Treatment of Cognitive Deficits After Traumatic Brain InjuryPhase 3NCT06337994
Memantine Hydrochloride for Treatment of Cognitive Dysfunction Due to Traumatic Brain Injury
A Phase 3 study testing Memantine Hydrochloride in people with Treatment of Cognitive Deficits After Traumatic Brain Injury, run by Assiut University at 1 site in Egypt.
Trial summary
Posttraumatic consequences are common causes of disability and long-term morbidity. They include cognitive dysfunction, seizures, headache, dizziness, fatigue, sensory deficits, neurodegeneration and psychiatric disorders (e.g. posttraumatic stress disorder, depression, anxiety, etc). Read more about this study
- Who is it for?
- Ages 18 to 55 yearsHealthy volunteers can take part
- Conditions the study is for
- Treatment of Cognitive Deficits After Traumatic Brain Injury
- What is being tested?
- Memantine Hydrochloride
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 60 participants
- Where
- 1 siteEgypt
- Study dates
- 1 Jan 2024to 1 Aug 2024
- Phase
- Phase 3
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 55 years
- All sexes
- Healthy volunteers accepted
- Adult
Who may be able to join
- Adults (age: 18 - 60 years old)
- History of primary traumatic closed head injury
- At least 6 months after TBI
- Mild/moderate previous TBI
- Normal neuroimaging of the brain at the period of the study.
Who cannot join
- Secondary injury or superimpose injury on a brain already affected by a mechanical injury
- patients with duration of illness less than 6 months
- History of open or severe head injuries
- Severe neurologic consequences after TBI
- Post traumatic seizures
- Posttraumatic hydrocephalus'
Show all 11Show fewer
- Posttraumatic abnormal neuroimaging of the brain
- History of chronic mental or neurologic disorders (e.g. comorbid schizophrenia, severe manic phase of bipolar disorder or intellectual disability).
- Substance abuse
- Pregnancy
- Individuals with the following physical conditions that are described in manufacturer's package including history of epilepsy or convulsion, renal dysfunction, factors increasing urine pH and severe liver dysfunction
Trial locations and contacts
1 site in 1 country.
Egypt1 site
Assiut University, Faculty of Medicine, Hospital of Neurology, Psychiatry and Neurosurgery
Asyut, 71516
About this study
Official title: Treatment of Post-traumatic Cognitive Dysfunction With Memantine Hydrochloride, an N-methyl-D-aspartate (NMDA)-Type Receptor Blocker: a Clinical Trial
Posttraumatic consequences are common causes of disability and long-term morbidity. They include cognitive dysfunction, seizures, headache, dizziness, fatigue, sensory deficits, neurodegeneration and psychiatric disorders (e.g. posttraumatic stress disorder, depression, anxiety, etc). Diffuse axonal injury and disruption of normal neuronal function are the most common and important pathologic features of traumatic primary closed head injury. depression, anxiety, etc). Excitotoxicity and apoptosis caused by activation of N-methyl-D-aspartate (NMDA) glutamate receptors, are two main suggested mechanisms of traumatic neuronal cell death and posttraumtic neurologic adverse consequences. Experimental and clinical studies have demonstrated that memantine hydrochloride, NMDA-type glutamate receptor antagonist, could have beneficial effect in treatment of posttraumatic cognitive dysfunction. Memantine may contribute to cognitive improvements in TBI by decreasing the synaptic 'noise' resulting from excessive NMDA receptor activation, inhibition of β-amyloid mediated toxicity and readjustment of the balance between inhibition and excitation on neuronal networks in the central nervous system (CNS).
