Monday, April 24, 2006

Abstract of the Day: Gingko Biloba and Dementia Prevention

DeKosky ST, Fitzpatrick A, Ives DG, Saxton J, Williamson J, Lopez OL, Burke G, Fried L, Kuller LH, Robbins J, Tracy R, Woolard N, Dunn L, Kronmal R, Nahin R, & Furberg C; for the GEMS Investigators. The Ginkgo Evaluation of Memory (GEM) study: Design and baseline data of a randomized trial of Ginkgo biloba extract in prevention of dementia. Contemp Clinical Trials. 2006 Apr 18; [Epub ahead of print].

Department of Neurology, University of Pittsburgh, 3471 Fifth Avenue, Suite 811, Pittsburgh, PA 15213, USA.

The epidemic of late life dementia, prominence of use of alternative medications and supplements, and initiation of efforts to determine how to prevent dementia have led to efforts to conduct studies aimed at prevention of dementia. The GEM (Ginkgo Evaluation of Memory) study was initially designed as a 5-year, randomized double-blind, placebo-controlled trial of Ginkgo biloba, administered in a dose of 120 mg twice per day as EGb761, in the prevention of dementia (and especially Alzheimer's disease) in normal elderly or those with mild cognitive impairment. The study anticipates 8.5 years of participant follow-up. Initial power calculations based on estimates of incidence rates of dementia in the target population (age 75+) led to a 3000-person study, which was successfully recruited at four clinical sites around the United States from September 2000 to June 2002. Primary outcome is incidence of all-cause dementia; secondary outcomes include rate of cognitive and functional decline, the incidence of cardiovascular and cerebrovascular events, and mortality. Following screening to exclude participants with incident dementia at baseline, an extensive neuropsychological assessment was performed and participants were randomly assigned to treatment groups. All participants are required to have a proxy who agreed to provide an independent assessment of the functional and cognitive abilities of the participant. Assessments are repeated every 6 months. Significant decline at any visit, defined by specific changes in cognitive screening scores, leads to a repeat detailed neuropsychological battery, neurological and medical evaluation and MRI scan of the brain. The final diagnosis of dementia is achieved by a consensus panel of experts. Side effects and adverse events are tracked by computer at the central data coordinating center and unblinded data are reviewed by an independent safety monitoring board. Studies such as these are necessary for this and a variety of other potential protective agents to evaluate their effectiveness in preventing or slowing the emergence of dementia in the elderly population.

PMID: 16627007 [PubMed - as supplied by publisher]
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Anthony H. Risser | |

Saturday, April 22, 2006

Obit: Tom Ferguson, M.D.

From Weblogsky: "Farewell to Dr. Tom"

Sunday, April 16, 2006

Media: Michael J. Fox and Parkinson's Disease

NBC's Dateline this evening covers Parkinson's Disease. Centering on the work of Michael J. Fox and his Foundation, it also includes segments with Muhammed Ali and his clinical center at the Barrow Neurological Institute in Phoenix and with several neuroscientists.
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Anthony H. Risser | |

Friday, April 14, 2006

Abstract of the Day: Malnutrition

Nakagawasai O, Yamadera F, Sato S, Taniguchi R, Hiraga H, Arai Y, Murakami H, Mawatari K, Niijima F, Tan-No K, & Tadano T. Alterations in cognitive function in prepubertal mice with protein malnutrition: relationship to changes in choline acetyltransferase. Behavior and Brain Research. 2006 Feb 15; 167(1): 111-117.

Department of Pharmacology, Tohoku Pharmaceutical University, 4-4-1 Komatsushima, Aoba-ku, Sendai 981-8558, Japan.

We have found that protein malnutrition (PM) causes a significant impairment of memory-related behavior on the 15th and 20th day after the start of PM (5% casein) feeding in prepubertal mice but not in postpubertal mice, as measured by a passive-avoidance task. This impairment was almost completely reversed by merely switching to a standard protein (20% casein) diet on the 10th day after the start of PM. However, the reversal was not observed when the switching to a standard protein regimen was done on the 15th day of the PM diet. Interestingly, the impairment of memory-related behavior on the 20th day was improved by the chronic administration of physostigmine (0.1 mg/kg/day x last 10 days, i.p.), a cholinesterase inhibitor. To correlate brain cholinergic neuron function with the memory-related behavior impairment induced by PM, microphotometry was used to determine the histological distribution of the imunofluorescence intensity for choline acetyltransferase (ChAT), a functional marker of presynapse in cholinergic neurons. The change in the intensity of fluorescence indicated that ChAT protein was decreased in the hippocampus (CA1, CA3 and dentate gyrus) on the 20th day after PM feeding in comparison with controls. These results suggest the possibility that the memory-related behavior deficits observed in prepubertal mice with PM are caused by a dysfunction of the cholinergic neurons in the hippocampus.

PMID: 16242790 [PubMed - indexed for MEDLINE]
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Anthony H. Risser | |

Saturday, April 08, 2006

Abstract of the Day: Mild Cognitive Impairment (MCI) & Dementia

Hodges JR, Erzinclioglu S, & Patterson K. Evolution of Cognitive Deficits and Conversion to Dementia in Patients with Mild Cognitive Impairment: A Very-Long-Term Follow-Up Study. Dementia and Geriatric Cognitive Disorders. 2006 Apr 4; 21(5-6): 380-391 [Epub ahead of print]

MRC Cognition and Brain Sciences Unit, Cambridge, UK.

Ten patients with mild cognitive impairment (MCI) underwent extensive neuropsychological evaluation at 12-monthly intervals for a minimum of 6 years. All 10 patients declined and 5 have now died. The onset of dementia, as defined by a fall in global cognitive function (MMSE <24) or activities of daily living (Clinical Dementia Rating Scale; CDR) ranged from 1 to 8 years with generally good concordance between these measures. The rate of decline on the MMSE was highly variable ranging from 0.86 to 2.83 points per year. Other than a consistent impairment on tests of episodic memory and category fluency (8 out of 10), other early cognitive deficits were difficult to define and tended to be unstable in the early stages. Impairment of semantic memory, visuo-spatial and attentional abilities eventually developed but the sequence of deficit acquisition was heterogeneous. These findings are discussed in the light of current views of MCI. Amnestic MCI may not be an accurate concept unless semantic memory impairment is also considered as an integral core deficit. Full-blown dementia may take many years to develop in patients with MCI but was a universal feature in this study. Copyright (c) 2006 S. Karger AG, Basel.

PMID: 16601329 [PubMed - as supplied by publisher]

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Anthony H. Risser | |

Friday, April 07, 2006

Daytrana (Methylphenidate Patch) & ADHD

From the website of The Washington Post:

FDA OKs First Attention Deficit Patch
By ANDREW BRIDGES
The Associated Press
Thursday, April 6, 2006; 8:06 PM

WASHINGTON -- The FDA on Thursday approved the first skin patch to treat attention deficit hyperactivity disorder in children.

The patch called Daytrana, designed to be worn for 9 hours, contains methylphenidate, which has been shown to help children with ADHD. It is the same stimulant that is in Ritalin. The patch is made by Noven Pharmaceuticals Inc. of Miami.

[ ... Read the full report ... ]
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Anthony H. Risser | |