LANDO pathway disruption for Alzheimer's disease (SJ-19-0020)

St. Jude Reference #SJ-19-0020

Description

Modulation of LC3-associated endocytosis or ‘LANDO’ has the potential to be a therapeutic target for a variety of diseases, including neurodegenerative diseases, solid malignancies, protein clearance diseases, and autoimmune diseases.

Modulation of LC3-associated endocytosis or ‘LANDO’ has the potential to be a therapeutic target for a variety of diseases, including neurodegenerative diseases, solid malignancies, protein clearance diseases, and autoimmune diseases.

Researchers at St. Jude showed that LANDO is involved in the accumulation of B-amyloid in the brain by microglia in Alzheimer’s Disease, acting in a manner to prevent or reverse neurodegenerative disease. Most current neurodegenerative disease therapeutics only deal with symptom management. Likewise, while promising cancer therapies continue to be identified and approved, novel cancer therapeutics that target LANDO would more fundamentally attack the root of tumor creation rather than the symptomatic tumor.

They have also demonstrated that LANDO is critical for the recycling of some receptors, with implications in cell types and settings beyond neurodegenerative diseases (such as solid malignancies, protein clearance diseases, and autoimmune diseases). The ability for LANDO to regulate receptor recycling is also of interest as a putative adjuvant therapy for currently existing immunotherapies that are reliant on efficient expression of certain immune receptors. LANDO is also protective against neuroinflammation by dampening cytokine production, making it a prime therapeutic avenue to suppress inflammation.

Keywords

LC3-associated endocytosis, LANDO, immunotherapy, neurodegenerative, cancer, B-amyloid, microglia, Alzheimer’s, solid malignancies, protein clearance diseases, and autoimmune diseases, receptor recycling, cytokine, inflammation.

Granted patents or published applications

Application published as WO 2020/152607 A1

Related scientific references

Heckmann BL, Teubner BJW, Boada-Romero E, Tummers B, Guy C, Fitzgerald P, Mayer U, Carding S, Zakharenko SS, Wileman T, Green DR. Noncanonical function of an autophagy protein prevents spontaneous Alzheimer's disease. Sci Adv. 2020 Aug 14;6(33):eabb9036. doi: 10.1126/sciadv.abb9036. eCollection 2020 Aug. PMID: 32851186 

Heckmann et al., “LC3-Associated Endocytosis Facilitates b-Amyloid Clearance and Mitigates Neurodegeneration in Murine Alzheimer’s Disease,” 2019, Cell 178, 1–16; July 25, 2019 ª 2019 Elsevier Inc.; https://doi.org/10.1016/j.cell.2019.05.056

Licensing opportunities

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