In the January Journal Club, we discussed the new drug J147 which
targets mitochondrial dysfunction to potentially treat Alzheimer's and other age - related diseases.
Not exact matches
With the microRNA signatures of
mitochondrial function and
dysfunction in RPE cells in hand, combined with a detailed mechanistic understanding of how these microRNAs are transferred from cell to cell, we can use small interfering RNAs to
target specific microRNAs and block their adverse effects on mitochondria function and their transfer to other RPE cells.
Dr. Falk is also PI of an NIH, pharma, and philanthropic funded translational research laboratory group at CHOP that investigates the causes and global metabolic consequences of
mitochondrial disease, as well as
targeted therapies, in C. elegans, zebrafish, mouse, and human tissue models of genetic - based respiratory chain
dysfunction, and directs multiple clinical treatment trials in
mitochondrial disease patients.
These findings suggest that specific MFN2 mutations cause tissue - selective
mitochondrial dysfunction with increased adipocyte proliferation and survival, confirm a novel form of excess adiposity with paradoxical suppression of leptin expression, and suggest potential
targeted therapies.
A customized dietary protocol,
targeted supplementation, and mind - body therapies enabled my dramatic recovery, as did addressing root causes of
dysfunction, including micronutrient deficiencies, heavy metal toxicity, hypothalamic - pituitary - adrenal axis
dysfunction, sex hormone imbalances, dysbiosis, stealth infections, blood sugar dysregulation, and aberrant
mitochondrial function.