to different degrees. Correlational findings further suggested that all fluency tasks involved executive control to some degree, while those with an added executive component (i.e., switching and shifting) were less dependent on semantic knowledge. Overall, our findings highlight the importance of including multiple verbal fluency tests in assessment batteries targeting preclinical dementia populations and suggest that individual fluency tasks may tap specific cognitive processes.Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-56330520231385327472008-07-08T08:08:00.001-07:002008-07-08T08:21:50.260-07:00New Online Dementia Resources from UCSFThe University of California, San Francisco (UCSF) Memory and Aging Center has recently revised their website and has launched a <i>YouTube</i> channel dedicated to educating patients, caregivers, and health professionals about neurodegenerative diseases and the dementias. The Center has also launched a <i>Facebook</i> webpage.<br /><br />The website can be examined at <a href="http://memory.ucsf.edu">UCSF website</a>.<br /><br />The<i> YouTube</i> channel - the first one I've heard of dedicated to these topics - can be found at <i><a href="http://www.youtube.com/ucsfmemoryandaging">YouTube</i> channel link</a>.<br /> <br />As noted by a UCSF contact:<br /><br />"Through the <i>YouTube</i> channel, we also hope to support the caregiver and the caregiver’s loved ones to help them cope with these illnesses.<br /> <br />"The channel features UCSF’s renowned clinical-researchers discussing disease characteristics – which are often subtle and not well known, even among members of the medical community. Personal stories of patients and family members are also featured, together with practical advice and coping strategies from healthcare professionals."<br /> <br />The <b>“Defeat Dementia”</b> <i>Facebook</i> group to help support patients, their families, friends, caregivers and others can be found at: <a href="http://www.facebook.com/group.php?gid=15060128066">link</a>.Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-70683576371334465342008-06-02T14:04:00.000-07:002008-06-02T14:07:36.747-07:00Alzheimer's DiseaseOn the <i>New York Times</i> website:<br /><br /><b>Earlier diagnosis giving Alzheimer's a new voice </b><br />By THE ASSOCIATED PRESS<br />Published: June 2, 2008<br />Filed at 4:26 p.m. ET<br /><br />"WASHINGTON (AP) -- Don Hayen has a handy way of deflecting the instant pity that comes when he reveals his Alzheimer's disease: "But I haven't lost my keys all day," he quickly jokes. Hayen is part of a growing new movement in Alzheimer's: Patients diagnosed early enough to still be articulate and demand better care and better research.<br /><br />They are giving a voice to a disease whose victims until now have remained largely silent, and powerless.<br /><br />It's a shift with big ramifications."<br /><br /><i>[ ... <a href="http://www.nytimes.com/aponline/health/AP-MED-HealthBeat-Alzheimers-Voice.html">Read the full article</a> ... ]</i>Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-48528908676886168292008-05-25T12:55:00.000-07:002008-05-25T14:06:24.116-07:00Three Brainy General-Readership BooksJust finished reading three excellent books with neuro themes, one a work of fiction and the other two are narrative accounts:<br /><br /><b>"Still Alice"</b> by <a href="http://www.lisagenova.com/">Lisa Genova</a> (available in paperback by iUniverse Press), is a very accurate dramatic fictional account of early-onset Alzheimer's disease.<br /><br /><b>"Insomniac"</b> by <a href="http://www.scrippscollege.edu/academics/faculty/gayle-greene.php">Gayle Greene</a> is a great account of the world of insomnia, from the vantage point of individuals living with sleep disorders (including the author) and from the vantage point of the clinical researchers who study the condition and who work on drug development and other facets of diagnosis, understanding, and treatment.<br /><br />Finally, <b>"Can't Remember What I Forgot"</b> by <a href="http://www.suehalpern.net/">Sue Halpern</a>, self described as a "behind-the-scenes foray into the world of cutting-edge memory research." It lives up to that description and does so in a very readable manner.<br /><br /><b>"Insomniac"</b> is published by the University of California Press and <b>"Can't Remember ..."</b> is published by Harmony Books.<br /><br /><br />Today, I am reading <b>"Netherland"</b> by Joseph O'Neill, published by Pantheon,, which was <a href="http://www.nytimes.com/2008/05/18/books/review/Garner-t.html?ex=1369368000&en=6efe703bcd909ba9&ei=5124&partner=permalink&exprod=permalink">released about a week ago to critical acclaim</a>. No neuro themes, but a compellingly good read.Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-21556176425215867312008-05-25T11:53:00.000-07:002008-05-25T12:05:11.969-07:00Analysis of the Neurotechnology Industry<b>The Ultimate Cure</b><br />by David Ewing Duncan <br /><i>CondeNast Portfolio</i><br />May 2008<br /><br />"The neurotech industry is engaged in a $2 trillion race to fix your brain. Many players will fail, but the payoff will be huge for those who succeed."<br /><br />[snip]<br /><br />"Neurotech’s returns are already enormous. In 2006, the industry brought in more than $120 billion—about $101 billion from drugs and the rest from neurodevices ($4.5 billion) and neurodiagnostics ($15 billion)—up 10 percent from the previous year, reports NeuroInsights, a market research and investment advisory firm. But industry analysts insist that this figure hardly begins to suggest the potential. For Alzheimer’s, a disease currently without an effective treatment for about 4.5 million sufferers in the U.S., 40 companies—including behemoths like Eli Lilly, GlaxoSmithKline, and Wyeth, as well as Targacept and a gaggle of similar upstarts—are testing 48 new drugs in human trials in a quest for the Prozac of dementia. The push has brought many small to midsize biotech firms together in partnerships with larger pharmaceutical companies to pursue everything from pain-control compounds derived from chili peppers to an antistroke medicine developed from vampire-bat saliva. There is so much activity in neurotech that last fall it got <a href="http://finance.yahoo.com/q?s=%5ENERV">its own index, NERV, on the Nasdaq, tracking the performance of 30 leading brain companies based in the United States</a>. Analysts estimate that the sector should continue to grow by about 10 percent a year, which would produce a brain-industrial complex worth more than $300 billion in the next 10 years."<br /><br />[snip] <br /><br /><i>[ ... <a href="http://www.portfolio.com/news-markets/national-news/portfolio/2008/05/12/Analysis-of-Neurotech-Industry">Read the full article</a> ... ]</i>Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-25747115275233663152008-05-24T14:19:00.000-07:002008-05-24T14:23:42.269-07:00Military Traumatic Brain Injury and RehabilitationAn interesting feature article in tomorrow's <i>New York Times Sunday Magazine</i>:<br /><br /><b>The Sergeant Lost Within</b><br />By DANIEL BERGNER<br />Published: May 25, 2008<br /><br />"Roadside bombs have caused hundreds of dire brain injuries to soldiers in Iraq. One of them is Shurvon Phillip, and a team of specialists has worked avidly trying to reach him."<br /><br />A good deal of the article deals with the <a href="http://www.ric.org/">Rehabilitation Institute of Chicago (RIC)</a>.<br /><br /><i>[ ... <a href="http://www.nytimes.com/2008/05/25/magazine/25injuries-t.html?ex=1369368000&en=0d6340cfb88e99ea&ei=5124&partner=permalink&exprod=permalink">Read the full article</a> ... ]</i>Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-18937759568963766972008-05-02T18:59:00.000-07:002008-05-02T19:05:32.256-07:00The Game BrainYep - another fine <i>New York Times</i> interview about neuro gymnastics:<br /><br /><b>Boomers, Exercise Your Brains, or Else You’ll...Uh...</b><br />By KATIE HAFNER<br />Published: May 3, 2008<br /><br />"The fear of a decaying brain has inspired a mini-industry of products from dietary supplements to computer games."<br /><br /><i>[ ... <a href="http://www.nytimes.com/2008/05/03/technology/03brain.html?ex=1367467200&en=df8d065d82006797&ei=5124&partner=permalink&exprod=permalink">Read the full article</a> ... ]</i>Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-19172046615748264662008-05-01T19:24:00.000-07:002008-05-02T19:28:58.595-07:00Upcoming Event: American Pain Society, 8-10 May 2008, Tampa FloridaThe annual meeting of the APS takes place next week in Florida. Visit the conference homepage for details: <a href="http://www.ampainsoc.org/meeting/">Link</a>.<br /><br />From the conference homepage:<br /><br /><b>Conference Purpose and Objectives</b><br /><br />"The 27th Annual Scientific Meeting of the American Pain Society will offer current information about the diagnosis, treatment, and management of acute pain, chronic cancer and noncancer pain, and recurrent pain. In-depth workshops are planned and are designed to enhance research or clinical skills pertinent to the management of pain; they will feature content appropriate for professionals at several experience levels.<br /><br />"Each year the APS Scientific Program Committee carefully reviews attendees’ evaluations in order to organize a scientific program which addresses a broad range of topics related to pain research and treatment.