valproic acid has been researched along with Amyotrophic Lateral Sclerosis in 14 studies
Valproic Acid: A fatty acid with anticonvulsant and anti-manic properties that is used in the treatment of EPILEPSY and BIPOLAR DISORDER. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of VOLTAGE-GATED SODIUM CHANNELS.
valproic acid : A branched-chain saturated fatty acid that comprises of a propyl substituent on a pentanoic acid stem.
Amyotrophic Lateral Sclerosis: A degenerative disorder affecting upper MOTOR NEURONS in the brain and lower motor neurons in the brain stem and SPINAL CORD. Disease onset is usually after the age of 50 and the process is usually fatal within 3 to 6 years. Clinical manifestations include progressive weakness, atrophy, FASCICULATION, hyperreflexia, DYSARTHRIA, dysphagia, and eventual paralysis of respiratory function. Pathologic features include the replacement of motor neurons with fibrous ASTROCYTES and atrophy of anterior SPINAL NERVE ROOTS and corticospinal tracts. (From Adams et al., Principles of Neurology, 6th ed, pp1089-94)
| Excerpt | Relevance | Reference |
|---|---|---|
| "This study provides a systematic review and meta-analysis of randomized controlled trials (RCTs) investigating the safety and efficacy of lithium in amyotrophic lateral sclerosis (ALS) patients." | 9.41 | Safety and efficacy of lithium in patients with amyotrophic lateral sclerosis: a systematic review and meta-analysis of randomized controlled trials. ( Al-Dardery, NM; Attia, AN; Hamad, AA; Meshref, M; Mohamed, SF, 2023) |
| "To determine whether valproic acid (VPA), a histone deacetylase inhibitor that showed antioxidative and antiapoptotic properties and reduced glutamate toxicity in preclinical studies, is safe and effective in amyotrophic lateral sclerosis (ALS) using a sequential trial design." | 9.14 | Randomized sequential trial of valproic acid in amyotrophic lateral sclerosis. ( de Jong, JM; de Jong, SW; de Visser, M; Groeneveld, GJ; Piepers, S; Scheffer, H; Schelhaas, HJ; Uijtendaal, EV; van den Berg, LH; van der Pol, WL; van der Tweel, I; Veldink, JH; Wokke, JH, 2009) |
| "The aim of this study was to evaluate the ability of lithium carbonate and valproate cotreatment to modify the survival rate and functional score of patients with definite sporadic amyotrophic lateral sclerosis (ALS)." | 7.80 | Clinical and biological changes under treatment with lithium carbonate and valproic acid in sporadic amyotrophic lateral sclerosis. ( Alcaraz-Zubeldia, M; Bayliss, L; Boll, MC; Burgos, J; Montes, S; Peñaloza-Solano, G; Rios, C; Vargas-Cañas, S, 2014) |
| "This study provides a systematic review and meta-analysis of randomized controlled trials (RCTs) investigating the safety and efficacy of lithium in amyotrophic lateral sclerosis (ALS) patients." | 5.41 | Safety and efficacy of lithium in patients with amyotrophic lateral sclerosis: a systematic review and meta-analysis of randomized controlled trials. ( Al-Dardery, NM; Attia, AN; Hamad, AA; Meshref, M; Mohamed, SF, 2023) |
| " We report here that, while dietary supplementation with high VPA dosage slows down motor neuron death, as assessed by measurement of a specific marker for cholinergic neurons in the spinal cord, it has no significant effect on lifespan." | 5.35 | Long-term dietary administration of valproic acid does not affect, while retinoic acid decreases, the lifespan of G93A mice, a model for amyotrophic lateral sclerosis. ( Bonamassa, B; Canistro, D; Contestabile, A; Crochemore, C; Paolini, M; Pena-Altamira, E; Virgili, M, 2009) |
| "To determine whether valproic acid (VPA), a histone deacetylase inhibitor that showed antioxidative and antiapoptotic properties and reduced glutamate toxicity in preclinical studies, is safe and effective in amyotrophic lateral sclerosis (ALS) using a sequential trial design." | 5.14 | Randomized sequential trial of valproic acid in amyotrophic lateral sclerosis. ( de Jong, JM; de Jong, SW; de Visser, M; Groeneveld, GJ; Piepers, S; Scheffer, H; Schelhaas, HJ; Uijtendaal, EV; van den Berg, LH; van der Pol, WL; van der Tweel, I; Veldink, JH; Wokke, JH, 2009) |
