How cells' recycling systems control protein cleanup in Alzheimer's disease
Endocytosis and Endolysosomal Trafficking of Receptor Tyrosine Kinases in the Regulation of Chaperone-Mediated Autophagy
This project looks at how cells' selective recycling pathway (chaperone-mediated autophagy) and certain growth-factor receptors affect the buildup of proteins linked to Alzheimer's disease.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of New Mexico Health Scis Ctr NIH-funded |
| Lab location | 1 site (Albuquerque, United States) |
| Project ID | NIH-11228376 on NIH RePORTER |
What this research studies
The researchers are studying chaperone-mediated autophagy (CMA), a selective cell process that removes specific damaged or excess proteins, to understand how it is regulated in aging and neurodegeneration. They focus on how receptor tyrosine kinases—especially the insulin and PDGF receptors—and the PI3K/AKT signaling pathway influence CMA activity. Experiments use molecular lab work and mouse models to map these signaling steps and test ways to boost CMA without the harmful side effects seen with some PI3K inhibitors. The goal is to identify druggable points in these pathways that could guide safer therapies to reduce harmful protein buildup in the brain.
Who could benefit from this research
Good fit: People with Alzheimer's disease or mild cognitive impairment, or those willing to donate samples for research on disease mechanisms, would be the most relevant candidates to follow this work.
Not a fit: Individuals seeking immediate symptom relief or people without neurodegenerative disease are unlikely to gain direct clinical benefit from this basic, lab-focused research.
Why it matters
Potential benefit: If successful, this work could point to new drug targets or approaches to boost cells' protein-cleanup systems and slow or prevent Alzheimer's-related protein buildup.
How similar studies have performed: Prior mouse studies showed class I PI3K inhibitors can activate CMA but caused serious side effects, so this project builds on that finding by exploring alternative, potentially safer regulatory targets downstream of receptor signaling.
Where this research is happening
Albuquerque, United States
- University of New Mexico Health Scis Ctr — Albuquerque, United States (Active)
Researchers
- Principal investigator: Endicott, Samuel Joseph — University of New Mexico Health Scis Ctr
- Study coordinator: Endicott, Samuel Joseph
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.