<br /><br />"Designed for a diverse group of scientists, pain clinicians, and other professionals, the 27th Annual Scientific Meeting features a prominent faculty presenting basic, translational, and clinical research advancements. <br /><br />Interact with cutting-edge researchers. <br /><br />Translate scientific discoveries into clinical practice. <br /><br />Network with your colleagues. <br /><br />Hear from policy makers about issues that directly affect you. <br /><br />Raise questions, debate the implications, plan follow-up studies, and discuss results. <br /><br />Discuss your own research and clinical observations. <br /><br />Meet with poster presenters to learn about their thinking and future research directions. <br /><br />Visit more than 150 booths that feature products and services specifically designed for multidisciplinary leaders who study and treat pain."Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-70968548931483496792008-04-12T10:43:00.000-07:002008-04-12T10:45:57.150-07:00I ...... MacIn tomorrow's <i>New York Times Sunday Magazine</i>:<br /><br /><b>Total Recall</b><br />By GARY MARCUS<br />Published: April 13, 2008<br /><br />"How much would you pay to have a small memory chip implanted in your brain if that chip would double the capacity of your short-term memory? Or guarantee that you would never again forget a face or a name?"<br /><br /><i>[...</i><a href="http://www.nytimes.com/2008/04/13/magazine/13wwln-essay-t.html?ex=1365652800&en=7200b19ac5d16085&ei=5124&partner=permalink&exprod=permalink">Read the full article</a><i>...]</i>Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-44440814552925402272008-04-11T22:56:00.000-07:002008-04-11T23:00:28.816-07:00Current Event: American Academy of Neurology (AAN) Annual Conference, ChicagoThe AAN conference takes place this week. Look for some interesting reports of dementia pharmaceutical clinical trials.<br /><br />Visit the conference website: [<a href="https://www.aan.com/go/am">Link</a>].Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-27665200826195009462008-04-06T10:45:00.000-07:002008-04-06T10:47:52.244-07:00Neuropsychology Abstract of the Day: Parkinson's Disease and OlfactionKranick SM, & Duda JE. <b>Olfactory dysfunction in Parkinson's disease.</b> <i>Neurosignals.</i> 2008; 16(1): 35-40.<br /><br />Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.<br /><br />Prior to the onset of the cardinal motor features of idiopathic Parkinson's disease (PD), other manifestations of neurodegeneration such as olfactory dysfunction are often apparent. Characterizing these potential biomarkers of preclinical PD is particularly important in identifying individuals who will go on to develop disabling symptoms, and thus be good candidates for new neuroprotective strategies. As shown by the Braak neuropathologic staging of PD, the olfactory system is among the first neuronal populations to display Lewy body pathology. Clinically, loss of smell can be easily tested in the office using several validated techniques and is often helpful to the physician in distinguishing idiopathic PD from other forms of parkinsonism. Recent findings have indicated that a decline in olfaction may be observed in selected at-risk patients, which has significant implications for identifying potential study populations. Ongoing studies of olfactory dysfunction may also reveal potential for use as a medication-independent biomarker of disease progression in addition to use as a biomarker for the diagnosis of PD.<br /><br />Publication Types: Review<br /><br />PMID: 18097158 [PubMed - indexed for MEDLINE]Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-59837448424099415392008-04-05T04:59:00.000-07:002008-04-05T05:01:35.450-07:00Neuropsychology Abstract of the Day: Parkinson's DiseasePagonabarraga J, Kulisevsky J, Llebaria G, García-Sánchez C, Pascual-Sedano B, & Gironell A. <b>Parkinson's disease-cognitive rating scale: A new cognitive scale specific for Parkinson's disease.</b> <i>Movement Disorders.</i> 2008 Mar 31 [Epub ahead of print].<br /><br />Movement Disorders Unit, Neurology Department, Sant Pau Hospital, Autonomous University of Barcelona, and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain.<br /><br />Cognitive defects associated with cortical pathology may be a marker of dementia in Parkinson's disease (PD). There is a need to improve the diagnostic criteria of PD dementia (PDD) and to clarify the cognitive impairment patterns associated with PD. Current neuropsychological batteries designed for PD are focused on fronto-subcortical deficits but are not sensitive for cortical dysfunction. We developed a new scale, the Parkinson's Disease-Cognitive Rating Scale (PD-CRS), that was designed to cover the full spectrum of cognitive defects associated with PD. We prospectively studied 92 PD patients [30 cognitively intact (CogInt), 30 mild cognitive impairment (MCI), 32 PDD] and 61 matched controls who completed the PD-CRS and neuropsychological tests assessing the cognitive domains included