NRF for Traumatic Brain Injury
Recruiting in Palo Alto (17 mi)
+1 other location
Age: 18+
Sex: Male
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Academic
Recruiting
Sponsor: Icahn School of Medicine at Mount Sinai
Disqualifiers: Non-English speaking, Under 18
No Placebo Group
Approved in 1 Jurisdiction
Trial Summary
What is the purpose of this trial?The purpose of this study is to evaluate the effectiveness of NeuroResource Facilitation, a novel/innovative intervention, in reducing recidivism in offenders with brain injury (BI).
Do I need to stop my current medications for the trial?
The trial information does not specify whether you need to stop taking your current medications.
What data supports the effectiveness of the treatment NeuroResource Facilitation (NRF) for Traumatic Brain Injury?
Research suggests that treatments promoting brain recovery, like NRF, may help after a traumatic brain injury by supporting brain cell growth and repair. Although NRF specifically isn't mentioned, similar strategies that encourage brain healing processes show promise in aiding recovery.
12345How is the treatment NeuroResource Facilitation (NRF) unique for traumatic brain injury?
NeuroResource Facilitation (NRF) is unique because it focuses on enhancing the body's natural protective mechanisms by activating the Nrf2 pathway, which helps increase the expression of genes that protect against oxidative damage after a traumatic brain injury. This approach is different from other treatments that may not specifically target these endogenous protective pathways.
23678Eligibility Criteria
This trial is for English-speaking adults over 18 with a history of brain injury, who are returning to specific counties in the U.S. within six months of release from incarceration. They must show significant cognitive impairment on certain tests.Inclusion Criteria
Returning to 6 county area (Bucks, Chester, Delaware, Montgomery, Philadelphia and Schuylkill)
I am 18 years old or older.
Proficient in English
+3 more
Exclusion Criteria
I am younger than 18 years old.
Non-English Speaking
Trial Timeline
Screening
Participants are screened for eligibility to participate in the trial
2-4 weeks
Treatment
Participants receive specialized care management through NeuroResource Facilitation (NRF) both in prison and after release, with weekly to monthly meetings depending on resource needs.
up to 36 months
Weekly to monthly visits (in-person)
Follow-up
Participants are monitored for recidivism and engagement with health/medical resources, productive activities, and community support.
up to 36 months post release
Participant Groups
The study is testing NeuroResource Facilitation (NRF), an innovative approach aimed at reducing repeat offenses among individuals with traumatic brain injuries by providing them with specialized support and resources.
2Treatment groups
Active Control
Group I: NeuroResource FacilitationActive Control1 Intervention
As part of the NRF intervention group, participants will receive specialized care management, both in prison and after the participant goes home. While in the State Correctional Institution (SCI), participants will meet weekly to monthly depending on resource needs, and how close participant is to release with a NeuroResource Facilitator in person who will help participants to understand more about their challenges. Participants may also be referred to a group run by the Facilitator in conjunction with staff from the prison. The facilitator will also tell the participant about resources that are available to help after the participant's release and help participants get connected to them.
Group II: Standard of CareActive Control1 Intervention
As part of the SoC, participants will receive the re-entry services normally receive if not in the study including (but not limited to) Treatment Services, Educational and Vocational Training, Mental Health Management, Reentry and Transitional Services, Population Management and Community Corrections.
NeuroResource Facilitation (NRF) is already approved in United States for the following indications:
🇺🇸 Approved in United States as NeuroResource Facilitation for:
- Support for individuals with traumatic brain injuries
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
Icahn School of Medicine at Mount SinaiNew York, NY
Brain Injury Association of PennsylvaniaCarlisle, PA
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Who Is Running the Clinical Trial?
Icahn School of Medicine at Mount SinaiLead Sponsor
Brain Injury Association of PennsylvaniaCollaborator
References
Experimental neuroprotective agents: nursing challenge. [2019]Neuroprotective agents are investigational drugs that can potentially suppress the development of secondary brain injury following cerebral traumatic injury. Currently, critical care nurses in research centers are challenged to care for these patients during the clinical trial phase of these drugs. Soon, if these drugs pass the trial phase and are approved, critical care nurses in all settings may be administering neuroprotective agents to brain injury patients, identifying side effects, and evaluating their effects on secondary brain injury.
Utility of serum nuclear factor erythroid 2-related factor 2 as a potential prognostic biomarker of severe traumatic brain injury in adults: A prospective cohort study. [2022]Nuclear factor erythroid 2-related factor 2 (Nrf2) may harbor endogenous neuroprotective role. We strived to ascertain the prognostic significance of serum Nrf2 in severe traumatic brain injury (sTBI).
