Bioactive Peptides: Inhibition of Neuroinflammation & Neurodegeneration

University of Oklahoma Background
There is currently no treatment available to stop or slow the progression of Alzheimer’s disease (AD). A vicious cycle between neuroinflammation and neurodegeneration is triggered and sustained by amyloid β (Aβ) soluble aggregates in the brain of patients with AD. The defense proteins CAP37, cathepsin G (CG) and neutrophil elastase (NE), expressed in neutrophils and certain brain cells have shown promise for interrupting these pathogenic pathways. CAP37, CG and NE bind Aβ, which inhibits aggregation into neurotoxic/proinflammatory species. They also binds and inhibits pro-inflammatory receptors RAGE and TLR4 and pro-inflammatory ligand S100A9. Therapeutic peptides derived from CAP37, CG, or NE could provide a multi-targeted strategy to inhibit both neuroinflammation and neurodegeneration to synergistically inhibit AD progression.
Technology Overview
Bioactive peptides derived from CG and CAP37 have been identified. They mimic the effects of full-length proteins and thus could be used for inhibition of the neurotoxic and proinflammatory effects of Aβ in AD and related diseases.

A peptide inhibits Aβ aggregation (A), Aß neurotoxicity (B) and targets receptors of Aβ aggregates (RAGE (C) and TLR4 (D)), as well as S100A9, another AD-associated pro-inflammatory mediator.
Stage of Development

Technology Readiness Level (TRL): 2

Further investigation underway to support the use of these peptides as a viable therapeutic strategy for AD.

In vitro: Investigate anti-inflammatory effects on human microglia
In vivo: Investigate the ability of these peptides to penetrate the brain


Multi-targeted strategy
Potential ability to cross the bloodbrain barrier by RAGE-mediated transcytosis

Inhibition of amyloid-β aggregation, neuroinflammation and neurodegeneration for the treatment of:

Alzheimer’s disease


Seeking industry partner for further development

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