Crossroads of Fragile X and Alzheimers Research

Crossroads of Fragile X and Alzheimers Research

Researchers investigate treatment targets which may address both Fragile X Syndrome and Alzheimer’s disease Last week researchers at VIB Leuven in Belgium published evidence that a brain pathway involving the protein APP (Amyloid Precursor Protein) plays a vital role in development of Fragile X syndrome, one of the most common causes of autism. Scientists led by Dr. Emanuela Pasciuto in the laboratory of Prof Claudia Bagni published findings of their study in the journal Neuron. The team identified the molecular mechanisms behind the elevated levels and metabolism of APP protein in a mouse model. This dysregulation affects brain development and behavior, at a stage where the infant’s neuronal connections i.e. synapses are being formed and remodeled. Using a newly developed agent the team was able to reduce the cellular dysfunction and behavioral alterations paving way for potential new therapies for autism in the future. Dysregulated ADAM10-Mediated Processing of APP during a Critical Time Window Leads

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Using Fenobam to Reduce APP and Abeta in Fragile X Mice

Using Fenobam to Reduce APP and Abeta in Fragile X Mice

With a $130,000 grant from FRAXA Research Foundation over 2008-2008, Drs. James Malter and Cara Westmark at the University of Wisconsin studied the relationship between the fragile X protein FMRP and APP, a protein important to the pathology of Alzheimer’s Disease. APP may also contribute to the pathology of fragile X, and its major metabolite, Aß, may contribute to abnormal protein synthesis via a positive feedback loop. This project sought to restore normal dendritic protein synthesis in fragile X mice by breaking into this loop.

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