Read the detailed description
Posttraumatic consequences are common causes of disability and long-term morbidity. Traumatic brain injuries (TBIs) are traditionally classified into primary and secondary injuries. Primary brain injury is usually mechanically induced and occurs at the moment of injury while secondary injury is not mechanically induced, delayed from the moment of injury and may superimpose a previously injured brain by mechanical forces. Primary brain injury may be associated with focal scalp injury, skull fractures, brain contusion caused by contact (i.e. an object striking the head or the brain striking the inside of the skull) as well as diffuse axonal brain injury which is usually caused by acceleration-deceleration forces or rotational acceleration of the brain as a result of unrestricted movement of the head, shearing and tensile forces and compressive strains. Diffuse axonal injury and disruption of normal neuronal function are the most common and important pathologic features of TBI. The latter is mostly microscopic damage and is often not visible in neuroimaging. Consequences of TBI include cognitive dysfunction, seizures, headache, dizziness, fatigue, sensory deficits, neurodegeneration and psychiatric disorders (e.g. posttraumatic stress disorder, depression, anxiety, etc). Excitotoxicity and apoptosis are two main suggested mechanisms of traumatic neuronal cell death. The N-methyl-D-aspartate (NMDA) glutamate receptors are implicated in these mechanisms. Furthermore, the activation of NMDA receptors by glutamate promotes the production of reactive oxygen species (ROS) and nitric oxide (NO) which further exacerbate secondary cell injury. NMDA receptor plays a pivotal role in learning and memory. Experimental and clinical studies have demonstrated that memantine hydrochloride, NMDA-type glutamate receptor antagonist, could have beneficial effect in treatment of posttraumatic cognitive dysfunction. Memantine is an FDA-approved drug for the treatment of moderate to severe Alzheimer's disease and is also used clinically for the treatment of some patients with Parkinson's disease. Memantine is effective in blocking excessive activity of NMDA-type glutamate receptors and reduces the progression of dementia. Memantine has shown to be neuroprotective in animal models of cerebral and spinal cord ischemia and in models of TBI. Memantine may contribute to cognitive improvements in TBI by decreasing the synaptic 'noise' resulting from excessive NMDA receptor activation, inhibition of β-amyloid mediated toxicity and readjustment of the balance between inhibition and excitation on neuronal networks in the CNS. It showed beneficial effects in treating post-injury synaptic dysfunction in the neocortex, partially reversing deficits in long-term potentiation (LTP), mitigating pathologic NMDAR loss, and reducing tau phosphorylation and β-amyloid expression. Memantine spares hippocampal neurons after a single moderate/severe or repetitive TBI and normalizes LTP, β-amyloid and tau expressions, and neuroinflammation abnormalities in a repeat experimental model of TBI. In rodent studies, memantine dramatically increased adult hippocampal neurogenesis. Memantine does not have the significant negative side effects, such as hallucinations and coma of other NMDAR antagonists. High doses (≥20 mg/d) may cause non-serious side effects, e.g. dizziness, anxiety, restlessness or agitation,
- Being tested
- Memantine Hydrochloride
- Keywords
- Traumatic brain injury, closed head injury, cognition, memory, N-methyl-D-aspartate (NMDA)-type receptors, NMDA blocker, memantine hydrochloride
- Medical subject headings
- Brain Injuries, Traumatic, Head Injuries, Closed
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Memantine HydrochlorideDrug
Also called Active arm
Memantine was added to each patient's current medication, with the initial dosage of 5 mg/day (once daily). The dosage was then increased to 10 mg/day after a week and maintained till the end of the study. In the case of intolerance to this increase, the dosage was flexibly adjusted according to the condition of the patient.
| Study group | Role | What they receive |
|---|---|---|
| Drug treatment (interventional) | Active comparator | - number of participant: >/= 60. This open-label clinical trial consisted of 24 weeks of memantine intake period, followed by 4-week (or more) post-trial observation period to monitor the drug adverse effects (e.g. sleep problems, sleepiness, sedation, anxiety, weight change and hypotension). Clinic visits will be scheduled at baseline and follow-ups after 6, 12, 18, 24 weeks of treatment initiation. Concomitant medications were essentially kept unchanged during the trial, i.e. the intake of antidepressant or antianxiologic psychotropic medications, psychotherapy to treat depressive or anxiety symptoms does not exclude participation in the study.
Memantine was added to each patient's current medication, with the initial dosage of 5 mg/day (once daily). The dosage was then increased to 10 mg/day after a week and maintained till the end of the study. In the case of intolerance to this increase, the dosage was flexibly adjusted according to the condition of the patient. Receives: Drug: Memantine Hydrochloride |
| No intervention | No intervention | number of participants: >/= 40 |
What is being measured
The primary outcome is the main question the study is designed to answer.
The severity of traumatic brain injury (TBI)
(1) The severity of TBI at onset which was assessed according to (a) Glasgow coma scale (GCS) determined at the time of injury. (b)The duration of loss of consciousness (LOC) at the time of injury: (c) The time elapsed from injury to the moment when patients can demonstrate continuous memory of what is happening around them (i.e. orientation).
