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Multiple System Atrophy News - February 2003 _____________________________________________________

Table of Contents

1. SUPPORT GROUP NEWS
a. View the Latest News from Shy-Drager.com
i. Annual Russell Wood Lecture - Denver, CO - April 2003
ii. SDS/MSA Support Group Regional Meeting - Houston, TX - May 2003

b. NAF Annual Membership Meeting - Atlanta, GA - March 2003

2. MULTIPLE SYSTEM ATROPHY RESEARCH NEWS
a. NIH FUNDED RESEARCH PROJECTS
i. Autonomic Disorders Program Project
ii. Molecular Substrates of Aging and Neuron Death

3. ODDS AND ENDS
a. Charmayne's MSA/Shy-Drager website has moved.

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1. SUPPORT GROUP NEWS

a. View the latest news published on the SDS/MSA Support Group

website:http://www.shy-drager.com

Of special note this month is the preliminary Calendar of Events for 2003

http://www.shy-drager.com/Calendar_of_Events.htm

Be sure to check back regularly for updates on these upcoming events:

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i. Annual Russell Wood Lecture - details forthcoming Denver, Colorado area Late April time frame

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ii. SDS/MSA Support Group Regional Meeting - details forthcoming Houston, Texas area

Early May time frame

Dr. Jankovic will be the Hosting Doctor

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b. NAF Annual Membership Meeting - Atlanta, GA

The BOARD OF DIRECTORS of THE NATIONAL ATAXIA FOUNDATION cordially invites you to THE 2003 ANNUAL MEMBERSHIP MEETING

March 6-9, 2003

at the Sheraton Gateway Hotel
1900 Sullivan Road
Atlanta, GA 30337
Phone: 1-770-997-1100
Toll Free: 1-800-784-9400

...

For more information please see: http://www.ataxia.org/amm2003/registrationinst.html

Note: The ataxias are a group of neurodegenerative disorders, some with a hereditary cause, that affect balance and coordination. The National Ataxia Foundation recognizes the cerebellar form of MSA (also known as OPCA - olivoponto cerebellar atrophy or degeneration) as a "sporadic (non-hereditary) ataxia".

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2. MULTIPLE SYSTEM ATROPHY RESEARCH NEWS

a. NIH FUNDED RESEARCH PROJECTS

Grant Number: 5P50NS032352-08
PI Name: LOW, PHILLIP A.
Project Title: AUTONOMIC DISORDERS PROGRAM PROJECT

Abstract: Autonomic dysfunction including orthostatic hypertension (OH) is a major health problem, causing significant morbidity and mortality. Its pathophysiology remains poorly understood and hence its management lacks a solid scientific base. The PPG focuses on the pathophysiology and treatment of autonomic failure. Project 1 (Low) incorporates a novel strategy of cholinesterase inhibition in the treatment of OH, an approach that promises to improve OH without supine hypertension. A second blinded treatment trial will evaluate if sodium chloride will expand plasma volume and if urinary sodium excretion is a suitable surrogate measure of plasma volume status. A series of studies, including the use of microneurography to measure sympathetic impulses, will evaluate the pathophysiology of postural tachycardia syndrome (POTS). A novel approach of amplitude modulation of the EEG in POTS shows a selective reduction of a frequency band of 0.02-0.05 Hz; this component is of particular interest since it may have a brainstem origin. The venous capacitance bed will be evaluated (Projects) to determine if there is excessive transcapillary efflux and changes in compliance in POTS and the effects of aging. The relative importance of the mesenteric, systematic and cerebrovascular circulations in OH will be evaluated. Project (Benarroch) will expand its studies on the neurochemical organization of autonomic control regions of the medulla in multiple system atrophy (MSA) and the parkinsonian syndromes. These include quantitative evaluates of new cellular groups (nucleus ambiguus, nuclease retroambiguus) and new receptors (including angiotensin II) that are likely to provide insights into the pathophysiology of autonomic failure in MSA. Project (Joyner) will undertake a detailed evaluation of the effects of denervation (mild in POTS and severe in neurogenic OH) and aging on the venous capacity and compliance. Project (Brimijoin) will focus on the response of the pre-ganglionic neuron to denervation and will study the mechanism of spinal intermediolateral column cell loss, using he model of immune- mediated pre-ganglionic autonomic neuropathy. The roles of apoptosis, excitotoxicity, growth factors, and aging will be evaluated and related to MSA.

