riluzole has been researched along with Acute Confusional Senile Dementia in 19 studies
Riluzole: A glutamate antagonist (RECEPTORS, GLUTAMATE) used as an anticonvulsant (ANTICONVULSANTS) and to prolong the survival of patients with AMYOTROPHIC LATERAL SCLEROSIS.
| Excerpt | Relevance | Reference |
|---|---|---|
| "This Editorial highlights a remarkable study in the current issue of the Journal of Neurochemistry in which Hascup and coworkers provide novel data showing that riluzole, an anti-glutamatergic drug, may be a promising early intervention strategy for Alzheimer's disease (AD), aimed at restoring glutamate neurotransmission prior to amyloid beta (Aβ) plaque accumulation and cognitive decline." | 8.02 | Hippocampal hyperglutamatergic signaling matters: Early targeting glutamate neurotransmission as a preventive strategy in Alzheimer's disease: An Editorial Highlight for "Riluzole attenuates glutamatergic tone and cognitive decline in AβPP/PS1 mice" on pa ( Gulyaeva, NV, 2021) |
| "In recent years several new treatments have been introduced in neurology, sumatriptan in migraine, riluzole in amyotrophic lateral sclerosis, interferon-beta in multiple sclerosis and rivastigmine in Alzheimer's disease." | 4.80 | [New therapies in neurology, but who benefits?]. ( de Haan, RJ; Vermeulen, M, 1999) |
| "This Editorial highlights a remarkable study in the current issue of the Journal of Neurochemistry in which Hascup and coworkers provide novel data showing that riluzole, an anti-glutamatergic drug, may be a promising early intervention strategy for Alzheimer's disease (AD), aimed at restoring glutamate neurotransmission prior to amyloid beta (Aβ) plaque accumulation and cognitive decline." | 4.02 | Hippocampal hyperglutamatergic signaling matters: Early targeting glutamate neurotransmission as a preventive strategy in Alzheimer's disease: An Editorial Highlight for "Riluzole attenuates glutamatergic tone and cognitive decline in AβPP/PS1 mice" on pa ( Gulyaeva, NV, 2021) |
| "The neurodegenerative disorders (Parkinson's disease, Alzheimer's dementia, Huntington's disease, cerebellar degeneration) are common medical and social problems." | 2.40 | [Neurodegeneration: aging and dementia. Etiopathogenic role of electron transport disorders. Therapeutic possibilities]. ( Klivényi, P; Vécsei, L, 1997) |
| "Current medications for Alzheimer's disease help manage symptoms and behavioral problems." | 1.91 | Riluzole and its prodrugs for the treatment of Alzheimer's disease. ( Al-Horani, RA, 2023) |
| "Riluzole is a glutamate modulator and used as treatment in amyotrophic lateral sclerosis." | 1.56 | Riluzole: a therapeutic strategy in Alzheimer's disease by targeting the WNT/β-catenin pathway. ( Guillevin, R; Lecarpentier, Y; Vallée, A; Vallée, JN, 2020) |
| "Riluzole is known to increase the glutamate transporter EAAT2's ability to scavenge excess glutamate, regulating synaptic transmission." | 1.46 | Age and Alzheimer's disease gene expression profiles reversed by the glutamate modulator riluzole. ( Davidson, RL; Gray, JD; Kogan, JF; McEwen, BS; Morrison, JH; Okamoto, M; Pereira, AC; Rubin, TG, 2017) |
| "Neurodegenerative diseases including Alzheimer's disease are complex to tackle because of the complexity of the brain, both in structure and function." | 1.46 | Using Drugs as Molecular Probes: A Computational Chemical Biology Approach in Neurodegenerative Diseases. ( Emon, MA; Hofmann-Apitius, M; Karki, R; Kodamullil, AT; Younesi, E, 2017) |
