This week researchers from the Institute for Neurodegenerative Disease, Massachusetts General Hospital (MGH), Harvard Medical School, released results from a study showing that a key protein associated with the development of Alzheimer’s disease, Amyloid precursor protein (APP), could potentially play an important role in eye and muscle health. The study, entitled, “FE65 and FE65L1 amyloid precursor protein–binding protein compound null mice display adult-onset cataract and muscle weakness,” demonstrated that in a mouse model where proteins binding to APP, called FE65 and FE65L1, are deleted, they cause cataracts and muscle weakness. If the findings, which were published in the latest edition of the Federation of American Societies for Experimental Biology (FASEB) Journal, are confirmed in clinical studies, FE65 and FE65L1 proteins could be a future therapeutic target for cataracts, muscular dystrophy and Alzheimer’s disease.
The researchers made this valuable discovery by comparing 4 groups of mice with distinct protein deficiencies, including:
- Mice without the FE65 protein
- Mice without FE65L1
- Mice without both FE65 and FE65L1
- Mice that had normal protein composition (control mice)
After a comparative analysis between the groups, the findings showed that mice lacking both FE65 and FE65L1 developed severe lens degeneration that may be an indication of cataracts and muscle weakness. For mice missing only one protein, milder symptoms of muscle degeneration were observed; while no changes were found in the control group…….
Source: Muscular Dystrophy News