Measured: Baseline
The symptoms of depression
(2) Beck's Depression Inventory - II (BDI-II)
Measured: Baseline
The symptoms of anxiety
(3) Hamilton Anxiety Rating Scale (HAM-A):
Measured: baseline
The cognitive function
The validated versions of Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) will be used to assess cognition. Each takes ~10-15 min to be administered.
Measured: baseline
Secondary outcomes (2)
Quality of life after drug treatment
(1) The brief WHO quality of life questionnaire (WHOQOL-brief) will be used for assessment. WHO defines Quality of Life as an individual's perception of their position in life in the context of the culture and value systems in which they live and in relation to their goals, expectations, standards and concerns.
Measured: 8, 16, and 24 weeks
Re-evaluation of the cognitive function after drug treatment
The validated versions of Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) were used to assess cognition as described above.
Measured: 8, 16, and 24 weeks
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted29 Mar 2024
- Study start1 Jan 2024
- Primary completion1 Jun 2024
- Study completion1 Aug 2024
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (10)Papers the sponsor has linked to this study.
- Other trials for Treatment of Cognitive Deficits After Traumatic Brain InjuryStudies of the same condition, open and under way.
- More trials run by Assiut UniversityThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 3
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Model description
- parallel assignment
- Masking
- None (open label)
- Enrolment
- 60 participants (actual)
Sponsor and investigators
- Lead sponsor
- Assiut University
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Sherifa Ahmed Hamed, Assiut University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06337994
- Sponsor's protocol ID
- AUH-Neurol-TBI_2024
- Status last verified
- Aug 2024
- First submitted
- 23 Mar 2024
- Last updated
- 7 Aug 2024
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Bramlett HM, Dietrich WD. Long-Term Consequences of Traumatic Brain Injury: Current Status of Potential Mechanisms of Injury and Neurological Outcomes. J Neurotrauma. 2015 Dec 1;32(23):1834-48. doi: 10.1089/neu.2014.3352. Epub 2014 Dec 19.
PubMed 25158206Guerriero RM, Giza CC, Rotenberg A. Glutamate and GABA imbalance following traumatic brain injury. Curr Neurol Neurosci Rep. 2015 May;15(5):27. doi: 10.1007/s11910-015-0545-1.
PubMed 25796572Effgen GB, Morrison B 3rd. Memantine Reduced Cell Death, Astrogliosis, and Functional Deficits in an in vitro Model of Repetitive Mild Traumatic Brain Injury. J Neurotrauma. 2017 Feb 15;34(4):934-942. doi: 10.1089/neu.2016.4528. Epub 2016 Aug 8.
PubMed 27450515Chamoun R, Suki D, Gopinath SP, Goodman JC, Robertson C. Role of extracellular glutamate measured by cerebral microdialysis in severe traumatic brain injury. J Neurosurg. 2010 Sep;113(3):564-70. doi: 10.3171/2009.12.JNS09689.
PubMed 20113156Girouard H, Wang G, Gallo EF, Anrather J, Zhou P, Pickel VM, Iadecola C. NMDA receptor activation increases free radical production through nitric oxide and NOX2. J Neurosci. 2009 Feb 25;29(8):2545-52. doi: 10.1523/JNEUROSCI.0133-09.2009.
PubMed 19244529Sattler R, Xiong Z, Lu WY, Hafner M, MacDonald JF, Tymianski M. Specific coupling of NMDA receptor activation to nitric oxide neurotoxicity by PSD-95 protein. Science. 1999 Jun 11;284(5421):1845-8. doi: 10.1126/science.284.5421.1845.
PubMed 10364559Lipton SA. The molecular basis of memantine action in Alzheimer's disease and other neurologic disorders: low-affinity, uncompetitive antagonism. Curr Alzheimer Res. 2005 Apr;2(2):155-65. doi: 10.2174/1567205053585846.
PubMed 15974913Chen HS, Wang YF, Rayudu PV, Edgecomb P, Neill JC, Segal MM, Lipton SA, Jensen FE. Neuroprotective concentrations of the N-methyl-D-aspartate open-channel blocker memantine are effective without cytoplasmic vacuolation following post-ischemic administration and do not block maze learning or long-term potentiation. Neuroscience. 1998 Oct;86(4):1121-32. doi: 10.1016/s0306-4522(98)00163-8.