in the PD-CRS. Acceptability, construct validity, reliability, and the discriminative properties of the PD-CRS were examined. The PD-CRS included items assessing fronto-subcortical defects and items assessing cortical dysfunction. Construct validity, test-retest and inter-rater reliability of PD-CRS total scores showed an intraclass correlation coefficient >0.70. The PD-CRS showed an excellent test accuracy to diagnose PDD (sensitivity 94%, specificity 94%). The PD-CRS total scores and confrontation naming item scores-assessing "cortical" dysfunction-independently differentiated PDD from non-demented PD. Alternating verbal fluency and delayed verbal memory independently differentiated the MCI group from both controls and CogInt. The PD-CRS appeared to be a reliable and valid PD-specific battery that accurately diagnosed PDD and detected subtle fronto-subcortical deficits. Performance on the PD-CRS showed that PDD is characterized by the addition of cortical dysfunction upon a predominant and progressive fronto-subcortical impairment. (c) 2008 Movement Disorder Society.<br /><br />PMID: 18381647 [PubMed - as supplied by publisher]Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-56517543777438316062008-03-27T14:26:00.000-07:002008-03-27T14:28:46.226-07:00Neuropsychology Abstract of the Day: Frontotemporal DementiaWittenberg D, Possin KL, Rascovsky K, Rankin KP, Miller BL, & Kramer JH. <b>The Early Neuropsychological and Behavioral Characteristics of Frontotemporal Dementia.</b> <i>Neuropsychological Review.</i> 2008 Feb 29 [Epub ahead of print]<br /><br />Memory and Aging Center, University of California—San Francisco Medical Center, San Francisco, CA, USA.<br /><br />Frontotemporal lobar degeneration (FTLD) represent a constellation of disorders that may be overlooked or misdiagnosed, despite being fairly common presenile neurodegenerative diseases. Although the cognitive disorder can be difficult to document, particularly early in the dementia course, neuropsychological evaluation can assist in the diagnosis. Neuropsychologists are in an excellent position to draw from related disciplines like personality theory and social psychology to better assess the types of changes that characterize the prodromal and early phases of the disease. This review summarizes the current state of the field in the diagnosis of FTLD and discusses the emerging role of neuropsychology in elucidating the brain organization of complex processes including empathy, behavioral control and inhibition, reward systems, appetitive behaviors, emotional regulation, and goal-orientation. As this review underscores, frontotemporal dementia remains a powerful model for studying brain-behavior relationships.<br /><br />PMID: 18311522 [PubMed - as supplied by publisher]Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-49113530189879208402008-03-19T19:54:00.000-07:002008-03-19T19:56:35.047-07:00Neuropsychology Abstract of the Day: Mild Cognitive Impairment (MCI)Bondi MW, Jak AJ, Delano-Wood L, Jacobson MW, Delis DC, & Salmon DP. <b>Neuropsychological Contributions to the Early Identification of Alzheimer's Disease.</b> <i>Neuropsychological Review.</i> 2008 Mar 18.<br /><br />A wealth of evidence demonstrates that a prodromal period of Alzheimer's disease (AD) exists for some years prior to the appearance of significant cognitive and functional declines required for the clinical diagnosis. This prodromal period of decline is characterized by a number of different neuropsychological and brain changes, and reliable identification of individuals prior to the development of significant clinical symptoms remains a top priority of research. In this review we provide an overview of those neuropsychological changes. In particular, we examine specific domains of cognition that appear to be negatively affected during the prodromal period of AD, and we review newer analytic strategies designed to examine cognitive asymmetries or discrepancies between higher-order cognitive functions versus fundamental skills. Finally, we provide a critical examination of the clinical concept of Mild Cognitive Impairment and offer suggestions for an increased focus on the impact of cerebrovascular disease (CVD) and CVD risk during the prodromal period of AD.<br /><br />PMID: 18347989 [PubMed - as supplied by publisher]Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-14287352914048665892008-03-18T08:46:00.000-07:002008-03-18T08:51:19.713-07:00Pediatric Brain TumorsFrom today's <i>New York Times</i>:<br /><br /><b>A Daring Treatment, a Little Girl’s Survival</b><br />By DENISE GRADY<br />Published: March 18, 2008<br /><br />Melanie Joy McDaniel is a study subject but also a reminder of how medical research can change lives.