National Institute on Aging

NEW YORK, June 22, 2026 (GLOBE NEWSWIRE) -- CurePSP announced the latest recipients of the Collaborative Approaches to Resources, Education and Support (CARES) grants, awarding a total of $155,000 to four projects spanning seven leading medical institutions in the U.S. and Canada. “Now in its fourth year, CARES advances best practices for progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and multiple system atrophy (MSA),” said Jessica Shurer, Director of Clinical Affairs and Advocacy. “Projects must involve at least two CurePSP Centers of Care and focus on person-centered care, access, underserved populations or medical education.” Rush University and the University of Pennsylvania will adapt PERSEVERE: a structured, 12-week peer mentorship program that trains experienced Lewy body dementia care partners to support newer ones, currently under a National Institute on Aging-funded national randomized trial. The team will develop a curriculum for PSP and CBD care partners and gather community feedback to inform a pilot program. The University of Miami, Northwestern University and the University of California, San Diego will survey clinicians and people with lived experience to identify barriers to accessing interdisciplinary care for PSP, CBD and MSA, diseases that have historically relied on care models designed for Parkinson's, and propose outcome measures to guide the development of care frameworks tailored specifically to these conditions. The University of Alberta and the University of Toronto, co-funded in partnership with Parkinson Canada, will use data mapping, provider interviews and patient focus groups to identify barriers to timely diagnosis of PSP, CBD and MSA in underserved populations across two Canadian provinces. The University of British Columbia and the University of California, San Diego, also co-funded with Parkinson Canada, will evaluate an eight-week virtual wellness program for people living with atypical parkinsonism, incorporating chair yoga, vocal exercises and peer support sessions. About CurePSP CurePSP is the leading nonprofit organization dedicated to the awareness, care and cure for three neurodegenerative diseases: progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and multiple system atrophy (MSA). As a catalyst for new treatments and a cure, CurePSP establishes important partnerships and funds critical research internationally. Through its advocacy and support efforts, CurePSP enhances education, care delivery and quality of life for people living with PSP, CBD and MSA and their families. Science, community and hope are at the heart of CurePSP's mission and all its services. CurePSP is a registered 501(c)(3) charity within the United States (EIN: 52-1704978). Contact: Kristophe Diaz, PhD Chief Executive Officer 646-725-1453 diaz@curepsp.org

Oligomerix, a clinical-stage biotechnology company based at the Albert Einstein College of Medicine in the Bronx, New York, has received a USD 1.9 million NIH Phase II SBIR Fast-Track grant to fund preclinical safety studies required before initiating a Phase Ib trial of OLX-07010, its oral small molecule tau inhibitor, in Alzheimer’s disease patients. The award, from the National Institute on Aging, signals continued NIH interest in tau-directed small molecule approaches as a complement to approved amyloid-targeting biologics. OLX-07010 is designed to inhibit tau protein self-association, the process by which soluble tau monomers aggregate into pathological oligomers and fibrils implicated in neuronal loss. The compound has demonstrated activity in multiple transgenic animal models and has completed Phase Ia human safety testing. The new funding will support a 13-week repeat-dose toxicology study in a non-rodent species — an FDA-required step before 3-month dosing in patients — complementing previously completed rodent studies. A favorable preclinical safety profile to date supports progression, though clinical efficacy remains to be established. All currently FDA-approved disease-modifying Alzheimer’s therapies — lecanemab (Leqembi) and donanemab (Kisunla) — target amyloid-beta and require intravenous or subcutaneous administration. Oral tau inhibitors remain an unvalidated but actively pursued class, with programs at several academic and industry groups. Oligomerix’s once-daily oral formulation and small molecule mechanism represent a differentiated approach in terms of administration and manufacturing cost. The grant reflects a broader NIH funding pattern supporting early-stage small molecule neurodegeneration programs through the SBIR mechanism, particularly those addressing modalities underrepresented among approved therapies. Oligomerix is also developing candidates for progressive supranuclear palsy and frontotemporal dementia, both tau-driven rare diseases with no approved treatments. This article was generated with AI assistance and reviewed and edited by the AllSci editorial team Explore more at AllSci News: https://allsci.com/news/ Your email address will not be published. Required fields are marked * Comment * Name * Email * Website Privacy Terms About Us Copyright © 2026. AllSci Corp. All rights reserved.

