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Protein Regulates Movement Of Mitochondria In Brain Cells
ScienceDaily (June 16, 2009) — Scientists have identified a protein in
the brain that plays a key role in the function of mitochondria – the
part of the cell that supplies energy, supports cellular activity, and
potentially wards off threats from disease. The discovery, which was
reported June 15 in the Journal of Cell Biology, may shed new light on
how the brain recovers from stroke.
"Understanding the molecular machinery that helps distribute
mitochondria to different parts of the cell has only recently begun to
be understood," said University of Rochester Medical Center neurologist
David Rempe, M.D., Ph.D., the lead author of the study. "We know that in
some disease states that mitochondria function is modified, so
understanding how their activity is modulated is important to
understanding how the brain responds to a pathological state."
Read more/source:
http://www.sciencedaily.com/releases/2009/06/090615093925.htm
CeNeRx BioPharma Obtains Rights To Novel Drug Candidate For
Prevention And Treatment Of Neurodegeneration Disorders
Article Date: 17 Jun 2009 - 3:00 PDT
CeNeRx BioPharma, Inc., a clinical stage company developing and
commercializing innovative treatments for diseases of the central
nervous system (CNS), announced that it has obtained the rights to
develop and market a novel agent for the prevention and treatment of
neuropathies and neurodegenerative disorders. The drug candidate,
CXB909, is a small molecule, orally active agent that enhances the
effects of nerve growth factor (NGF). CeNeRx intends to initiate a Phase
l trial of CXB909 for the treatment of chemotherapy-induced peripheral
neuropathy (CIPN) later this year.
"Nerve growth factor has long been of interest as a potential therapy
for neuropathies and neurodegenerative diseases, but recombinant NGF
lacks key qualities needed for successful CNS drugs," said Dr. Daniel
Burch, Executive Vice President of R&D and Chief Medical Officer of
CeNeRx. "In preclinical studies, our small molecule agent CXB909 has
been shown to increase the action of native NGF, but without the
pharmacokinetic and administration challenges of recombinant NGF. Most
notably, CXB909 crosses the blood brain barrier, has a long half-life
and is orally available. The preclinical data for this agent is very
promising, and we look forward to assessing it in the clinic for
neuropathic and neurodegenerative conditions that currently have no
treatment options."
Read more/source:
http://www.medicalnewstoday.com/articles/154197.php
Copyright (c) 2008 Published by Elsevier B.V.
The mitochondrial cocktail: Rationale for combined nutraceutical
therapy in mitochondrial cytopathies
References and further reading may be available for this article. To
view references and further reading you must purchase this article.
M.A. Tarnopolsky, a,
aDepartment of Pediatrics and Medicine, McMaster University, 1200 Main
St. W., HSC-2H26, Hamilton, Ontario, Canada L8N 3Z5
Received 23 April 2008;
accepted 2 May 2008.
Available online 4 July 2008.
Abstract
Mitochondrial cytopathies ultimately lead to a reduction in aerobic
energy transduction, depletion of alternative energy stores, increased
oxidative stress, apoptosis and necrosis. Specific combinations of
nutraceutical compounds can target many of the aforementioned
biochemical pathways. Antioxidants combined with cofactors that can
bypass specific electron transport chain defects and the provision of
alternative energy sources represents a specific targeted strategy. To
date, there has been only one randomized double-blind clinical trial
using a combination nutraceutial therapy and it showed that the
combination of creatine monohydrate, coenzyme Q10, and α-lipoic acid
reduced lactate and markers of oxidative stress in patients with
mitochondrial cytopathies. Future studies need to use larger numbers
of patients with well defined clinical and surrogate marker outcomes
to clarify the potential role for combination nutraceuticals
("mitochondrial cocktail") as a therapy for mitochondrial cytopathies.
Keywords: Antioxidant; MELAS; LHON; Mitochondrial myopathy;
Neuroprotection
This review is part of the Advanced Drug Delivery Reviews theme issue
on "Mitochondrial Medicine and Mitochondrion-based Therapeutics".