| "Treatment with riluzole restored glutamate regulation and rescued memory deficits in the TauP301L model." | 1.43 | Riluzole rescues alterations in rapid glutamate transients in the hippocampus of rTg4510 mice. ( Hickman, JE; Hunsberger, HC; Reed, MN, 2016) |
| "Riluzole-treated TauP301L mice exhibited improved performance in the water radial arm maze and the Morris water maze, associated with a decrease in glutamate release and an increase in glutamate uptake in the dentate gyrus, cornu ammonis 3 (CA3), and cornu ammonis 1 (CA1) regions of the hippocampus." | 1.42 | Riluzole rescues glutamate alterations, cognitive deficits, and tau pathology associated with P301L tau expression. ( Gerhardt, GA; Hickman, JE; Hunsberger, HC; Libell, EM; Reed, MN; Rudy, CC; Speer, RR; Weitzner, DS, 2015) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 3 (15.79) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 9 (47.37) | 24.3611 |
| 2020's | 7 (36.84) | 2.80 |
| Authors | Studies |
|---|---|
| Bulic, B | 1 |
| Pickhardt, M | 1 |
| Mandelkow, E | 1 |
| Hroch, L | 1 |
| Benek, O | 1 |
| Guest, P | 1 |
| Aitken, L | 1 |
| Soukup, O | 1 |
| Janockova, J | 1 |
| Musil, K | 1 |
| Dohnal, V | 1 |
| Dolezal, R | 1 |
| Kuca, K | 1 |
| Smith, TK | 1 |
| Gunn-Moore, F | 1 |
| Musilek, K | 1 |
| Saba, K | 1 |
| Patel, AB | 1 |
| Chintha, N | 1 |
| Jupudi, S | 1 |
| Palathoti, N | 1 |
| Bharathi J, J | 1 |
| Justin, A | 1 |
| Al-Horani, RA | 1 |
| Findley, CA | 1 |
| McFadden, SA | 1 |
| Cox, MF | 1 |
| Sime, LN | 1 |
| Peck, MR | 1 |
| Quinn, K | 1 |
| Bartke, A | 1 |
| Hascup, KN | 1 |
| Hascup, ER | 1 |
| Vallée, A | 1 |
| Vallée, JN | 1 |
| Guillevin, R | 1 |
| Lecarpentier, Y | 1 |
| Gulyaeva, NV | 1 |
| Matthews, DC | 1 |
| Mao, X | 1 |
| Dowd, K | 1 |
| Tsakanikas, D | 1 |
| Jiang, CS | 1 |
| Meuser, C | 1 |
| Andrews, RD | 1 |
| Lukic, AS | 1 |
| Lee, J | 1 |
| Hampilos, N | 1 |
| Shafiian, N | 1 |
| Sano, M | 1 |
| David Mozley, P | 1 |
| Fillit, H | 1 |
| McEwen, BS | 3 |
| Shungu, DC | 1 |
| Pereira, AC | 3 |
| Okamoto, M | 2 |
| Gray, JD | 2 |
| Larson, CS | 1 |
| Kazim, SF | 1 |
| Soya, H | 1 |
| Ittner, AA | 1 |
| Gladbach, A | 1 |
| Bertz, J | 1 |
| Suh, LS | 1 |
| Ittner, LM | 1 |
| Ren, SC | 1 |
| Shao, H | 1 |
| Ji, WG | 1 |
| Jiang, HH | 1 |
| Xu, F | 1 |
| Chen, PZ | 1 |
| Mi, Z | 1 |
| Wen, B | 1 |
| Zhu, GX | 1 |
| Zhu, ZR | 1 |
| Hunsberger, HC | 2 |
| Weitzner, DS | 1 |
| Rudy, CC | 1 |
| Hickman, JE | 2 |
| Libell, EM | 1 |
| Speer, RR | 1 |
| Gerhardt, GA | 1 |
| Reed, MN | 2 |
| Kogan, JF | 1 |
| Davidson, RL | 1 |
| Rubin, TG | 1 |
| Morrison, JH | 1 |
| Emon, MA | 1 |
| Kodamullil, AT | 1 |
| Karki, R | 1 |
| Younesi, E | 1 |
| Hofmann-Apitius, M | 1 |
| Klivényi, P | 1 |
| Vécsei, L | 1 |
| Maloteaux, JM | 1 |
| Vermeulen, M | 1 |
| de Haan, RJ | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Glutamatergic Dysfunction in Cognitive Aging: Riluzole in Mild Alzheimer's Disease[NCT01703117] | Phase 2 | 50 participants (Actual) | Interventional | 2013-11-30 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