Institution: MAYO CLINIC ROCHESTER
200 1ST ST SW
ROCHESTER, MN 55905
Project Start: 01-JAN-1995
Project End: 31-AUG-2005

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Grant Number: 5P01AG009215-13

PI Name: TROJANOWSKI, JOHN Q.
Project Title: MOLECULAR SUBSTRATES OF AGING AND NEURON DEATH

Abstract: Mechanisms of brain dysfunction and death due to neurodegenerative diseases of the central nervous system (CNS) are poorly understood, but the emergence of profound cognitive and/or motor impairments in these heterogenous diseases is a manifestation of the progressive and massive degeneration of selectively vulnerable populations of neurons that distinguishes neurodegenerative diseases from normal aging. Additionally, intracellular filamentous inclusions are neuropathological hallmarks of many neurodegenerative diseases despite their heterogeneity. For example, abnormal alpha-synuclein filaments aggregate to form Lewy bodies (Lbs) in neurons and they are signature lesions of Parkinson's disease (PD), dementia with Lbs (DLB) and an Alzheimer's disease (AD) subtype known as the LB variant of AD (LBVAD), while multiple system atrophy (MSA) is characterized by glial cytoplasmic inclusions (GCIs) composed of alpha-synuclein filaments aggregate to form Lewy bodies (Lbs) in neurons and they are signature lesions of Parkinson's disease (PD), dementia with Lbs (DLB) and an Alzheimer's disease (AD) subtype known as the LB variant of AD (LBVAD), while multiple system atrophy (MSA) is characterized by glial cytoplasmic inclusions (GCIs) composed of alpha-synuclein filaments. Although these inclusions often were regarded as epiphenomena unrelated to mechanisms of brain degeneration, this view has undergone dramatic revisions after the discoveries that: mutations in the alpha- synuclein cause familial PD in rare kindreds, alpha-synuclein is a major component of Lbs and GCIs, and wild type, as well as mutant alpha-synuclein form filaments in vitro similar to those in Lbs and GCIs. Moreover, the presence of abundant alpha-synuclein Lbs in the most common variant of sporadic AD (i.e., LBVAD), >60% of familial AD brains and >50% of Down's syndrome brains with AD provides an opportunity to elucidate mechanisms of the enigmatic, but frequent overlap of AD and PD. Finally, we also have shown that beta- and gamma-synucleins accumulate in dystrophic hippocampal processes in PD and DLB. Thus, we hypothesize that accumulations of synuclein filaments or aggregates play a mechanistic role in neurodegenerative diseases characterized by abundant synuclein pathology, and this Program Project grant describes four complementary Projects to test this hypothesis with the support of an Administrative, Clinical, and Neuropathology Core. The Projects are highly synergistic and pursue research conducted on disease brains with authentic human synuclein pathology (Project 1), as well as on mechanisms of synuclein pathologies using in vitro (Project 2), transgenic fly (Project 3) and transgenic mouse (Project 4) models. This Program Project will provide new insights into mechanisms of synuclein pathologies and their role in brain degeneration, which are likely to accelerate efforts to improve the diagnosis and therapy of these and other neurodegenerative disorders characterized by filamentous brain lesions.

Institution: UNIVERSITY OF PENNSYLVANIA
3451 Walnut Street
PHILADELPHIA, PA 191046205

Project Start: 01-AUG-1990
Project End: 30-APR-2005

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3. ODDS & ENDS

a. Charmayne's MSA/Shy-Drager website has moved.

Don't lose touch with this great site, please change your bookmarks to:

http://www.bischel.com/MSAindex.html

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To subscribe to the MSA Online Support Group

Please visit http://groups.yahoo.com/group/shydrager

To view past issues of Multiple System Atrophy News please go to: http://americanautonomicsociety.org and click on "Patient Resources" then on "Multiple System Atrophy News"

Did you know? Much of the research news about MSA comes from leads from you, our readers. Please, if you know of any research studies accepting MSA patients kindly share this information by contacting the MSA News editor at pbower@accesscable.net ______________________________________________________

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