Retrotope And Collaborators To Present Poster At American Academy of Neurology On Stabilized PUFA Drug Efficacy In Multiple Alzheimer’s Models

D-PUFA stabilized fatty acid drug combination reverses Alzheimer’s cognitive losses and improves oxidation stress markers in the brain of two different mouse models.

LOS ALTOS, CA, April 21, 2017 – Retrotope and its collaborators, Dr. Brian Bennett of Queens University, Kingston, ON, Canada, and Dr. Mark Mattson, the National Institute of Aging, will present a joint poster at AAN, Boston this week entitled “Isotope-reinforced Polyunsaturated Lipids (D-PUFAs) Mitigate Symptoms in Different Alzheimer’s Disease Mouse Models”. The results demonstrate that combinations of Retrotope’s deuterated polyunsaturated fatty acid (D-PUFA) drugs are active vs. inactive fat controls at both lowering amyloid beta fragments in brain in the APP/PS1 NIH Alzheimer’s mouse and reversing multiple cognition deficits in an aldehyde dehydrogenase 2 (ALDH2-/-) early onset knockout mouse. Further collaborators from Vanderbilt University and the University of Arkansas Stable Isotope Laboratory are additional authors who assisted in analyzing tissues for oxidation markers and tissue drug incorporation.

Dr. Mikhail Shchepinov, CSO and co-founder of Retrotope, commented: “The neurodegenerative disease community has long recognized that lipid peroxidation damage was associated with Alzheimer’s disease. We have further been able to show with these data that downregulating lipid peroxidation by fortifying the susceptible polyunsaturated fats active in key brain membranes, can halt or reverse the disease process in these animals. This discovery challenges some of the long held tenets of the causes of Alzheimer’s disease. Our data suggests that damaged amyloid precursor and other (e.g. tau) proteins are toxic to cells, but don’t alone cause the disease. We believe they trigger a specific type of lipid peroxidation, and that the lipid peroxidation is required as a final common pathway to cell death, and symptoms. By controlling the lipid peroxidation, one may be able to arrest the disease, and even recover function.”

Alzheimer’s disease is becoming one of the most serious challenges to healthcare around the world. It is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills, and eventually the ability to carry out the simplest tasks. Experts suggest that more than 5 million Americans may have Alzheimer’s, and it is the most common cause of dementia among older adults. There is currently no approved therapy that stops or reverses the progression of the disease despite tens of billions in research and clinical trials.

About D-PUFAs

D-PUFAs are patented, orally available, modified fatty-acid therapeutics that stabilize (“fireproof”) mitochondrial and cellular membranes against attack and restore cellular health. Retrotope and others have discovered that lipid peroxidation, the free-radical degradation of fatty acids in mitochondrial and cellular membranes, may be required in a wide range of degenerative disease phenotypes. The degradation products of these fats involved in critical cell functions like mitochondrial ATP generation create toxic cascades that lead to cell death, disease onset and progression.

About Retrotope

Retrotope, a privately-held, clinical-stage pharmaceutical company, is creating a new category of drugs to treat degenerative diseases. Composed of proprietary compounds that are chemically stabilized forms of essential nutrients, these compounds are being studied as disease modifying therapies for many intractable diseases such as Parkinson’s, Alzheimer’s, mitochondrial myopathies, and retinopathies. RT001, Retrotope’s first lead candidate, is for the treatment of Friedreich’s ataxia, a fatal orphan disease. For more information about Retrotope, please visit www.retrotope.com.

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