April 25, 2007

AAN Meeting 2007: ALS Advances at a Glance

Roberta Friedman, Ph.D., Research Department Information Coordinator

The 2007 annual meeting of the American Academy of Neurology in Boston, April 30-May 5, provides ALS researchers from around the world an opportunity to learn about the most recent advances in the field that will lead toward more effective therapies. Platform presentations and poster sessions will highlight important progress in understanding what occurs in the human body to produce ALS and how to develop new strategies for treating the disease. Sessions throughout the meeting will focus on developing areas of research with direct implications for ALS. Please visit us at booth #2112.

The ALS Association is making available this preview of the meeting with emphasis on new developments relevant to the disease: 

A special scientific session including formal presentation of The Sheila Essey Award presented to Christopher Henderson, Ph.D., of Columbia University takes place on Wednesday at 3:45, in Room 311, followed by talks covering biomarker candidates, genome screening, and the link to ALS of variants in a gene for a set of detoxifying enzymes called paraoxinases.

Presidential Plenary Session, Tuesday, May 1, 9:00 a.m. 12:00 p.m., Hynes Convention Center Auditorium including:

“ALS: From Mutations to Mechanisms and Medicines”/Robert H. Brown, Jr., M.D., D.Phil, Presenter

Scientific Session, Tuesday, May 1, 2 3:30 p.m., Room 311, Clinical trials results; Nogo A; Antisense and more

Hot Topics Plenary Session, Tuesday, May 1, 5:15 p.m. 6:15 p.m., Hynes Convention Center Auditorium including:

  • “Brain Computer Interface” / John P. Donoghue, Ph.D., Presenter
  • “Progranulin Mutations in FTDP-17: Genetic and Clinical Implications”/ Michael Hutton, Ph.D., Presenter

Thursday afternoon features a session on Frontotemporal Dementia, 3:30 p.m., Room 210, concluding at 5:05 p.m. with a talk on links between the frontotemporal dementias and ALS by Bradley Boeve, M.D.

Progress in RNAi strategies for ALS and considerations for clinical trials in ALS will be presented as part of a Therapy of Genetic Disorders conference on Friday, at the Sheraton Hotel. Presenters include Michael Benatar MBChB, D.Phil, and Timothy Miller, M.D., Ph.D. Don Cleveland, Ph.D., will give an overview from 9:55 to 10:30 a.m.

Stop by our booth or visit www.alsa.org/research to learn more about ALS and ALS research and to get your copy of our new research newsletter, RESEARCH ALS TODAY.

SITE FEATURE: Our monthly ALS Research Journal News features recent advances relating to the disease as published in the scientific literature. Send suggestions and comments to [email protected].

To be included on our mailing list, email [email protected].


The ALS Association Guide of ALS Highlights at AAN 2007, Boston

Tuesday, May 1, 2007, 7:00 a.m., Posters (Attended 7 -8:30 a.m.), Anterior Horn

P01.082 deltoid denervation in ALS patients predicts diaphragm denervation.
Posters 01.079-86 discuss various outcome measures relevant to ALS clinical trials.
P01.095 neurodegenerative diseases are more common in relatives of ALS patients compared with relatives of controls.

2-3:30 p.m., Session, Anterior Horn
S06.001-.006: Trial results minocycline, phenylbutyrate; ALS incidence in Europe; Nogo-A in ALS and FTD; antinsense findings in rat model; microglia role in inherited ALS.

Wednesday, May 2, 2007, Sessions

Room 306, Neurogenetics and Gene Therapy:
2:45 p.m. S29.004 DNA variants in two genes are statistically associated with ALS susceptibility. Both of these genes have well-defined functions that may relate to the disease process of sporadic ALS.
3:15 p.m. S29.006 progranulin acts as a modifier of the course of disease in patients with ALS through earlier onset and shorter survival.

3:45 -4:45 p.m., Room 311, The Sheila Essey Award presentation and platform session:

  • muscle Nogo-A as a prognostic marker in lower motor neuron syndromes
  • genome-wide, SNP genotyping of publicly available samples from American and Italian sporadic ALS patients and controls 
  • findings support the association between the paroxonases and ALS.

4:30 p.m., Room 310, Brain computer interfacing in ALS and in nervous system injury

Posters, 4:00 p.m. (Attended 5:30 7 p.m.)
P05.116 mutant SOD1cells show marked reduction in the mRNA half-life of VEGF compared to wild-type (U251 glioma).
P05.117 gene expression in spinal motor neurons from mutant SOD1 mice: mitochondria and endoplasmic reticular function change early in disease.
P05.118 angiogenic genes may confer risk for the development of ALS.
P05.119 in hypoxic conditions, VEGF levels were decreased by 50 % in ALS patients.
P05.120 zebrafish embryos overexpressing mutant SOD1A4V showed abnormally branched and shorter axons compared to their littermates.
P05.121 stress-activated protein kinases and ALS: inhibitor slightly prolonged survival of mtSOD1
Also featured are posters on role of Hfe mutation and of microglia in ALS.

Thursday, May 3, 2007, 11:30 a.m., Posters (Attended Noon 1:30 p.m.)

P07.050 screen of all the exonic and flanking intronic sequences of 3 causative genes and 7 related genes for ALS
P07.054 chromosome 9p locus for ALS/FTD has been narrowed down to a 7.14cM region but no mutations found.
P07.076 genetics of ALS-FTD

2 6 p.m., Room 210, Integrated Neuroscience Session on FTD and ALS , highlights:
IN4-2.003 Tau isolated from ALS with cognitive impairment is phosphorylated and shows increase in polymer formation.
5:05 p.m. IN4-3.004 Links between Frontotemporal Lobar Degeneration, PSP, CBD and ALS

4:00 p.m., Posters (Attended 5:30 7 p.m.)
P08.033 CSF erythropoietin concentrations in neurodegenerative disease: in the same range or reduced versus controls
P08.034 angiogenin plays a role in onset for sporadic ALS; implicates the T allele of rs11701 in North America.
P08.036 increased progranulin in affected areas in ALS and in ALS with FTD, whereas in FTD expression is reduced.
P08.035 and P08.037 consider evidence for inflammation and oxidative stress in ALS
P08.145 viral delivery of transcription-mediated siRNA suppressed mutant SOD1 in muscle; did not maintain grip strength.

Friday, May 4, 2007, 9 a.m. 5 p.m., Sheraton Hotel, Therapy of Genetic Disorders, highlights:

  • siRNA producing mice showed a stable knockdown effect on SOD1 expression over four generations, onset delayed
  • An anti-inflammatory / anti-apoptotic agent and an anti-oxidative agent appear most promising for preventative and therapeutic trials respectively in patients with familial ALS.
  • Early treatment (30 days) of SOD1G93A rats extends survival by 30 days, compared with treatment initiated close to disease onset (65 days), which extended survival by 10 days.

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Call for Clinical Pilot Study Proposals (for TREAT ALS)

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