The Harvard Gazette, Combination Therapy Shows Promise for Delaying ALS
New cocktail may extend survival by 25 percent
In a study, researchers reported that the combination of minocycline and creatine resulted in additive neuroprotection in the case of amyotrophic lateral sclerosis, also known as Lou Gehrig’s Disease. After treatment with combination therapy, survival for mice with ALS was extended by 25 percent — or an additional 35 days — when compared to baseline.
Foundations Give Pitt $100,000 for ALS Research (2013)
The University of Pittsburgh School of Medicine has received a $100,000 grant to fund research into amyotrophic lateral sclerosis, the neurodegenerative disease also known as ALS or Lou Gehrig’s disease.
Pitt Findings on Lou Gehrig’s Disease May Hold Hope (2013)
A person diagnosed this year with amyotrophic lateral sclerosis, better known as ALS or Lou Gehrig’s disease, will receive basically the same prognosis as the New York Yankee did — an average life expectancy of two to five years.
Melatonin May Hold Promise Against ALS (2013)
A new study by researchers at the University of Pittsburgh School of Medicine may hold promise for the understanding and treatment of amyotrophic lateral sclerosis, the neurodegenerative disease more commonly known as ALS or Lou Gehrig’s disease.
Pitt Gets $100,000 for ALS Study (2013)
There is no cure, or any effective treatment, for amyotrophic lateral sclerosis, also called Lou Gehrig’s disease, the disease Neil Alexander was diagnosed with in June 2011.
Melatonin inhibits the caspase-1/cytochrome c/caspase-3 cell death pathway, inhibits MT1 receptor loss and delays disease progression in a mouse model of amyotrophic lateral sclerosis
Caspase-mediated cell death contributes to the pathogenesis of motor neuron degeneration in the mutant SOD1G93A transgenic mouse model of amyotrophic lateral sclerosis (ALS), along with other factors such as inflammation and oxidative damage. By screening a drug library, we found that melatonin, a pineal hormone, inhibited cytochrome c release in purified mitochondria and prevented cell death in cultured neurons. In this study, we evaluated whether melatonin would slow disease progression in SOD1G93A mice.
Increased stem cell proliferation in the spinal cord of adult amyotrophic lateral sclerosis transgenic mice
Harnessing the regenerative potential of the central nervous system to repopulate depleted cellular populations from endogenous stem cells would be a novel approach for the treatment of neurological diseases resulting from cell death.
Minocycline Inhibits Cytochrome C Release and Delays Progression (Mayo/Elsevier)
Minocycline mediates neuroprotection in experimental models of neurodegeneration. It inhibits the activity of caspase-1, caspase-3, inducible form of nitric oxide synthetase (iNOS) and p38 mitogen-activated protein kinase (MAPK). Although minocycline does not directly inhibit these enzymes, the effects may result from interference with upstream mechanisms resulting in their secondary activation.
Functional Role of Caspase-1 and Caspase-3 in an ALS Transgenic Mouse Model
Mutations in the copper/zinc superoxide dismutase (SOD1) gene produce an animal
model of familial amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative
disorder. To test a new therapeutic strategy for ALS, we examined the effect of
caspase inhibition in transgenic mice expressing mutant human SOD1 with a
substitution of glycine to alanine in position 93 (mSOD1G93A).
Inhibition of ICE slows ALS in mice
Amyotrophic lateral sclerosis (ALS) is
a progressive age-dependent disease
involving degeneration of motor neurons in
the brain, brainstem and spinal cord. ALS is
universally fatal, with the median survival of
patients being five years from diagnosis.