pentylenetetrazole has been researched along with Acute Confusional Senile Dementia in 16 studies
Pentylenetetrazole: A pharmaceutical agent that displays activity as a central nervous system and respiratory stimulant. It is considered a non-competitive GAMMA-AMINOBUTYRIC ACID antagonist. Pentylenetetrazole has been used experimentally to study seizure phenomenon and to identify pharmaceuticals that may control seizure susceptibility.
pentetrazol : An organic heterobicyclic compound that is 1H-tetrazole in which the hydrogens at positions 1 and 5 are replaced by a pentane-1,5-diyl group. A central and respiratory stimulant, it was formerly used for the treatment of cough and other respiratory tract disorders, cardiovascular disorders including hypotension, and pruritis.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Seizures are a known co-occurring symptom of Alzheimer's disease, and they can accelerate cognitive and neuropathological dysfunction." | 5.42 | Low brain ascorbic acid increases susceptibility to seizures in mouse models of decreased brain ascorbic acid transport and Alzheimer's disease. ( Harrison, FE; Kang, JQ; Kennard, JA; Warner, TA, 2015) |
| "Many of the neurochemical changes associated with aging brain, particularly lower choline acetyltransferase and higher monoamine oxidase, occur with greater severity in senile dementia, Alzheimer's type (SDAT)." | 4.76 | Chemotherapy of cognitive disorders in geriatric subjects. ( Gershon, S; Goodnick, P, 1984) |
| "Epilepsy is a common neurological disorder affecting more than 70 million people worldwide." | 1.91 | ( Gao, Y; Jiang, X; Liang, X; Liu, W; Lu, H; Wang, N; Xing, B; Xu, X; Zhao, Q; Zhou, L, 2023) |
| "The risk of seizures is 10-fold higher in patients with Alzheimer's disease than the general population, yet the mechanisms underlying this susceptibility and the effects of these seizures are poorly understood." | 1.72 | The role of mTORC1 activation in seizure-induced exacerbation of Alzheimer's disease. ( Barbour, AJ; Eberwine, G; Gourmaud, S; Irwin, DJ; Jensen, FE; O'Brien, WT; Roberts, N; Stewart, DA; Talos, DM; Vassar, R, 2022) |
| "Epileptic seizures constitute a significant comorbidity of Alzheimer's disease (AD), which are recapitulated in transgenic mouse models of amyloidogenesis." | 1.56 | Hyperexcitability and seizures in the THY-Tau22 mouse model of tauopathy. ( Basquin, M; Blum, D; Boison, D; Buée, L; Ferry, B; Gomez-Murcia, V; Laurent, C; Parrot, S; Sandau, U, 2020) |
| "Alzheimer's disease is a common age associated neurodegenerative disorder associated with an elevated risk of seizures that may be fundamentally connected to cognitive dysfunction." | 1.46 | Seizure susceptibility in the APP/PS1 mouse model of Alzheimer's disease and relationship with amyloid β plaques. ( Nuñez, A; Reyes-Marin, KE, 2017) |
| "Spontaneous seizures were not detected more often in APParc mice than in their wild-type control mice." | 1.43 | Increased Epileptiform EEG Activity and Decreased Seizure Threshold in Arctic APP Transgenic Mouse Model of Alzheimer's Disease. ( Graff, C; Gurevicius, K; Miszczuk, D; Pitkänen, A; Rönnbäck, A; Tanila, H; Winblad, B; Ziyatdinova, S, 2016) |