<br /><br /><i>[ ... <a href="http://www.nytimes.com/2008/03/18/health/18seco.html?ex=1363579200&en=8baaf61beb69f9c7&ei=5124&partner=permalink&exprod=permalink">Read the full article</a> ... ]</i>Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-26727223977529260252008-02-26T16:17:00.000-08:002008-02-26T16:20:35.897-08:00Neuropsychology Abstract of the Day: Mild Cognitive Impairment (MCI)Karas G, Sluimer J, Goekoop R, van der Flier W, Rombouts S, Vrenken H, Scheltens P, Fox N, & Barkhof F. <b>Amnestic Mild Cognitive Impairment: Structural MR Imaging Findings Predictive of Conversion to Alzheimer Disease.</b> <i>American Journal of Neuroradiology.</i> 2008 Feb 22 [Epub ahead of print].<br /><br />Department of Diagnostic Radiology, Image Analysis Center, Alzheimer Center, and Department of Clinical Neurology, VU University Medical Center, Amsterdam, the Netherlands; Dementia Research Group, Department of Clinical Neurology, Institute of Neurology, London, UK; Department of Physics and Medical Technology, Alzheimer Center, VU University Medical Center and Leiden Institute for Brain and Cognition, Leiden, the Netherlands; Department of Psychology, Leiden University, Leiden, the Netherlands; and Department of Radiology, Leiden University Medical Center, Leiden, the Netherlands.<br /><br />BACKGROUND AND PURPOSE: Mild cognitive impairment (MCI) is considered by many to be a prodromal phase of Alzheimer disease (AD). We used voxel-based morphometry (VBM) to find out whether structural differences on MR imaging could offer insight into the development of clinical AD in patients with amnestic MCI at 3-year follow-up. MATERIALS AND METHODS: Twenty-four amnestic patients with MCI were included. After 3 years, 46% had progressed to AD (n = 11; age, 72.7 +/- 4.8 years; women/men, 8/3). For 13 patients (age, 72.4 +/- 8.6 years; women/men, 10/3), the diagnosis remained MCI. Baseline MR imaging at 1.5T included a coronal heavily T1-weighted 3D gradient-echo sequence. Localized gray matter differences were assessed with VBM. RESULTS: The converters had less gray matter volume in medial (including the hippocampus) and lateral temporal lobe, parietal lobe, and lateral temporal lobe structures. After correction for age, sex, total gray matter volume, and neuropsychological evaluation, left-sided atrophy remained statistically significant. Specifically, converters had more left parietal atrophy (angular gyrus and inferior parietal lobule) and left lateral temporal lobe atrophy (superior and middle temporal gyrus) than stable patients with MCI. CONCLUSION: By studying 2 MCI populations, converters versus nonconverters, we found atrophy beyond the medial temporal lobe to be characteristic of patients with MCI who will progress to dementia. Atrophy of structures such as the left lateral temporal lobe and left parietal cortex may independently predict conversion.<br /><br />PMID: 18296551 [PubMed - as supplied by publisher]Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-39805098373889934622008-02-25T17:19:00.000-08:002008-02-25T17:22:08.783-08:00Neuroscience in the New Yorker: Numbers and ApproximationsFrom this week's <i>New Yorker</i>:<br /><br /><b>Numbers Guy</b><br />Are our brains wired for math?<br />by Jim Holt <br />March 3, 2008<br /><br /><i>[ ... <a href="http://www.newyorker.com/reporting/2008/03/03/080303fa_fact_holt">Read the full article</a> ... ]</i>Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-35115219663374524002008-02-25T06:28:00.000-08:002008-02-25T06:31:35.386-08:00Drug Development: Glutamate and SchizophreniaFrom Sunday's <i>New York Times</i>:<br /><br /><b>Daring to Think Differently About Schizophrenia</b><br />By ALEX BERENSON<br />Published: February 24, 2008<br /><br />"A new drug aimed at treating schizophrenia turns its focus away from dopamine and instead on the effects of glutamate, another powerful neurotransmitter."<br /><br /><i>[ ... <a href="http://www.nytimes.com/2008/02/24/business/24drug.html?ex=1361595600&en=67418fd0e3a5343f&ei=5124&partner=permalink&exprod=permalink">Read the article</a> ... ]</i>Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-1069729669420495542008-02-23T18:11:00.000-08:002008-02-23T18:14:22.808-08:00Neuropsychology Abstract of the Day: Schizophrenia Clinical TrialsHill SK, Sweeney JA, Hamer RM, Keefe RS, Perkins DO, Gu H, McEvoy JP, & Lieberman JA. <b>Efficiency of the CATIE and BACS neuropsychological batteries in assessing cognitive effects of antipsychotic treatments in schizophrenia.</b> <i>Journal of the International Neuropsychological Society.</i> 2008 Mar; 14(2): 209-221.<br /><br />Center for Cognitive Medicine, Department of Psychiatry, University of Illinois at Chicago, Chicago, Illinois.