PubMed 9697119Dogan A, Eras MA, Rao VL, Dempsey RJ. Protective effects of memantine against ischemia-reperfusion injury in spontaneously hypertensive rats. Acta Neurochir (Wien). 1999;141(10):1107-13. doi: 10.1007/s007010050491.
PubMed 10550658Mei Z, Qiu J, Alcon S, Hashim J, Rotenberg A, Sun Y, Meehan WP 3rd, Mannix R. Memantine improves outcomes after repetitive traumatic brain injury. Behav Brain Res. 2018 Mar 15;340:195-204. doi: 10.1016/j.bbr.2017.04.017. Epub 2017 Apr 13.
PubMed 28412305
Study at a glance
From the registry record, last updated by the sponsor on 7 Aug 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Treatment of Post-traumatic Cognitive Dysfunction With Memantine Hydrochloride, an N-methyl-D-aspartate (NMDA)-Type Receptor Blocker: a Clinical Trial
- ClinicalTrials.gov ID
- NCT06337994
- Acronym / sponsor ID
- AUH-Neurol-TBI_2024
- Keywords
- Traumatic brain injury, closed head injury, cognition, memory, N-methyl-D-aspartate (NMDA)-type receptors, NMDA blocker, memantine hydrochloride
- Phase
- Phase 3
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 60 participants (actual)
- Lead sponsor
- Assiut UniversityUniversity, hospital or other
- Study start
- 1 Jan 2024 (actual)
- Primary completion
- 1 Jun 2024 (actual)
- Study completion
- 1 Aug 2024 (actual)
- First posted
- 29 Mar 2024 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Posttraumatic consequences are common causes of disability and long-term morbidity. They include cognitive dysfunction, seizures, headache, dizziness, fatigue, sensory deficits, neurodegeneration and psychiatric disorders (e.g. posttraumatic stress disorder, depression, anxiety, etc). Diffuse axonal injury and disruption of normal neuronal function are the most common and important pathologic features of traumatic primary closed head injury. depression, anxiety, etc). Excitotoxicity and apoptosis caused by activation of N-methyl-D-aspartate (NMDA) glutamate receptors, are two main suggested mechanisms of traumatic neuronal cell death and posttraumtic neurologic adverse consequences. Experimental and clinical studies have demonstrated that memantine hydrochloride, NMDA-type glutamate receptor antagonist, could have beneficial effect in treatment of posttraumatic cognitive dysfunction. Memantine may contribute to cognitive improvements in TBI by decreasing the synaptic 'noise' resulting from excessive NMDA receptor activation, inhibition of β-amyloid mediated toxicity and readjustment of the balance between inhibition and excitation on neuronal networks in the central nervous system (CNS).
Detailed description
Posttraumatic consequences are common causes of disability and long-term morbidity. Traumatic brain injuries (TBIs) are traditionally classified into primary and secondary injuries. Primary brain injury is usually mechanically induced and occurs at the moment of injury while secondary injury is not mechanically induced, delayed from the moment of injury and may superimpose a previously injured brain by mechanical forces. Primary brain injury may be associated with focal scalp injury, skull fractures, brain contusion caused by contact (i.e. an object striking the head or the brain striking the inside of the skull) as well as diffuse axonal brain injury which is usually caused by acceleration-deceleration forces or rotational acceleration of the brain as a result of unrestricted movement of the head, shearing and tensile forces and compressive strains. Diffuse axonal injury and disruption of normal neuronal function are the most common and important pathologic features of TBI. The latter is mostly microscopic damage and is often not visible in neuroimaging. Consequences of TBI include cognitive dysfunction, seizures, headache, dizziness, fatigue, sensory deficits, neurodegeneration and psychiatric disorders (e.g. posttraumatic stress disorder, depression, anxiety, etc). Excitotoxicity and apoptosis are two main suggested mechanisms of traumatic neuronal cell death. The N-methyl-D-aspartate (NMDA) glutamate receptors are implicated in these mechanisms. Furthermore, the activation of NMDA receptors by glutamate promotes the production of reactive oxygen species (ROS) and nitric oxide (NO) which further exacerbate secondary cell injury. NMDA receptor plays a pivotal role in learning and memory. Experimental and clinical studies have demonstrated that memantine hydrochloride, NMDA-type glutamate receptor antagonist, could have beneficial effect in treatment of posttraumatic cognitive dysfunction. Memantine is an FDA-approved drug for the treatment of