IMMUNOLOGY2026™ Conference Recordings For Attendees-Harnessing Neuroimmune Interactions for Disease Modification in Alzheimer's & Parkinson's

Harnessing Neuroimmune Interactions for Disease Modification in Alzheimer's & Parkinson's

Video Transcription

Video Summary

The speaker argued that the brain is not truly immune-privileged but immune-specialized, with constant communication between peripheral immunity and CNS microglia. Using mouse and human studies, they showed that acute inflammation alters microglial signaling, while chronic inflammation and aging drive immune dysregulation, immunosenescence, and even autoimmunity. This may contribute to Alzheimer’s and Parkinson’s disease long before symptoms appear. They emphasized that midlife inflammation, genetic risk, infections, and chronic inflammatory diseases can shape later neurodegeneration.  <br /><br />A major focus was TNF biology: soluble TNF appears harmful, while membrane-bound TNF may be protective. A selective soluble-TNF inhibitor (Xpro) improved inflammatory and neurodegenerative biomarkers in early Alzheimer’s trials, with further trials underway. In Parkinson’s, the lab found immune exhaustion, mitochondrial dysfunction, and altered iron metabolism in peripheral immune cells, suggesting disease-relevant changes may begin outside the brain. Overall, the message was to look beyond the brain and use peripheral immune profiling to stratify patients and guide therapies.

Meta Tag

Date April 18, 2026 12:30 PM - 2:30 PM

Room 104C

Session Autoimmunity, Neurodegeneration and Aging

Speaker Malu Tansey

Track Basic Autoimmunity (BA)

Year 2026

Keywords

microglia

neuroinflammation

TNF

immunosenescence

Alzheimer's disease

Parkinson's disease

April 18, 2026 12:30 PM - 2:30 PM

104C

Autoimmunity, Neurodegeneration and Aging

Malu Tansey

Basic Autoimmunity (BA)

2026