<br /><br />Efficient and reliable assessments of cognitive treatment effects are essential for the comparative evaluation of procognitive effects of pharmacologic therapies. Yet, no studies have addressed the sensitivity and efficiency with which neurocognitive batteries evaluate cognitive abilities before and after treatment. Participants were primarily first episode schizophrenia patients who completed baseline (n = 367) and 12-week (n = 219) assessments with the BACS (Brief Assessment of Cognition in Schizophrenia) and CATIE (Clinical Antipsychotic Trials of Intervention Effectiveness) neuropsychological batteries in a clinical trial comparing olanzapine, quetiapine, and risperidone. Exploratory factor analysis revealed that performance on both batteries was characterized by a single factor of generalized cognitive deficit for both baseline performance and cognitive change after treatment. Both batteries estimated similar levels of change following treatment, although the BACS battery required half the administration time. Because a unitary factor characterized baseline cognitive abilities in early psychosis as well as cognitive change after treatment with atypical antipsychotic medications, short batteries such as the BACS may efficiently provide sufficient assessment of procognitive treatment effects with antipsychotic medications. Assessment of cognitive effects of adjunctive therapies targeting specific cognitive domains or impairments may require more extensive testing of the domains targeted to maximize sensitivity for detecting specific predicted cognitive outcomes. (JINS, 2008, 14, 209-221.)Presented in part at the annual International Neuropsychology Society meeting in Portland, OR, February 2007; and the 2007 International Congress for Schizophrenia Research in Colorado Springs, CO.<br /><br />PMID: 18282319 [PubMed - in process]Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-58738512524749536912008-02-21T14:10:00.000-08:002008-02-21T14:12:40.182-08:00MemoryA press release rom the NIH:<br /><br /><b>Genetic Tags Reveal Secrets of Memories’ Staying Power in Mice</b><br /><br />A better understanding of how memory works is emerging from a newfound ability to link a learning experience in a mouse to consequent changes in the inner workings of its neurons. Researchers, supported in part by the National Institutes of Health's National Institute of Mental Health (NIMH), have developed a way to pinpoint the specific cellular components that sustain a specific memory in genetically-engineered mice.<br /><br />"Remarkably, this research demonstrates a way to untangle precisely which cells and connections are activated by a particular memory," said NIMH Director Thomas Insel, M.D. "We are actually learning the molecular basis of learning and memory."<br /><br />For a memory to last long-term, the neural connections holding it need to be strengthened by incorporating new proteins triggered by the learning. Yet, it's been a mystery how these new proteins — born deep inside a neuron — end up becoming part of the specific connections in far-off neuronal extensions that encode that memory. <br /><br />By tracing the destinations of such migrating proteins, the researchers located the neural connections, called synapses, holding a specific fear memory. In the process, they discovered these synapses are distinguished by telltale molecular tags that enable them to capture the memory-sustaining proteins.<br /><br />Mark Mayford, Ph.D., and Naoki Matsuo, Ph.D., of the Scripps Research Institute, report on their findings in the February 22, 2008 issue of the journal <i>Science</i>.<br /><br />The Scripps researchers have been applying their new technique in a series of studies that focus on progressively finer details of the molecular machinery of memory.<br /><br />"Inside neurons involved in a specific memory, we're tracing molecules activated by that learning to see how it ultimately changes neural connections," explained Mayford.<br /><br />In a study published in the August 31, 2007 <i>Science</i>, Mayford and colleagues showed the same neurons activated by a learning experience are also activated when that memory is retrieved. The more neurons involved in the learning, the stronger the memory.<br /><br />The researchers determined this by genetically engineering a strain of mice with traceable neurons in the brain's fear center, called the amygdala. Inserted genes caused activated neurons to glow red when the animals learned to fear situations where they received shocks, in a process known as fear conditioning — and to glow green when the memory was later retrieved. The researchers then chemically prevented further expression of those neurons, so that resulting neural and behavioral changes could be confidently attributed to that learning experience at a later time. The study revealed which circuits and neurons were involved in the specific learning experience.