"Particularly a deficiency in the mitochondrial respiratory chain complex I and cristae disruption have been consistently described in PD. Moreover, the products of PD-familial genes, including alpha-synuclein, Parkin, PINK1, DJ-1, LRRK2 and HTR2A, were shown to localize to the mitochondria under certain conditions.It seems that PD has a mitochondrial component so events that would modulate normal mitochondrial functions may compromise neuronal survival. "
Mitochondrial metabolism modulation: a new therape... [CNS Neurol Disord Drug Targets. 2010] - PubMed result
A Blog by HEIRS on Health Education, Information and Support Resources
This blog provides information and resources for healthier living, wellness and a number of health topics including specific medical conditions. It is also a resource for conditions commonly considered to be environmental illnesses including CFS, FM, PTSD, obesity, diabetes, insulin resistance, MCS, heart disease, and a number of other conditions that are potentiated by contaminants in the air, soil and water including autism, sick building syndrome and sickness behavior just to name a few. This blog will try to focus on less scientific and more real-world news and application.
Showing posts with label mitochondrial dysfunction. Show all posts
Showing posts with label mitochondrial dysfunction. Show all posts
Sunday, March 7, 2010
Wednesday, February 17, 2010
Sunday, September 6, 2009
A Chemical in Cigarettes Induces Cell Stress & Possible Cell Death
Original Post: Acrolein induces a cellular stress response and triggers mitochondrial apoptosis in A549 cells.:
Summary: "Acrolein is an important contaminant in cigarette smoke which strigger the cellular stress response. If this process can not reduce the effects of the contaminant then mitochondrial cell death ensues."
Summary: "Acrolein is an important contaminant in cigarette smoke which strigger the cellular stress response. If this process can not reduce the effects of the contaminant then mitochondrial cell death ensues."
Thursday, September 3, 2009
A systematic review of experimental treatments for mitochondrial dysfunction in sepsis and multiple organ dysfunction syndrome.
Wednesday, September 2, 2009
N-acetylcysteine, coenzyme Q10 and superoxide dismutase mimetic prevent mitochondrial cell dysfunction and cell death induced by d-galactosamine in primary culture of human hepatocytes.
N-acetylcysteine, coenzyme Q10 and superoxide dismutase mimetic prevent mitochondrial cell dysfunction and cell death induced by d-galactosamine in primary culture of human hepatocytes.: "URL: N-acetylcysteine, coenzyme Q10 and superoxide dismutase mimetic prevent mitochondrial cell dysfunction and cell death induced by d-galactosamine in primary culture of human hepatocytes."
Labels:
mitochondrial dysfunction,
NAC,
q10,
SOD,
vitamin research
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