Pathway-Dependent Inhibition Of Proteopathic Seed Transmission
Tech ID: 28942 / UC Case 2018-028-0
UCLA researchers in
the Department of Neurology have developed a
novel approach to stop the propagation of proteopathic diseases, which could
be applied to wide range of neurodegenerative disorders including Alzheimer’s
disease and Parkinson’s disease.
Proteopathy is a common feature of many neurodegenerative disorders,
including Alzheimer’s disease and Parkinson’s disease. Alzheimer’s disease
market alone is expected to reach over 2.9 billion USD by 2020. Available
treatments are largely ineffective, and currently there is no successful approach
for modifying the disease to stop its progression. A method to neutralize the spread
of proteopathy that contributes to neurodegeneration would revolutionize how we
treat proteopathic neurodegenerative disorders.
Researchers at UCLA have developed a novel approach to stop the
propagation of proteopathic diseases. Recent data has shown that the
proteopathy disease propagation occurs when misfolded or aggregate-prone
disease-specific proteins spread to other cells. There, these proteopathic “seeds”
serve as a template to cause other proteins to misfold, in a manner similar to
that of prions. Researchers in
the Department of Neurology at UCLA have identified a specific molecular pathway that can
be inhibited to stop proteopathic seed delivery, representing a promising
strategy to control progression of neurodegenerative disorders.
- Alzheimer’s disease
- Parkinson’s disease
- Lewy body dementia
- Front of temporal dementia
- Amyotrophic lateral sclerosis
- Proteopathic diseases
- Gives insight into proteopathic disease
- Applicable across multiple proteopathic diseases
- Allow discovery of
new small molecule drugs for neurodegenerative disorders
State Of Development
- Identified a specific molecular pathway to stop proteopathic tau seed
- Identified small molecule leads that could modulate the pathway and
inhibit the seed transmission
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