<br /><br />In the new study, Mayford and Matsuo adapted this approach to discover how fear learning works at a deeper level — inside neurons of the brain's memory hub, called the hippocampus.<br /><br />Evidence suggested that proteins called AMPA receptors (http://www.nimh.nih.gov/science-news/2007/faster-acting-antidepressants-closer-to-becoming-a-reality.shtml) strengthen memories by becoming part of the synapses encoding them. To identify these synapses, the researchers genetically engineered a strain of mice to express AMPA receptors traceable by a green glow. After fear conditioning had triggered new AMPA receptors deep in the neuron's nucleus, they chemically suppressed any further expression of the proteins. This allowed time for the receptors to migrate to their appointed synapses. Hours later, green fluorescence revealed the fate of the specific AMPA receptors born in response to the learning.<br /><br />As expected, the newly synthesized AMPA receptors had traveled and become part of only certain hippocampus synapses — presumably the ones holding the memory. Synaptic connections are made onto small nubs on the neuron called spines. These spines come in three different shapes called thin, stubby and mushroom. While little was known about the function of these differently shaped spines, the fact that they are altered in various forms of mental retardation, like Fragile-X syndrome, suggests a critical importance in mental function.<br /><br />The researchers discovered the synapses that received the AMPA receptors with memory were limited to the mushroom type. The mushroom spines also figured prominently in the same neurons when the fear conditioning was reversed by repeatedly exposing the animals to the feared situation without getting shocked — a procedure called extinction learning. This indicated that the same neurons activated when a fear is learned are also activated when it is lost. The surge in mushroom spine capture of the receptors appeared within hours of learning and was gone after a few days, but appeared to be critical for cementing the memory.<br /><br /><i>[ ... <a href="http://www.nih.gov/news/health/feb2008/nimh-21.htm">Read the full press release</a> ... ]</i>Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-74258930821361132662008-02-05T14:15:00.000-08:002008-02-05T14:17:03.257-08:00Upcoming Event: Univ. of Minnesota, 08 February 20082008 Center for Bioethics Seminar Series<br /><br /><b>“Ethics and Public Health Emergencies: How Should We Prepare for Pandemic Flu?”</b><br />Friday, February 8, 2008<br />12:15–1:30 pm, 3-100 Mayo, University of Minnesota Campus<br /><br />Presented by<br /><b>Debra DeBruin, PhD<br />Director of Education and Assistant Professor, Center for Bioethics; Department of Medicine<br />University of Minnesota Medical School</b><br /><br />Dr. DeBruin has served as a health policy fellow for the United States Senate, and worked as a <br />consultant to the National Academy of Science’s Institute of Medicine and the National Bioethics Advisory Commission. She has also been a member of a number of working groups relevant to public health, including the Minnesota Privacy and Security Project Solutions Workgroup, the Minnesota Privacy and Security Project Legal Workgroup, the Minnesota Center for Healthcare Ethics’ Pandemic Influenza Ethics Work Group, and the State of Minnesota Department of Administration’s Work Group on Genetic Information. Currently, she is leading a team from the University of Minnesota Center for Bioethics along with the Minnesota Center for Health Care Ethics to provide guidance to the Minnesota Department of Health on ethical issues in pandemic planning. In addition to her work in public health policy, she teaches and conducts research in the ethics of research.<br /><br />Seminars are free and open to the public. Refreshments will be provided.<br /><br />Objectives:<br /><br />Following this seminar, participants will be able to:<br /> 1) Identify ethical issues that arise in the context of a public health emergency such as influenza pandemic.<br /> 2) Discuss moral considerations relating to the allocation of scarce resources.<br /> 3) Consider strategies for devising and implementing an ethical framework in pandemic planning.<br /><br />Continuing Medical Education Credit (CME) Available<br /><br />The University of Minnesota designates this educational activity for a maximum of 1 AMA PRA Category 1 <br />Credit ™. Physicians should only claim credit commensurate with the extent of their participation in the activity.<br />The University of Minnesota is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.<br />Pre-registration is preferred if you are attending for CME credit. Please call 612-624-8478 to pre-register. <br />Registration will also be available on site.Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-28983638019157845642008-02-05T09:43:00.000-08:002008-02-05T09:45:16.776-08:00Current Event: International Neuropsychological Society (INS) Meeting, Hawaii<b>36th Annual International Neuropsychological Society (INS) Meeting</b><br /><br />February 6, 2008 to February 9, 2008<br />Waikoloa, Hawaii, USA<br />Hilton Waikoloa Village<br /><br /><a href="http://www.the-ins.org/meetings/detail/index.cfm?id=40">Meeting webpage</a>Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-25497957208590501452008-02-05T09:40:00.000-08:002008-02-05T09:42:17.133-08:00Neuropsychology Abstract of the Day: AphasiaBaldo JV, Klostermann EC, & Dronkers NF. <b>It's either a cook or a baker: Patients with conduction aphasia get the gist but lose the trace.</b> <i> Brain and Language</i>. 2008 Feb 1 [Epub ahead of print]<br /><br />VA Northern California Health Care System, Center for Aphasia and Related Disorders, 150 Muir Road (126s), Martinez, CA 94553, USA.<br /><br />Patients with conduction aphasia have been characterized as having a short-term memory deficit that leads to relative difficulty on span and repetition tasks. It has also been observed that these same patients often get the gist of what is said to them, even if they are unable to repeat the information verbatim. To study this phenomenon experimentally, patients with conduction aphasia and left hemisphere-injured controls were tested on a repetition recognition task that required them to listen to a sentence and immediately point to one of three sentences that matched it. On some trials, the distractor sentences contained substituted words that were semantically-related to the target, and on other trials, the distractor sentences contained semantically-distinct words. Patients with conduction aphasia and controls performed well on the latter condition, when distractors were semantically-distinct. However, when the distractor sentences were semantically-related, the patients with conduction aphasia were impaired at identifying the target sentence, suggesting that these patients could not rely on the verbatim trace. To further understand these results, we also tested elderly controls on the same task, except that a delay was introduced between study and test. Like the patients with conduction aphasia, the elderly controls were worse at identifying target sentences when there were semantically-related distractors. Taken together, these results suggest that patients with conduction aphasia rely on non-phonologic cues, such as lexical-semantics, to support their short-term memory, just as normal participants must do in long-term memory tasks when the phonological trace is no longer present.<br /><br />PMID: 18243294 [PubMed - as supplied by publisher]Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.comtag:blogger.com,1999:blog-8201655.post-74973527608145290602008-02-05T09:13:00.000-08:002008-02-05T09:37:08.108-08:00Progressive Inflammatory Neuropathy (PIN) - Post 2From today's <i>New York Times</i>:<br /><br /><b>A Medical Mystery Unfolds in Minnesota</b><br />By DENISE GRADY<br />Published: February 5, 2008<br /><br />[snip]<br /><br />By then, November 2007, other cases had begun to turn up. Ultimately, there were 12 — 6 men and 6 women, ranging in age from 21 to 51. Doctors and the plant owner, realizing they had an outbreak on their hands, had already called in the Minnesota Department of Health, which, in turn, sought help from the federal Centers for Disease Control and Prevention.<br /><br />Though the outbreak seemed small, the investigation took on urgency because the disease was serious, and health officials worried that it might indicate a new risk to other workers in meatpacking.<br /><br />“It is important to characterize this because it appears to be a new syndrome, and we don’t truly know how many people may be affected throughout the U.S. or even the world,” said Dr. Jennifer McQuiston, a veterinarian from the disease centers.<br /><br />In early November, Dr. Aaron DeVries, a health department epidemiologist, visited the plant and combed through medical records. The disease bore no resemblance to mad cow disease or to trichinosis, the notorious parasite infection that comes from eating raw or undercooked pork. Nor did it spread person to person — the workers’ relatives were unaffected — or pose any threat to people who ate pork.<br /><br />A survey of the workers confirmed what the plant’s nurses had suspected: those who got sick were employed at or near the “head table,” where workers cut the meat off severed hog heads.<br /><br />[snip]<br /><br /><i>[ ... <a href="http://www.nytimes.com/2008/02/05/health/05pork.html?ex=1359867600&en=8963fa660fb20f05&ei=5124&partner=permalink&exprod=permalink">Read the full article</a> ... ]</i>Anthony Risserhttp://www.blogger.com/profile/11099026972556006040noreply@blogger.com