"ADCS-ADL is a 23-item inventory developed as a Rater-administered questionnaire answered by the participant's caregiver. It measures performance of basic and instrumental activities of daily living by participants. The total score ranges from 0 to 78, with lower scores indicating greater disease severity.~Obtained for correlation with neuroimaging" (NCT01703117)
Timeframe: baseline to 6 months
| Intervention | score on a scale (Mean) | |
|---|---|---|
| BASELINE | 6 MONTHS | |
| Placebo | 68.0500000 | 64.3000000 |
| Riluzole | 68.3636364 | 65.5000000 |
The ADAS comprises two subscales, cognitive and non-cognitive. The Cognitive Subscale (ADAScog) is a psychometric instrument that includes 11 tasks and evaluates memory, attention, reasoning, language, orientation, and praxis, scored from 0 to 70. The full ADAS total is scored by summing the number of errors made on each task on a range from 0 to 150 so that higher scores indicate worse performance.The non-cognitive component was not used in this study. Obtained for correlation with neuroimaging biomarkers. (NCT01703117)
Timeframe: baseline to 6 months
| Intervention | score on a scale (Mean) | |
|---|---|---|
| BASELINE | 6 MONTHS | |
| Placebo | 17.9005000 | 18.8495000 |
| Riluzole | 22.4981818 | 21.8022727 |
In vivo measurement of glutamate with 1H magnetic resonance spectroscopy (MRS) (a neuroimaging study) in posterior cingulate as a marker of target engagement at three and six months compared to baseline.In vivo brain levels of glutamate, tCr and other major metabolites were obtained using 1H MRS and a 2x2x2-cm3 Posterior Cingulate Cortex voxel of interest in approximately 6.5 minutes using the constant-time point-resolved spectroscopy (CT-PRESS) technique with TE 30 ms, 129 constant-time increments (t1) of 0.8ms, and TR 1500 ms and a receive-only 8-channel phased-array head coil.The levels of glutamate and other metabolites were expressed semi-quantitatively as ratios of peak areas relative to that of the unsuppressed water signal (W) from the same voxels. For consistency with earlier MRS literature, levels of the same metabolites were also expressed as peak ratios relative to tCr area in the same voxel. (NCT01703117)
Timeframe: Change from baseline to 6 months
| Intervention | Ratios (Mean) | |||||
|---|---|---|---|---|---|---|
| BASELINE (Glu/W) | 3 MONTHS (Glu/W) | 6 MONTHS (Glu/W) | BASELINE (Glu/tCr) | 3 MONTHS (Glu/tCr) | 6 MONTHS (Glu/tCr) | |
| Placebo | 0.0677906 | 0.0646162 | 0.0633453 | 0.2367567 | 0.2285644 | 0.2162526 |
| Riluzole | 0.0598059 | 0.0579899 | 0.0609985 | 0.2280186 | 0.2080647 | 0.2339366 |
"Change from baseline to 6 months in cerebral glucose metabolism measured with FDG PET in posterior cingulate cortex, hippocampus, precuneus, and medial temporal, lateral temporal, inferior parietal, and frontal lobes, referred to collectively as our pre-specified regions of interest.~Fluorodeoxyglucose (FDG)-positron emission tomography (PET) is an imaging procedure that measures glucose metabolism in the brain.It is a well-established Alzheimer's disease biomarker and predictor of disease progression. For each FDG PET scan, 5 mCi of fluorodeoxyglucose was administered followed by a 40 minute uptake period during which the participant was in a resting state. Images were acquired on a Siemens Biograph 64mCT scanner as a series of 4 frames of 5 minutes each. Using SPM12 (Wellcome Trust), motion correction was performed and frames averaged into a static image. Each 6 month scan was coregistered to the baseline FDG scan, which was co-registered to the participant's T1-weighted MRI scan." (NCT01703117)