moderate to severe Alzheimer's disease and is also used clinically for the treatment of some patients with Parkinson's disease. Memantine is effective in blocking excessive activity of NMDA-type glutamate receptors and reduces the progression of dementia. Memantine has shown to be neuroprotective in animal models of cerebral and spinal cord ischemia and in models of TBI. Memantine may contribute to cognitive improvements in TBI by decreasing the synaptic 'noise' resulting from excessive NMDA receptor activation, inhibition of β-amyloid mediated toxicity and readjustment of the balance between inhibition and excitation on neuronal networks in the CNS. It showed beneficial effects in treating post-injury synaptic dysfunction in the neocortex, partially reversing deficits in long-term potentiation (LTP), mitigating pathologic NMDAR loss, and reducing tau phosphorylation and β-amyloid expression. Memantine spares hippocampal neurons after a single moderate/severe or repetitive TBI and normalizes LTP, β-amyloid and tau expressions, and neuroinflammation abnormalities in a repeat experimental model of TBI. In rodent studies, memantine dramatically increased adult hippocampal neurogenesis. Memantine does not have the significant negative side effects, such as hallucinations and coma of other NMDAR antagonists. High doses (≥20 mg/d) may cause non-serious side effects, e.g. dizziness, anxiety, restlessness or agitation,
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Number of arms
- 2
- Model description
- parallel assignment
| Arm | Type | Receives |
|---|---|---|
| Drug treatment (interventional) | Active comparator | Drug: Memantine Hydrochloride- number of participant: >/= 60. This open-label clinical trial consisted of 24 weeks of memantine intake period, followed by 4-week (or more) post-trial observation period to monitor the drug adverse effects (e.g. sleep problems, sleepiness, sedation, anxiety, weight change and hypotension). Clinic visits will be scheduled at baseline and follow-ups after 6, 12, 18, 24 weeks of treatment initiation. Concomitant medications were essentially kept unchanged during the trial, i.e. the intake of antidepressant or antianxiologic psychotropic medications, psychotherapy to treat depressive or anxiety symptoms does not exclude participation in the study. Memantine was added to each patient's current medication, with the initial dosage of 5 mg/day (once daily). The dosage was then increased to 10 mg/day after a week and maintained till the end of the study. In the case of intolerance to this increase, the dosage was flexibly adjusted according to the condition of the patient. |
| No intervention | No intervention | –number of participants: >/= 40 |
Who may qualify
- Ages
- 18 to 55 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (5 listed)
- Adults (age: 18 - 60 years old)
- History of primary traumatic closed head injury
- At least 6 months after TBI
- Mild/moderate previous TBI
- Normal neuroimaging of the brain at the period of the study.
Key exclusion criteria (11 listed)
- Secondary injury or superimpose injury on a brain already affected by a mechanical injury
- patients with duration of illness less than 6 months
- History of open or severe head injuries
- Severe neurologic consequences after TBI
- Post traumatic seizures
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Memantine HydrochlorideAlso: Active armMemantine was added to each patient's current medication, with the initial dosage of 5 mg/day (once daily). The dosage was then increased to 10 mg/day after a week and maintained till the end of the study. In the case of intolerance to this increase, the dosage was flexibly adjusted according to the condition of the patient. | Drug | Drug treatment (interventional) |
Primary outcome
The severity of traumatic brain injury (TBI)
Time frame: Baseline
(1) The severity of TBI at onset which was assessed according to (a) Glasgow coma scale (GCS) determined at the time of injury. (b)The duration of loss of consciousness (LOC) at the time of injury: (c) The time elapsed from injury to the moment when patients can demonstrate continuous memory of what is happening around them (i.e. orientation).
The symptoms of depression
Time frame: Baseline
(2) Beck's Depression Inventory - II (BDI-II)
The symptoms of anxiety
Time frame: baseline
(3) Hamilton Anxiety Rating Scale (HAM-A):
The cognitive function
Time frame: baseline
The validated versions of Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) will be used to assess cognition. Each takes ~10-15 min to be administered.
