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Recent News and Articles on the Keywords: neurodenegerative + diseases + linked  Related to the article below (Last Update: 8/5/2008)

P EPTIDE A GGREGATION IN N EURODEGENERATIVE D ISEASE -
RM Murphy - Annual Reviews in Biomedical Engineering, 2002 - Annual Reviews
... 2). Huntington's disease is causally linked to an ... to be capable of transmitting disease. ...
1 Three aggregating polypeptides related to neurodenegerative disease. ...

The Paradigm of Huntington's Disease: Therapeutic Opportunities in Neurodegeneration -
J Leegwater-Kim, JHJ Cha - NeuroRX, 2004 - Elsevier
... by dissociating NMDA receptor-linked macromolecular complexes. ... 1 appears to slow
disease progression in ... a number of neurodenegerative disorders, including HD. ...

Generative naming in parkinson disease patients -
KA Bayles, MW Trosset, CK Tomoeda, EB Montgomery, … - Journal of Clinical and Experimental Neuropsychology, 1993 - informaworld.com
... neurodenegerative effects of Alzheimer?s disease (AD) (Appell, Kertesz, & Fisman,
1982; Becker, Huff, Nebes, Holland, & Boller, 1988; Branconnier, 1988; But- ...

[CITATION] Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral …
DR Rosen, T Siddique, D Patterson, DA Figlewicz, P … - Nature, 1993 - Day Neuromuscular Research Laboratory, Massachusetts General …

10 Principles of immune-virus interactions in the nervous system
PJ Tolbot, H Jacomy, E Gruslin - Clinical Neuroimmunology, 2005 - books.google.com
... strains or as a function of age) by a mechanism linked to macro ... and neurotoxic roles
have been attributed to microglial cells in neurodenegerative diseases. ...
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[PDF] CYTOTOXICITY OF PEROXYNITRITE AND NITRIC OXIDE INDUCED OXIDATIVE STRESS ON 3T3 FIBROBLAST CELL LINE -
DE GAMSIZ - 2003 - digital.sabanciuniv.edu
Page 1. CYTOTOXICITY OF PEROXYNITRITE AND NITRIC OXIDE INDUCED OXIDATIVE
STRESS ON 3T3 FIBROBLAST CELL LINE by Dilber Ece GAMSIZ ...

Pharmacological Intervention at Ionotropic Glutamate Receptor Complexes -
R Planells-Cases, J Lerma, A Ferrer-Montiel - Current Pharmaceutical Design, 2006 - ingentaconnect.com
... linked to ion chan- nels [2]. Since two recent reviews have rigorously described
the pharmacology of mGluRs and their implication in neu- rological diseases, ...

-
VJ Vodyanoy, AM Samoylov, OM Pustovyy - US Patent 7,138,255, 2006 - Google Patents
... Collins bodies Glutamate repeats Inherited neurodenegerative disorders Hungtington's ...
in the late stages of the disease and may ... or a free radical linked to an ...
-

[PDF] EUR Repository -
DF Majoor-Krakauer - ep.eur.nl
... 128-130 Parkin-linked cases (PARK2) generally exhibit selective ... to the three major
neurodenegerative disorders, dementia ... Epidemiology of motor-neuron diseases. ...

Abstracts
G Attardi - Mitochondrion, 2001 - Elsevier
... Nuclear genes, mitochondrial diseases ? Shoubridge EA ? Montreal Neurological Institute,
3801 ... dysfunction due to mutations in the X-linked TIMM8a gene ...

Source: Google Scholar
 
 

Mechanism for neurodenegerative diseases linked to transport proteins

 
 
Hampering the transport of proteins within cells may underlie several adult-onset neurodegenerative diseases, such as Huntington's, amyotrophic lateral sclerosis ( ALS ) and Kennedy disease.
Understanding how this cell transport is blocked in these diseases may offer targets for future therapy.

Researchers at the University of Illinois at Chicago ( UIC ) College of Medicine showed how a chemical pathway that is obstructed in Kennedy disease interferes with a cellular distribution system called " fast axonal transport " that moves proteins from where they are synthesized to where they are needed in the cell.

This transport system is critical in neurons because these cells can be as much as three feet long, says Scott Brady, at UIC.

" A breakdown in fast axonal transport would selectively kill neurons because neurons are especially dependent on the transport system," Brady said.

Kennedy disease is also known as spinal and bulbar muscular atrophy, or SBMA. Like the better-known ALS and Huntington's, it is a rare but devastating disease, affecting one in 40,000 people, usually between the ages of 30 and 50. Huntington's strikes about four times as many.

Neurodegenerative diseases like SBMA are caused by the lengthening of part of a gene that encodes repetitions of the amino acid glutamine in the protein. Although different genes are affected, all of the polyglutamine-expansion or "polyQ" diseases are characterized by symptoms that begin in middle age and by the loss of certain types of neurons through a pattern in which the neuron's terminals die before the cell body. PolyQ genes are expressed in many types of cells, but only neurons are affected.

Earlier studies had linked specific neurodegenerative diseases to mutations in proteins involved in intracellular transport. This led researchers to wonder if the deranged polyQ proteins inhibit fast axonal transport in several diseases, including SBMA, in which a mutation in the receptor for testosterone leads to the loss of motor neurons.
In the study, Brady and his co-workers were able to show that polyQ-AR, the mutated protein in SBMA, caused inhibition of fast axon transport by activating an enzyme called JNK that can inhibit these transport proteins.

Brady said this is the first proposed mechanism for polyQ diseases that explains why only nerve cells die and why the terminals die before the cell body. The link to the activation of the JNK enzyme suggests a new therapeutic target that might limit, delay or perhaps prevent progressive neurodegeneration, the researchers conclude.

The study is published in the journal Nature Neuroscience.

Source: University of Illinois at Chicago, 2006
 
 
 
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