Ligand-Guided Phagocytosis Based Therapy of Alzheimer's Disease

Description:

Hybrid protein that can prevent brain cell death in patients of neurodegenerative diseases.

 

The Invention

One major pathological indicator of Alzheimer’s disease is the presence of amyloid beta aggregates that block cell-to-cell communication in the brain. The body removes these aggregates through a process that activates the production of pro-inflammatory substances, exacerbates neuro-inflammation, and results in the death of neurons.

 

We have engineered hybrid proteins that are capable of “snatching” harmful amyloid beta aggregates and “re-directing” them to an alternative degradation route that does not instigate a toxic response in the brain. Our initial findings reveal that the hybrid proteins facilitate the removal of harmful amyloid beta and reduce the number of inflammatory initiators, which may be essential for preventing brain cell death in patients of Alzheimer’s disease and other neurodegenerative diseases.

 

Key Benefits

  • Removes amyloid beta aggregates (treats the disease, not just the symptoms)
  • Protein has a high specificity for amyloid beta
  • Uses a non-inflammatory pathway to clear amyloid beta

Applications

  • Pharmaceutical

Market Opportunity

Currently, there is approximately 6.7 million Americans and at least 50 million people worldwide living with with Alzheimer’s disease. These numbers are expected to double by 2050 due to the increasing geriatric population.

 

The global Alzheimer’s disease treatment market is forecasted to grow from $4.71 billion in 2021 to $8.98 billion in 2029 at a CAGR of 8.4%. Additionally, the U.S. brand name pharmaceutical manufacturing market is expected to grow from $239.8 billion in 2022 to $269.3 billion in 2028 at a CAGR of 2.3%.

 

The vast majority of current FDA approved drugs only alleviate some of the psychological and behavioral symptoms of Alzheimer’s. Moreover, many clinical drug trials have been halted due to brain inflammation in patients. This treatment will treat the disease itself, not just the symptoms, and use a non-inflammatory pathway to clear amyloid beta.

 

Development and Intellectual Property Status

Patent filed.

 

 

Patent Information:
Category(s):
All
For Information, Contact:
Michael Mosher
Director of Commercialization
University of Nevada, Las Vegas
702-895-5697
michael.mosher@unlv.edu
Inventors:
Nora Caberoy
Keywords:
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