Sept. 23, 2019
A minimally invasive optical induction system has been developed to transiently alter autophagic flux, specifically targeting and reducing pathological tau proteins.
The uncontrolled misfolding and aggregation of microtubule-associate protein Tau (MAPT) into neurofibrillary tangles (NFTs) has been identified as a common component in a number of neurodegenerative diseases, such as, Alzheimer’s disease, Pick’s disease, and other dementias. Efforts have shown that a deficiency in endogenous autophagic clearance results in a subsequent build-up of pathological tau (p-Tau) proteins, which contribute to the impairment of microtubule stability resulting in neuronal cell death. Transcription factor EB (TFEB), a regulator of autophagy flux, promotes the natural clearance of p-Tau and its regulation has the potential to prevent NFT pathology. Unfortunately, a constant activation of TFEB poses many risks to whole cell bioenergetics as well as increased toxicity in co-morbid conditions of ischemia or traumatic brain injury. Thus, it is of high importance to identify a mechanism to spatially and temporally control autophagy flux when necessary.
Researchers at the University of New Mexico have developed a minimally invasive optical induction system to transiently alter autophagic flux, specifically targeting and reducing pathological tau proteins. Utilizing a novel optogenetic gene expression system, the device drives TFEB gene expression upon optical stimulation. The light-regulatable gene expression of TFEB enables the directed control of autophagic flux, leading to the reduction of excessive p-Tau accumulation. Tunable control of TFEB expression may have beneficial effects on the prevention and treatment of neurodegenerative diseases.
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microtubule stability resulting
transcription factor eb
prevent nft pathology
traumatic brain injury
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