Timeframe: Change from baseline to 6 months
| Intervention | Standardized Uptake Value Ratios (SUVRs) (Mean) | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|
| Posterior cingulate | Precuneus | Temporal | Frontal | Parietal | Hippocampus | Right Hippocampus | AD Progression score | Post Cing - Precuneus | Orbitofrontal | |
| Placebo | -0.048 | -0.032 | -0.023 | -0.129 | -0.020 | -0.018 | -0.021 | 0.579 | -0.041 | -0.019 |
| Riluzole | -0.005 | -0.007 | 0.002 | -0.077 | -0.005 | -0.002 | 0.002 | 0.245 | -0.006 | 0.014 |
N-acetylaspartate (NAA) is a neuronal viability marker measured through magnetic resonance spectroscopy (1H MRS).In vivo brain levels of NAA, glutamate, tCr and other major metabolites were obtained using 1H MRS and a 2x2x2-cm3 Posterior Cingulate Cortex (PC) voxel of interest in approximately 6.5 minutes using the constant-time point-resolved spectroscopy (CT-PRESS) technique with TE 30 ms, 129 constant-time increments (t1) of 0.8ms, and TR 1500 ms and a receive-only 8-channel phased-array head coil.The levels of NAA and other metabolites were expressed semi-quantitatively as ratios of peak areas relative to that of the unsuppressed water signal (W) from the same voxels. For consistency with earlier MRS literature, levels of the same metabolites were also expressed as peak ratios relative to tCr area in the same voxel. (NCT01703117)
Timeframe: Changes from baseline to 6 months
| Intervention | Ratios (Mean) | |||||
|---|---|---|---|---|---|---|
| BASELINE (NAA/W) | 3 MONTHS (NAA/W) | 6 MONTHS (NAA/W) | BASELINE (NAA/tCr) | 3 MONTHS (NAA/tCr) | 6 MONTHS (NAA/tCr) | |
| Placebo | 0.4274546 | 0.4248429 | 0.4415926 | 1.4802620 | 1.4766125 | 1.4811814 |
| Riluzole | 0.3843874 | 0.3996655 | 0.3784181 | 1.4488809 | 1.4271889 | 1.4594796 |
"NPI assesses psychopathology in participants with dementia and other neurologic disorders. Information is obtained from a caregiver familiar with the participant's behavior. Total score ranges from 0 to 144; Higher scores indicate greater disease severity.~Obtained for correlation with neuroimaging" (NCT01703117)
Timeframe: baseline to 6 months
| Intervention | score on a scale (Mean) | |
|---|---|---|
| BASELINE | 6 MONTHS | |
| Placebo | 10.2000000 | 14.0500000 |
| Riluzole | 9.6363636 | 9.0909091 |
3 reviews available for riluzole and Acute Confusional Senile Dementia
| Article | Year |
|---|---|
Progress and developments in tau aggregation inhibitors for Alzheimer disease.
Topics: Alzheimer Disease; Animals; Clinical Trials as Topic; Humans; Hydrogen Bonding; Models, Molecular; P | 2013 |
[Neurodegeneration: aging and dementia. Etiopathogenic role of electron transport disorders. Therapeutic possibilities].
Topics: Aged; Aging; Alzheimer Disease; Calcium Channel Blockers; Cerebellar Diseases; Dementia; Electron Tr | 1997 |
[New therapies in neurology, but who benefits?].
Topics: Alzheimer Disease; Amyotrophic Lateral Sclerosis; Antiviral Agents; Carbamates; Humans; Interferon-b | 1999 |
1 trial available for riluzole and Acute Confusional Senile Dementia
| Article | Year |
|---|---|
Riluzole, a glutamate modulator, slows cerebral glucose metabolism decline in patients with Alzheimer's disease.