2 secondary outcomes
Quality of life after drug treatment
Time frame: 8, 16, and 24 weeks
Re-evaluation of the cognitive function after drug treatment
Time frame: 8, 16, and 24 weeks
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 7 Aug 2024.
- Background: PubMed 25158206Bramlett HM, Dietrich WD. Long-Term Consequences of Traumatic Brain Injury: Current Status of Potential Mechanisms of Injury and Neurological Outcomes. J Neurotrauma. 2015 Dec 1;32(23):1834-48. doi: 10.1089/neu.2014.3352. Epub 2014 Dec 19.
- Background: PubMed 25796572Guerriero RM, Giza CC, Rotenberg A. Glutamate and GABA imbalance following traumatic brain injury. Curr Neurol Neurosci Rep. 2015 May;15(5):27. doi: 10.1007/s11910-015-0545-1.
- Background: PubMed 27450515Effgen GB, Morrison B 3rd. Memantine Reduced Cell Death, Astrogliosis, and Functional Deficits in an in vitro Model of Repetitive Mild Traumatic Brain Injury. J Neurotrauma. 2017 Feb 15;34(4):934-942. doi: 10.1089/neu.2016.4528. Epub 2016 Aug 8.
- Background: PubMed 20113156Chamoun R, Suki D, Gopinath SP, Goodman JC, Robertson C. Role of extracellular glutamate measured by cerebral microdialysis in severe traumatic brain injury. J Neurosurg. 2010 Sep;113(3):564-70. doi: 10.3171/2009.12.JNS09689.
- Background: PubMed 19244529Girouard H, Wang G, Gallo EF, Anrather J, Zhou P, Pickel VM, Iadecola C. NMDA receptor activation increases free radical production through nitric oxide and NOX2. J Neurosci. 2009 Feb 25;29(8):2545-52. doi: 10.1523/JNEUROSCI.0133-09.2009.
- Background: PubMed 10364559Sattler R, Xiong Z, Lu WY, Hafner M, MacDonald JF, Tymianski M. Specific coupling of NMDA receptor activation to nitric oxide neurotoxicity by PSD-95 protein. Science. 1999 Jun 11;284(5421):1845-8. doi: 10.1126/science.284.5421.1845.
- Background: PubMed 15974913Lipton SA. The molecular basis of memantine action in Alzheimer's disease and other neurologic disorders: low-affinity, uncompetitive antagonism. Curr Alzheimer Res. 2005 Apr;2(2):155-65. doi: 10.2174/1567205053585846.
- Background: PubMed 9697119Chen HS, Wang YF, Rayudu PV, Edgecomb P, Neill JC, Segal MM, Lipton SA, Jensen FE. Neuroprotective concentrations of the N-methyl-D-aspartate open-channel blocker memantine are effective without cytoplasmic vacuolation following post-ischemic administration and do not block maze learning or long-term potentiation. Neuroscience. 1998 Oct;86(4):1121-32. doi: 10.1016/s0306-4522(98)00163-8.
- Background: PubMed 10550658Dogan A, Eras MA, Rao VL, Dempsey RJ. Protective effects of memantine against ischemia-reperfusion injury in spontaneously hypertensive rats. Acta Neurochir (Wien). 1999;141(10):1107-13. doi: 10.1007/s007010050491.
- Background: PubMed 28412305Mei Z, Qiu J, Alcon S, Hashim J, Rotenberg A, Sun Y, Meehan WP 3rd, Mannix R. Memantine improves outcomes after repetitive traumatic brain injury. Behav Brain Res. 2018 Mar 15;340:195-204. doi: 10.1016/j.bbr.2017.04.017. Epub 2017 Apr 13.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
The record lists no contact. Use the official record to reach the sponsor.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 3 study testing Memantine Hydrochloride in people with Treatment of Cognitive Deficits After Traumatic Brain Injury, run by Assiut University at 1 site in Egypt.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 11 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 7 Aug 2024. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Egypt. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 3 studies compare the treatment with the current standard treatment or a placebo in a large group, to confirm how well it works and watch for side effects.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
The severity of traumatic brain injury (TBI) (time frame: Baseline). The study lists 4 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT06337994, which also lists 10 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 7 Aug 2024.