Temporal and spatial dynamics of nrf2-antioxidant response elements mediated gene targets in cortex and hippocampus after controlled cortical impact traumatic brain injury in mice. [2021]The pathophysiological importance of oxidative damage after traumatic brain injury (TBI) has been extensively demonstrated. The transcription factor nuclear factor erythoid related factor 2 (Nrf2) mediates antioxidant and cytoprotective genes by binding to antioxidant response elements (ARE) present in nuclear DNA. In this study, we characterized the time course of Nrf2-ARE-mediated expression in the cortex and hippocampus using a unilateral controlled cortical impact model of focal TBI. Ipsilateral hippocampal and cortical tissue was collected for Western-blot protein analysis (n=6/group) or quantitative reverse transcription-polymerase chain reaction for mRNA (n=3/group) at 3, 6, 12, 24, 48, and 72 h or 1 week post-injury. Multiple genes mediated by Nrf2-ARE were altered post-TBI. Specifically, Nrf2 mRNA increased significantly post-TBI at 48 and 72 h in the cortex and at 48 and 72 h and 1 week in the hippocampus with a coincident increase in glial fibrillary acidic protein mRNA, thereby implying this response is likely occurring in astrocytes. Presumably linked to Nrf2 activation, heme-oxygenase-1, nicotinamide adenine dinucleotide phosphate-quinone-oxidoreductase 1, glutathione reductase, and catalase mRNA overlap throughout the post-injury time course. This study demonstrates the first evidence of such changes during the first week after focal TBI and that increases in expression of some Nrf2-ARE-mediated cytoprotective genes are not observed until 24-48 h post-injury. Unfortunately, this does not precede, but rather coincides with, the occurrence of lipid peroxidative damage. This is the first known comparison between the time course of peroxidative damage and that of Nrf2-ARE activation during the first week post-TBI. These results underscore the necessity to discover pharmacological agents to accelerate and amplify Nrf2-ARE-mediated expression early post-TBI.
Intranasal Nerve Growth Factor administration improves cerebral functions in a child with severe traumatic brain injury: A case report. [2022]Nerve growth factor (NGF) promotes neural recovery after experimental traumatic brain injury (TBI) supporting neuronal growth, differentiation and survival of brain cells and up-regulating the neurogenesis-associated protein Doublecortin (DCX). Only a few studies reported NGF administration in paediatric patients with severe TBI.
Neurorestorative treatments for traumatic brain injury. [2022]Traumatic brain injury (TBI) remains a major cause of death and permanent disability worldwide, especially in children and young adults. A total of 1.5 million people experience head trauma each year in the United States, with an annual economic cost exceeding $56 billion. Unfortunately, almost all Phase III TBI clinical trials have yet to yield a safe and effective neuroprotective treatment, raising questions regarding the use of neuroprotective strategies as the primary therapy for acute brain injuries. Recent preclinical data suggest that neurorestorative strategies that promote angiogenesis (formation of new blood vessels from pre-existing endothelial cells), axonal remodeling (axonal sprouting and pruning), neurogenesis (generation of new neurons) and synaptogenesis (formation of new synapses) provide promising opportunities for the treatment of TBI. This review discusses select cell-based and pharmacological therapies that activate and amplify these endogenous restorative brain plasticity processes to promote both repair and regeneration of injured brain tissue and functional recovery after TBI.
Transcription factor Nrf2 plays a pivotal role in protection against traumatic brain injury-induced acute intestinal mucosal injury in mice. [2009]Traumatic brain injury (TBI) can induce an acute intestinal mucosal injury. Nuclear factor erythroid 2-related factor 2 (Nrf2) has a unique role in many physiological stress processes, but its contribution to intestinal mucosal injury after TBI remains to be determined.
Expression and antioxidation of Nrf2/ARE pathway in traumatic brain injury. [2018]To explore the expression of Nrf2/ARE pathway in hindbrain tissue after the traumatic brain injury (TBI) and its anti-oxidative stress effect in the secondary nerve injury.
Endogenous neuroprotection factors and traumatic brain injury: mechanisms of action and implications for therapy. [2013]Throughout evolution the brain has acquired elegant strategies to protect itself against a variety of environmental insults. Prominent among these are signals released from injured cells that are capable of initiating a cascade of events in neurons and glia designed to prevent further damage. Recent research has identified a remarkably large number of neuroprotection factors (NPFs), whose expression is increased in response to brain injury. Examples include the neurotrophins (NGF, NT-3, NT-5, and BDNF), bFGF, IGFs, TGFs, TNFs and secreted forms of the beta-amyloid precursor protein. Animal and cell culture studies have shown that NPFs can attenuate neuronal injury initiated by insults believed to be relevant to the pathophysiology of traumatic brain injury (TBI) including excitotoxins, ischemia, and free radicals. Studies of the mechanism of action of these NPFs indicate that they enhance cellular systems involved in maintenance of Ca2+ homeostasis and free radical metabolism. Recent work has identified several low-molecular-weight lipophilic compounds that appear to mimic the action of NPFs by activating signal transduction cascades involving tyrosine phosphorylation. Such compounds, alone or in combination with antioxidants and calcium-stabilizing agents, have proved beneficial in animal studies of ischemic brain injury and provide opportunities for development of preventative/therapeutic approaches for TBI.