| "The aim of this study was to evaluate the ability of lithium carbonate and valproate cotreatment to modify the survival rate and functional score of patients with definite sporadic amyotrophic lateral sclerosis (ALS)." | 3.80 | Clinical and biological changes under treatment with lithium carbonate and valproic acid in sporadic amyotrophic lateral sclerosis. ( Alcaraz-Zubeldia, M; Bayliss, L; Boll, MC; Burgos, J; Montes, S; Peñaloza-Solano, G; Rios, C; Vargas-Cañas, S, 2014) |
| " We report here that, while dietary supplementation with high VPA dosage slows down motor neuron death, as assessed by measurement of a specific marker for cholinergic neurons in the spinal cord, it has no significant effect on lifespan." | 1.35 | Long-term dietary administration of valproic acid does not affect, while retinoic acid decreases, the lifespan of G93A mice, a model for amyotrophic lateral sclerosis. ( Bonamassa, B; Canistro, D; Contestabile, A; Crochemore, C; Paolini, M; Pena-Altamira, E; Virgili, M, 2009) |
| "Valproic acid (VPA) has long been used as an antiepileptic drug and recently as a mood stabilizer, and evidence is increasing that VPA exerts neuroprotective effects through changes in a variety of intracellular signalling pathways including upregulation of Bcl-2 protein with an antiapoptotic property and inhibiting glycogen synthase kinase 3-beta, which is considered to promote cell survival." | 1.32 | Benefit of valproic acid in suppressing disease progression of ALS model mice. ( Goto, M; Hamasaki, T; Miyaguchi, K; Sakoda, S; Sugai, F; Sumi, H; Yamamoto, Y; Zhou, Z, 2004) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 6 (42.86) | 29.6817 |
| 2010's | 5 (35.71) | 24.3611 |
| 2020's | 3 (21.43) | 2.80 |
| Authors | Studies |
|---|---|
| Gyawali, A | 1 |
| Latif, S | 1 |
| Choi, SH | 1 |
| Hyeon, SJ | 1 |
| Ryu, H | 3 |
| Kang, YS | 1 |
| Bankole, O | 1 |
| Scambi, I | 1 |
| Parrella, E | 1 |
| Muccilli, M | 1 |
| Bonafede, R | 1 |
| Turano, E | 1 |
| Pizzi, M | 1 |
| Mariotti, R | 1 |
| Hamad, AA | 1 |
| Attia, AN | 1 |
| Al-Dardery, NM | 1 |
| Mohamed, SF | 1 |
| Meshref, M | 1 |
| Boll, MC | 1 |
| Bayliss, L | 1 |
| Vargas-Cañas, S | 1 |
| Burgos, J | 1 |
| Montes, S | 1 |
| Peñaloza-Solano, G | 1 |
| Rios, C | 1 |
| Alcaraz-Zubeldia, M | 1 |
| Lee, J | 1 |
| Keum, G | 1 |
| Yoon, YJ | 1 |
| Kowall, NW | 1 |
| Wang, SY | 2 |
| Ren, M | 2 |
| Jiang, HZ | 2 |
| Wang, J | 2 |
| Jiang, HQ | 2 |
| Yin, X | 2 |
| Qi, Y | 2 |
| Wang, XD | 2 |
| Dong, GT | 1 |
| Wang, TH | 2 |
| Yang, YQ | 2 |
| Feng, HL | 3 |
| Wang, X | 1 |
| Ma, M | 1 |
| Teng, J | 1 |
| Che, X | 1 |
| Zhang, W | 1 |
| Feng, S | 1 |
| Zhou, S | 1 |
| Zhang, Y | 1 |
| Wu, E | 1 |
| Ding, X | 1 |
| Wang, Y | 1 |
| Zhang, CT | 1 |
| Leng, Y | 1 |
| Ma, CH | 1 |
| Zhang, J | 1 |
| Chuang, DM | 1 |
| Crochemore, C | 1 |
| Virgili, M | 1 |
| Bonamassa, B | 1 |
| Canistro, D | 1 |
| Pena-Altamira, E | 1 |
| Paolini, M | 1 |
| Contestabile, A | 1 |
| Piepers, S | 1 |
| Veldink, JH | 1 |
| de Jong, SW | 1 |
| van der Tweel, I | 1 |
| van der Pol, WL | 1 |
| Uijtendaal, EV | 1 |
| Schelhaas, HJ | 1 |
| Scheffer, H | 1 |
| de Visser, M | 1 |
| de Jong, JM | 1 |
| Wokke, JH | 1 |
| Groeneveld, GJ | 1 |
| van den Berg, LH | 1 |
| Sugai, F | 1 |
| Yamamoto, Y | 1 |
| Miyaguchi, K | 1 |
| Zhou, Z | 1 |
| Sumi, H | 1 |
| Hamasaki, T | 1 |
| Goto, M | 1 |
| Sakoda, S | 1 |
| Tremolizzo, L | 1 |
| Rodriguez-Menendez, V | 1 |
| Sala, G | 1 |
| Di Francesco, JC | 1 |
| Ferrarese, C | 1 |
| Rouaux, C | 1 |
| Panteleeva, I | 1 |
| René, F | 1 |
| Gonzalez de Aguilar, JL | 1 |
| Echaniz-Laguna, A | 1 |
| Dupuis, L | 1 |
| Menger, Y | 1 |
| Boutillier, AL | 1 |
| Loeffler, JP | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Randomized Clinical Trial, Double Blind, Placebo-controlled of Lithium and Valproate in Amyotrophic Lateral Sclerosis.[NCT03204500] | Phase 2 | 43 participants (Actual) | Interventional | 2016-05-31 | Completed | ||
| A Randomized, Double-Blind, Placebo-Controlled Sequential Clinical Trial of Sodium Valproate in ALS[NCT00136110] | Phase 3 | 165 participants (Actual) | Interventional | 2005-04-30 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
2 reviews available for valproic acid and Amyotrophic Lateral Sclerosis
| Article | Year |
|---|---|
Safety and efficacy of lithium in patients with amyotrophic lateral sclerosis: a systematic review and meta-analysis of randomized controlled trials.