Researchers discovered that mutations linked to blood cancers may help trigger Alzheimer’s disease by creating overly inflammatory immune cells in the brain. The unexpected finding could lead to new blood-based screening methods and potential treatments borrowed from cancer medicine.As people grow older, their cells steadily pick up new genetic mutations. A study from Boston Children's Hospital, published in Cell, has uncovered an unexpected twist in that process. Researchers found that microglia, the immune cells that reside in the brain, accumulate mutations in specific cancer-driving genes. Rather than causing cancer, however, these mutations may contribute to the development of Alzheimer's disease. The research was led by Christopher Walsh, MD, PhD, Chief of the Division of Genetics and Genomics at Boston Children's Hospital and an Investigator of the Howard Hughes Medical Institute. Collaborators included Alice Eunjung Lee, PhD, and August Yue Huang, PhD, also of the Division of Genetics and Genomics. All three are Professors at Harvard Medical School and Associate Members of the Broad Institute of MIT and Harvard. The team says the findings could point to new ways to diagnose and treat Alzheimer's disease. "We find that to some extent, Alzheimer's disease is a little like cancer -- driven by the same mutations that drive blood cancers like lymphoma and leukemia," said Walsh. "This is helpful because we have a lot of drugs to fight cancer and some of them might be useful therapeutically for Alzheimer's disease." Cancer Driver Mutations Found in Alzheimer's Brains To investigate, researchers analyzed 149 cancer-driving genes in brain tissue samples from 190 people with Alzheimer's disease and compared them with samples from 121 healthy brains. The Alzheimer's samples contained more single-letter DNA changes than the healthy tissue. Many of these alterations repeatedly appeared in the same five cancer driver genes, suggesting that microglia were accumulating mutations in a specific set of genes. Microglia serve as the brain's cleanup crew. These cells remove debris and help eliminate infected, damaged, or dying cells. Scientists had long believed that microglia remain confined to the brain and do not cross the blood brain barrier, unlike many other immune cells that circulate through the bloodstream. Unexpected Link Between Blood Cells and the Brain The mutations identified in microglia are commonly associated with blood cancers. That observation prompted the researchers to look for the same mutations in blood samples from people with Alzheimer's disease. They did not expect to find them. Instead, the blood cells from the same Alzheimer's patients carried the identical cancer-associated mutations. "It was actually a really unexpected finding that suggests a totally new mechanism for Alzheimer's disease pathogenesis," said Huang. "The findings mean that the blood's immune cells with cancer mutations are likely getting into the brain and contributing to disease." How Mutant Immune Cells May Fuel Alzheimer's The researchers propose that aging or injury can weaken the blood-brain barrier, allowing immune cells from the bloodstream to enter the brain. Once there, these cells may transform into microglia-like cells. At the same time, protein clumps that build up in the brain trigger microglia to multiply and respond. Cells that possess a biological advantage are more likely to expand, including the microglia-like cells carrying cancer-related mutations. According to the researchers, these mutated cells may create a more inflammatory and damaging environment than healthy microglia. As a result, nearby neurons can be harmed and die, contributing to the progression of Alzheimer's disease. Potential for New Alzheimer's Tests and Treatments The discovery could eventually lead to new approaches for detecting Alzheimer's risk. "Because it's hard to access brain tissue in a living patient, genetic screens using blood samples could be developed to test whether a person carries these mutations, and has an increased risk of developing Alzheimer's disease," said Lee. In a follow-up study posted as a preprint on bioRxiv, Huang and Lee found additional evidence supporting the connection. Their analysis showed that cancer driver mutations detected in blood samples increased Alzheimer's disease risk independently of APOE4, a well-established genetic risk factor for the disease. The research was conducted in collaboration with the Icahn School of Medicine at Mount Sinai. Funding was provided by the Howard Hughes Medical Institute, the National Institute on Aging, the NIH Common Fund through the Somatic Mosaicism Across Human Tissues (SMaHT) consortium, and the Suh Kyungbae Foundation (SUHF).