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Brain; Double-Blind Method; Female; Glucose; Humans; Mal | 2021 |
15 other studies available for riluzole and Acute Confusional Senile Dementia
| Article | Year |
|---|---|
Design, synthesis and in vitro evaluation of benzothiazole-based ureas as potential ABAD/17β-HSD10 modulators for Alzheimer's disease treatment.
Topics: 3-Hydroxyacyl CoA Dehydrogenases; Alzheimer Disease; Animals; Benzothiazoles; Cell Survival; CHO Cel | 2016 |
Riluzole restores memory and brain energy metabolism in AβPP-PS1 mouse model of Alzheimer's disease.
Topics: Alzheimer Disease; Amyloid beta-Protein Precursor; Animals; Brain; Disease Models, Animal; Energy Me | 2022 |
Topics: Acetylcholinesterase; Alzheimer Disease; Cholinesterase Inhibitors; Humans; Molecular Docking Simula | 2023 |
Riluzole and its prodrugs for the treatment of Alzheimer's disease.
Topics: Alzheimer Disease; Humans; Neuroprotective Agents; Prodrugs; Riluzole | 2023 |
Prodromal Glutamatergic Modulation with Riluzole Impacts Glucose Homeostasis and Spatial Cognition in Alzheimer's Disease Mice.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animals; Cognition; Diseas | 2023 |
Riluzole: a therapeutic strategy in Alzheimer's disease by targeting the WNT/β-catenin pathway.
Topics: Alzheimer Disease; beta Catenin; Gene Expression Regulation; Humans; Neuroprotective Agents; Riluzol | 2020 |
Hippocampal hyperglutamatergic signaling matters: Early targeting glutamate neurotransmission as a preventive strategy in Alzheimer's disease: An Editorial Highlight for "Riluzole attenuates glutamatergic tone and cognitive decline in AβPP/PS1 mice" on pa
Topics: Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animals; Cognitive Dysfunc | 2021 |
Riluzole reduces amyloid beta pathology, improves memory, and restores gene expression changes in a transgenic mouse model of early-onset Alzheimer's disease.
Topics: Alzheimer Disease; Animals; Astrocytes; Cognition; Disease Models, Animal; Gene Expression; Hippocam | 2018 |
p38 MAP kinase-mediated NMDA receptor-dependent suppression of hippocampal hypersynchronicity in a mouse model of Alzheimer's disease.
Topics: Alzheimer Disease; Animals; Disease Models, Animal; Dizocilpine Maleate; Electrodes, Implanted; Elec | 2014 |
Riluzole prevents soluble Aβ1-42 oligomers-induced perturbation of spontaneous discharge in the hippocampal CA1 region of rats.
Topics: Action Potentials; Alzheimer Disease; Amyloid beta-Peptides; Animals; CA1 Region, Hippocampal; Drug | 2015 |
Riluzole rescues glutamate alterations, cognitive deficits, and tau pathology associated with P301L tau expression.
Topics: Alzheimer Disease; Animals; Brain Chemistry; Cognition Disorders; Excitatory Amino Acid Antagonists; | 2015 |
Riluzole rescues alterations in rapid glutamate transients in the hippocampus of rTg4510 mice.
Topics: Alzheimer Disease; Animals; Disease Models, Animal; Glutamic Acid; Hippocampus; Memory Disorders; Mi | 2016 |
Age and Alzheimer's disease gene expression profiles reversed by the glutamate modulator riluzole.
Topics: Age Factors; Aging; Alzheimer Disease; Animals; Cognition; Cognitive Aging; Disease Models, Animal; | 2017 |
Using Drugs as Molecular Probes: A Computational Chemical Biology Approach in Neurodegenerative Diseases.
Topics: Alzheimer Disease; Amyotrophic Lateral Sclerosis; Computational Biology; Computer Simulation; Cyclos | 2017 |
[Clinical pharmacology and therapeutic aspects in certain degenerative neurological diseases].
Topics: Alzheimer Disease; Amyotrophic Lateral Sclerosis; Antiparkinson Agents; Cholinesterase Inhibitors; H | 1996 |