Andrew J Alt

Pharmacology Department.

2 publications 2004 – 2022
Arthritis, RheumatoidDisease Models, AnimalBradykininCD13 AntigensFibroblasts

What does Andrew J Alt research?

Andrew J Alt's research dives into the causes and potential treatments for inflammatory arthritis and neurological disorders. He studies how a protein called CD13 triggers inflammatory arthritis by activating a receptor known as B1R, which is overly active in patients with rheumatoid arthritis, a painful condition affecting the joints. In addition to arthritis, Alt has developed a compound called UBP296 that blocks certain brain receptors, aiming to find better therapies for various neurological conditions. His studies indicate that by targeting these specific receptors, it’s possible to create more effective treatments without unwanted side effects.

Key findings

  • Blocking the B1R receptor stops inflammation in human tissues and mouse models of rheumatoid arthritis, indicating a new treatment approach.
  • In his study of UBP296, it was shown to be more effective than previous compounds in inhibiting GLUK5-containing kainate receptors, suggesting improved options for neurological disorders.
  • CD13 protein levels were found to be elevated in patients with rheumatoid arthritis, linking it directly to the disease's inflammation process.

Frequently asked questions

Does Dr. Alt study rheumatoid arthritis?
Yes, Dr. Alt studies the mechanisms of rheumatoid arthritis and has identified new potential drug targets for treating the condition.
What treatments has Dr. Alt researched?
Dr. Alt has researched treatments for rheumatoid arthritis by targeting the B1R receptor and has developed a compound called UBP296 for neurological disorders.
Is Dr. Alt's work relevant to patients with neurological disorders?
Yes, his research on UBP296 aims to improve treatment options for patients suffering from various neurological conditions.

Publications in plain English

Soluble CD13 induces inflammatory arthritis by activating the bradykinin receptor B1.

2022

The Journal of clinical investigation

Tsou PS, Lu C, Gurrea-Rubio M, Muraoka S, Campbell PL +26 more

Plain English
Researchers discovered that a protein called CD13, which leaks into the bloodstream, causes inflammatory arthritis by activating a receptor called B1R found on joint cells. They confirmed this by showing that blocking B1R with drugs stopped the inflammation in multiple types of arthritis in mice and in human joint tissue samples. This matters because B1R could be a new drug target to treat rheumatoid arthritis and other inflammatory diseases by preventing CD13 from triggering joint inflammation.

PubMed

Characterisation of UBP296: a novel, potent and selective kainate receptor antagonist.

2004

Neuropharmacology

More JC, Nistico R, Dolman NP, Clarke VR, Alt AJ +9 more

Plain English
This study focused on a new compound called UBP296, which blocks a specific type of brain receptor called the GLUK5-containing kainate receptor. Researchers found that UBP296 is highly effective at inhibiting these receptors, performing better than previous compounds, and it specifically reduced calcium levels triggered by glutamate in cells with these receptors. This research is significant because it enhances our understanding of how GLUK5 receptors work, which may lead to better treatments for neurological conditions. Who this helps: Patients with neurological disorders.

PubMed

Publication data sourced from PubMed . Plain-English summaries generated by AI. Not medical advice.