News & Media
NeurAegis Announces Publication of Preclinical Animal Data Supporting Calpain-2 as a Promising Therapeutic Target for Concussion
SOUTHBOROUGH, Mass., July 1, 2020 /PRNewswire/ — NeurAegis, Inc., a neuropharmaceutical company pioneering the development of breakthrough treatments for neurological disorders, today announced the publication of a paper titled “Calpain-2 as a therapeutic target in repeated concussion-induced neuropathy and behavioral impairment” in Science Advances. The studies reported in the publication were performed in the laboratory of NeurAegis’ scientific founder, Dr. Michel Baudry, at Western University of Health Sciences, Pomona, CA, where the neurodegenerative role of the protease calpain-2 in repeated concussions was investigated. These studies lend further scientific rationale for the Company’s focus on developing novel calpain-2 inhibitors as therapeutic agents for concussion.
NeurAegis Scientific Founder Michel Baudry Awarded $3.8M Grant from the Department of Defense to Advance Product Candidate for Treating Traumatic Brain Injury and Concussion
SOUTHBOROUGH, Mass., Sept. 5, 2019 /PRNewswire/ — NeurAegis, Inc., a privately held pharmaceutical company pioneering the development of breakthrough treatments for neurological disorders, announced today that its scientific founder, Dr. Michel Baudry, has been awarded a multi-year, $3.8 million grant from the Department of Defense’s Combat Casualty Care Research Program. This project is focused on optimizing a neuroprotective drug candidate for traumatic brain injury (TBI) and concussion and the DOD funds will support medicinal chemistry and preclinical studies in preparation for a first-in-human Phase I clinical trial.
SELECTED PUBLICATIONS AND POSTERS
Prolonged calpain-2 activation in hippocampus plays a critical role in seizure-induced neuropathology
Calpain has been proposed to play a critical role in the development of epilepsy, since this calcium-dependent protease is activated after seizures and is involved in neurodegeneration. In the present study we used conditional calpain-2 knock-out mice and a selective calpain-2 inhibitor to analyze the role of calpain-2 in epilepsy using the kainic acid model of epilepsy elicited by repeated injections of low doses of kainic acid. Neurodegeneration was evident in various hippocampal subfields, and in particular in the hilus of the dentate gyrus 7 days after KA-induced seizures.
Differential Activation of Calpain-1 and Calpain-2 following Kainate-Induced Seizure Activity in Rats and Mice.
Systemic injection of kainate produces repetitive seizure activity in both rats and mice. It also results in short-term synaptic modifications aswell as delayed neurodegeneration. The signaling cascades involved in both short-term and delayed responses are not clearly defined. The calcium-dependent protease calpain is activated in various brain structures following systemic kainate injection, although the precise involvement of the two major brain calpain isoforms, calpain-1 and calpain-2, remains to be defined.
Calpain-2 as a therapeutic target for acute neuronal injury.
Protection against TBI-Induced Neuronal Death with Post-Treatment with a Selective Calpain-2 Inhibitor in Mice.
Traumatic brain injury (TBI) is a significant public health problem in the United States. In 2010 alone, an estimated 2.5 million TBI patients presented for treatment, and it is likely that many more cases are never reported. The financial burden for the society is enormous, as many patients with TBI completely lose the ability to be self-sufficient and require long-term medical and rehabilitative care. Among the different types of TBI, penetrating TBI produces the worst outcomes and highest morality rates.
Calpain-1 and Calpain-2: The Yin and Yang of Synaptic Plasticity and Neurodegeneration.
Many signaling pathways participate in both synaptic plasticity and neuronal degeneration. While calpains participate in these phenomena, very few studies have evaluated the respective roles of the two major calpain isoforms in the brain, calpain-1 and calpain-2. We review recent studies indicating that calpain-1 and calpain-2 exhibit opposite functions in both synaptic plasticity and neurodegeneration. Calpain-1 activation is required for the induction of long-term potentiation (LTP) and is generally neuroprotective, while calpain-2 activation limits the extent of potentiation and is neurodegenerative.