Tel.: +1 905 521 2100x76593; fax: +1 905 577 8380.
; fax: +1 905 577 8380.
Hello all,
Just wanted to add a few other "perspective points" to the fine comments
already made. First, this abstract from Dr. Filla "presents the results
of a retrospective analysis" of FA patients taking a low dose of
Idebeneone for up to five years. I'd like to emphasize "retrospective"
-- looking back at and analyzing data from studies completed in the past.
We can not tell from the abstract how long ago the study was completed -
maybe that will be clear when we get the full article. I do know that
Dr. Filla has been seeing FA patients and monitoring their hearts for
over a dozen years, so the data reported in this abstract could well be
from a study completed years ago - maybe from the period right after
Idebenone was "discovered" in FA by Dr. Rustin when he gave the same low
dose of Idebenone (5mg/kg) to a few patients and reported reduction of
Left Ventricle Hypertrophy (wall thickness) in some of them.
Because Dr. Filla has been seeing FA patients and monitoring their
hearts for years, FARA asked him to serve on FARA's Cardiac Panel. Panel
members have been asked to assemble all the data they have on FA hearts
so the group can draw some conclusions and insights that might be
helpful in achieving a much deeper understanding of FA cardiology and
designing approaches to clinical trials that could improve clinical
management and therapy. It is for the same reason that some of the FARA-MDA
supported FA Clinical Research Network centers have been collecting FA
cardiology records.
So, Dr. Filla has published this retospective report, in part, as a
result of our effort to assemble FA cardiology data. Although, as others
have observed, this abstract does not appear to move the ball forward
very far in terms of Idebenone therapy, we should keep in mind that
these are additional pieces of data that help complete the picture. Good
scientists like Dr. Filla know that it is very important to publish
study results even when they do not appear to represent a success or a
breakthrough. Otherwise, other scientists would be likely later to move
down the same paths.
Warm regards to all,
Ron
Ronald J. Bartek
President
Friedreich's Ataxia Research Alliance (FARA)
P. O. Box 1537
Springfield, VA 22151
Tel (703) 426-1576
FARA website: http://www.CureFA.org
Email: fara@CureFA.org
Please register in the FARA Patient Registry at http://www.curefa.org/registry/
and for e-news at
http://visitor.constantcontact.com/email.jsp?m=1101190303489
Creating zinc monkey wrenches in the treatment of epigenetic disorders.
alin JH, Butler KV, Kozikowski AP.
University of Illinois at Chicago, Department of Medicinal Chemistry,
833 South Wood Street, Chicago, IL 60612, USA.
The approval of suberoylanilide hydroxamic acid by the FDA for the
treatment of cutaneous T-cell lymphoma in October, 2006 sparked a
dramatic increase in the development of inhibitors for the class of
enzymes known as the histone deacetylases (HDACs). In recent years, a
large number of combination therapies involving histone deacetylase
inhibitors (HDACIs) have been developed for the treatment of a variety
of malignancies and neurodegenerative disorders. Promising evidence has
been reported for the treatment of pancreatic cancer, prostate cancer,
and leukemia as well as a number of other previously difficult to treat
cancers. Drug combination approaches have also shown promise for the
treatment of mood disorders including bipolar disorder and depression.
In addition to these drug combination approaches, HDACIs alone have
demonstrated effectiveness in the treatment of Parkinson's disease,
Alzheimer's disease, Rubinstein-Taybi syndrome, Rett syndrome,
Friedreich's ataxia, Huntington's disease, multiple sclerosis, anxiety,
and schizophrenia. Adverse inflammatory affects observed with traumatic
brain injury and arthritis have also been alleviated by treatment with
certain HDACIs. Based on the diverse utility and wide range of
mechanistic actions observed with this class of drugs, the future
development of better drug combination therapies and more selective
HDACIs is warranted.
