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Targeting Inflammation to Reduce Effects of Alzheimer Disease: RJ Tesi, MD
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The president and chief executive officer of INmune Bio detailed the mechanistic advantages of XPro1595 as a potentially therapeutic benefit for patients with Alzheimer disease and dementia. [WATCH TIME: 5 minutes]
WATCH TIME: 5 minutes
"If nerve cells are dead, you’re not going to recover, you have to relearn. The bottom line is the therpapies for Alzheimer disease that are trying to reestablish dead nerve cells is a losers game. Sick nerve cells will get better, but most importantly, you want to reestablish synaptic function."
At the 2022 Clinical Trials on Alzheimer Disease (CTAD) conference, held November 29 to December 2, in San Francisco, California, a lot of the focus was on anti-amyloid therapies and their impacts on Alzheimer disease (AD). Although promising, many of those within the field, including RJ Tesi, MD, believe it will take a combination of therapies and approaches to truly make a significant impact on the lives of those with the neurodegenerative condition. INmune Bio, a clinical stage biotechnology company, is currently developing XPro1595, a protein biologic designed to decrease neuroinflammation.
As chronic inflammation continues to worsen, patients experience cognitive decline. This inflammation can come from a variety of sources, and the combination and intensity of each of these risk factors can ultimately set the innate immune system astray. XPro1595 is unique in that it targets soluble tumor necrosis factor (TNF). TNF is a potent immune signaling molecule that sits at the apex of inflammation and coordinates immune responses that are both beneficial and detrimental to the patient. It’s been previously reported that TNF is routinely elevated in patients with AD, and considered one of the first inflammatory markers linked to the disease.
Tesi, the president and chief executive officer of INmune, sat down with NeurologyLive® at CTAD 2022 to discuss the therapy and the reasons why it may be potentially beneficial. Additionally, he provided perspective on the role of neuroinflammation in AD, the reasons for developing agents that don’t focus on tau or amyloid-ß, and the future plans of the drug.