Topics: Amyotrophic Lateral Sclerosis; Humans; Lithium; Randomized Controlled Trials as Topic; Valproic Acid | 2023 |
Therapeutic targeting of epigenetic components in amyotrophic lateral sclerosis (ALS).
Topics: Amyotrophic Lateral Sclerosis; Animals; Epigenesis, Genetic; Histone Deacetylase Inhibitors; Histone | 2014 |
1 trial available for valproic acid and Amyotrophic Lateral Sclerosis
| Article | Year |
|---|---|
Randomized sequential trial of valproic acid in amyotrophic lateral sclerosis.
Topics: Adult; Aged; Amyotrophic Lateral Sclerosis; Disease Progression; Double-Blind Method; Enzyme Inhibit | 2009 |
11 other studies available for valproic acid and Amyotrophic Lateral Sclerosis
| Article | Year |
|---|---|
Monocarboxylate transporter functions and neuroprotective effects of valproic acid in experimental models of amyotrophic lateral sclerosis.
Topics: Amyotrophic Lateral Sclerosis; Animals; Disease Models, Animal; Mice; Mice, Transgenic; Monocarboxyl | 2022 |
Beneficial and Sexually Dimorphic Response to Combined HDAC Inhibitor Valproate and AMPK/SIRT1 Pathway Activator Resveratrol in the Treatment of ALS Mice.
Topics: AMP-Activated Protein Kinases; Amyotrophic Lateral Sclerosis; Animals; Disease Models, Animal; Femal | 2022 |
Clinical and biological changes under treatment with lithium carbonate and valproic acid in sporadic amyotrophic lateral sclerosis.
Topics: Amyotrophic Lateral Sclerosis; Cadmium; Cause of Death; Disability Evaluation; Enzyme Inhibitors; Fe | 2014 |
Notch pathway is activated in cell culture and mouse models of mutant SOD1-related familial amyotrophic lateral sclerosis, with suppression of its activation as an additional mechanism of neuroprotection for lithium and valproate.
Topics: Amyotrophic Lateral Sclerosis; Animals; Cells, Cultured; Disease Models, Animal; Embryo, Mammalian; | 2015 |
Valproate Attenuates 25-kDa C-Terminal Fragment of TDP-43-Induced Neuronal Toxicity via Suppressing Endoplasmic Reticulum Stress and Activating Autophagy.
Topics: Amyotrophic Lateral Sclerosis; Animals; Autophagy; Cell Line; DNA-Binding Proteins; Endoplasmic Reti | 2015 |
Downregulation of Homer1b/c in SOD1 G93A Models of ALS: A Novel Mechanism of Neuroprotective Effect of Lithium and Valproic Acid.
Topics: Amyotrophic Lateral Sclerosis; Animals; Apoptosis; Cell Line; Genetic Predisposition to Disease; Hom | 2016 |
Combined lithium and valproate treatment delays disease onset, reduces neurological deficits and prolongs survival in an amyotrophic lateral sclerosis mouse model.
Topics: Adjuvants, Immunologic; Age Factors; Amyotrophic Lateral Sclerosis; Animals; Anticonvulsants; Behavi | 2008 |
Long-term dietary administration of valproic acid does not affect, while retinoic acid decreases, the lifespan of G93A mice, a model for amyotrophic lateral sclerosis.
Topics: Acetylcholinesterase; Amyotrophic Lateral Sclerosis; Animal Feed; Animals; Antineoplastic Agents; Ch | 2009 |
Benefit of valproic acid in suppressing disease progression of ALS model mice.
Topics: Age of Onset; Amyotrophic Lateral Sclerosis; Animals; Cell Count; Cell Death; Dicarboxylic Acids; Di | 2004 |
Valproate and HDAC inhibition: a new epigenetic strategy to mitigate phenotypic severity in ALS?
Topics: Amyotrophic Lateral Sclerosis; Histone Deacetylase Inhibitors; Humans; Phenotype; Valproic Acid | 2005 |
Sodium valproate exerts neuroprotective effects in vivo through CREB-binding protein-dependent mechanisms but does not improve survival in an amyotrophic lateral sclerosis mouse model.
Topics: Amyotrophic Lateral Sclerosis; Animals; Cell Line, Tumor; CREB-Binding Protein; Disease Models, Anim | 2007 |