PMID: 19541531 [PubMed - as supplied by publisher]
Source:
Curr Opin Chem Biol. 2009 Jun 19. [Epub ahead of print]
http://www.ncbi.nlm.nih.gov/pubmed/19541531
Abstract kindly supplied by Juan Carlos Baiges
See:
http://friedreichscientificnews.blogspot.com/2009/06/creating-zinc-monkey-wrenches-in.html
Genetic Markers To Help Fight Diabetes Discovered
ScienceDaily (June 24, 2009) - Translational Genomics Research Institute
(TGen) scientists have identified five genetic biomarkers that could
help lead to improved treatments, with fewer side-effects, for patients
with diabetes.
TGen Senior Investigator Dr. Johanna DiStefano presented the findings in
New Orleans on June 6, 2009, at the 69th Scientific Sessions of the
American Diabetes Association.
"We identified genetic variants that may predict how well someone will
respond to the common anti-diabetes drug, Actos," said Dr. DiStefano,
Director of TGen’s Diabetes, Cardiovascular & Metabolic Diseases
Division. "The implications of these findings include determining which
patients will best respond to the drug for the prevention or treatment
of diabetes. In addition, this work lays the foundation for personalized
medicine for patients with this disease."
Personalized medicine involves the rapid application of laboratory
discoveries to therapies, depending on the individual genetic make-up of
each patient.
Source/read more:
http://www.sciencedaily.com/releases/2009/06/090616103215.htm
Behind the Scenes: Nanoparticles Explored for Preventing Cell Damage
By Cecile Gonzalez , National Science Foundation
posted: 26 June 2009 08:24 am ET
Sudipta Seal is enthralled by nanoparticles, particularly those of a
rare earth metal called cerium. The particles are showing potential for
a wide range of applications, from medicine to energy.
Seal is a professor of materials science and engineering at the
University of Central Florida (UCF), and several years ago he and his
colleagues engineered nanoparticles of cerium oxide (CeO2), a material
long used in ceramics, catalysts and fuel cells. The novel
nanocrystalline form is non-toxic and biocompatible — ideal for medical
applications.
Since then, the researchers found that cerium oxide nanoparticles have
two additional medical benefits: they behave like an antioxidant,
protecting cells from oxidative stress, and they can be fine tuned to
potentially deliver medical treatments directly into cells.
Oxidative stress = major headache
Oxidative stress has been implicated as a cause of arthritis, heart
disease and even aging. It also plays a role in several incurable
blinding diseases, such as diabetic retinopathy, age-related macular
degeneration, and retinal degeneration.
Oxidative stress occurs when too many reactive oxygen species (ROS) are
present. These powerful molecules are generated by exposure to ionizing
radiation and by commonplace reduction–oxidation reactions within cells.
(Peroxide and free radicals are two examples of ROS.)
Usually, enzymes known as antioxidants protect cells from oxidative
stress by disarming ROS and minimizing their toxic effects. But
sometimes, the number of ROS overwhelms a biological system, causing
damage to proteins, DNA and other cellular materials.
Engineering nanoparticles with antioxidant powers
Seal and his colleagues — James McGinnis, a vision scientist at the
University of Oklahoma Health Sciences Center, Artem Masunov, a
theoretical chemist at UCF, and William Self, a molecular and micro-biologist
at UCF — engineered special cerium oxide nanoparticles, which they call
"nanoceria," for tailored biomedical applications.
In a nanocrystalline form, cerium oxide is a powerful antioxidant
because its latticework crystal structure has many vacancies that can
capture oxygen and the material has a large surface area.
Self showed that nanoceria mimic the activity of superoxide dismutases,
an antioxidant that can stop the deadly chain reactions caused by ROS.
Nanoceria are also able to regenerate their antioxidant abilities. "Due
to this catalytic property," explains Seal, "repeated dosing with
nanoceria may not be needed, as it is with certain antioxidant vitamins."
In a biological paradox, ROS are actually required for some beneficial
cellular reactions. Fortunately, nanoceria do not deactivate all ROS.
Rather, says Seal, "they reduce the amount of ROS to a certain low level,
thus striking a perfect balance."
Source/read more:
http://www.livescience.com/health/090626-bts-nanoparticles.html
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