| "Seizures are a known co-occurring symptom of Alzheimer's disease, and they can accelerate cognitive and neuropathological dysfunction." | 1.42 | Low brain ascorbic acid increases susceptibility to seizures in mouse models of decreased brain ascorbic acid transport and Alzheimer's disease. ( Harrison, FE; Kang, JQ; Kennard, JA; Warner, TA, 2015) |
| "In rodent seizure models, tanshinone IIA showed anticonvulsive activity in the mouse 6-Hz psychomotor seizure test in a biphasic manner and modified seizure thresholds in a complex manner for the mouse i." | 1.39 | Tanshinone IIA exhibits anticonvulsant activity in zebrafish and mouse seizure models. ( Buenafe, OE; Crawford, AD; De Borggraeve, W; de Witte, P; Esguerra, CV; Huang, H; Luyten, W; Maes, J; Orellana-Paucar, A; Ying, X, 2013) |
| "Seizures are a common phenotype in all of these neurological disorders, yet the underlying molecular mechanism(s) of seizure induction and propagation remain largely unknown." | 1.36 | Alzheimer's disease and Down syndrome rodent models exhibit audiogenic seizures. ( Malter, JS; Westmark, CJ; Westmark, PR, 2010) |
| "Many potential treatments for Alzheimer's disease target amyloid-beta peptides (Abeta), which are widely presumed to cause the disease." | 1.34 | Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model. ( Cheng, IH; Gerstein, H; Mucke, L; Palop, JJ; Roberson, ED; Scearce-Levie, K; Wu, T; Yan, F; Yu, GQ, 2007) |
| "Reports suggest that Alzheimer's disease (AD) patients show a high life-time prevalence of seizure-like disorders." | 1.32 | Increased seizure threshold and severity in young transgenic CRND8 mice. ( Del Vecchio, RA; Gold, LH; Hyde, LA; Novick, SJ; Wong, G, 2004) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 2 (12.50) | 18.7374 |
| 1990's | 1 (6.25) | 18.2507 |
| 2000's | 2 (12.50) | 29.6817 |
| 2010's | 7 (43.75) | 24.3611 |
| 2020's | 4 (25.00) | 2.80 |
| Authors | Studies |
|---|---|
| Zhou, L | 1 |
| Gao, Y | 1 |
| Lu, H | 1 |
| Liu, W | 1 |
| Xu, X | 1 |
| Xing, B | 1 |
| Liang, X | 1 |
| Wang, N | 1 |
| Jiang, X | 1 |
| Zhao, Q | 1 |
| Jahan, R | 1 |
| Yousaf, M | 1 |
| Khan, H | 1 |
| Bibi, N | 1 |
| Ijaz, M | 1 |
| Rehan, T | 1 |
| Shah, SA | 1 |
| Gomez-Murcia, V | 1 |
| Sandau, U | 1 |
| Ferry, B | 1 |
| Parrot, S | 1 |
| Laurent, C | 1 |
| Basquin, M | 1 |
| Buée, L | 1 |
| Boison, D | 1 |
| Blum, D | 1 |
| Gourmaud, S | 1 |
| Stewart, DA | 1 |
| Irwin, DJ | 1 |
| Roberts, N | 1 |
| Barbour, AJ | 1 |
| Eberwine, G | 1 |
| O'Brien, WT | 1 |
| Vassar, R | 1 |
| Talos, DM | 1 |
| Jensen, FE | 1 |
| Popova, I | 1 |
| Malkov, A | 1 |
| Ivanov, AI | 1 |
| Samokhina, E | 1 |
| Buldakova, S | 1 |
| Gubkina, O | 1 |
| Osypov, A | 1 |
| Muhammadiev, RS | 1 |
| Zilberter, T | 1 |
| Molchanov, M | 1 |
| Paskevich, S | 1 |
| Zilberter, M | 1 |
| Zilberter, Y | 1 |
| Reyes-Marin, KE | 1 |
| Nuñez, A | 1 |
| Buenafe, OE | 1 |
| Orellana-Paucar, A | 1 |
| Maes, J | 1 |
| Huang, H | 1 |
| Ying, X | 1 |
| De Borggraeve, W | 1 |
| Crawford, AD | 1 |
| Luyten, W | 1 |
| Esguerra, CV | 1 |
| de Witte, P | 1 |
| Warner, TA | 1 |
| Kang, JQ | 1 |
| Kennard, JA | 1 |
| Harrison, FE | 1 |
| Ziyatdinova, S | 1 |
| Rönnbäck, A | 1 |
| Gurevicius, K | 1 |
| Miszczuk, D | 1 |
| Graff, C | 1 |
| Winblad, B | 1 |
| Pitkänen, A | 1 |
| Tanila, H | 1 |
| Westmark, CJ | 1 |
| Westmark, PR | 1 |
| Malter, JS | 1 |
| Abuznait, AH | 1 |
| Cain, C | 1 |
| Ingram, D | 1 |
| Burk, D | 1 |
| Kaddoumi, A | 1 |
| Del Vecchio, RA | 1 |
| Gold, LH | 1 |
| Novick, SJ | 1 |
| Wong, G | 1 |
| Hyde, LA | 1 |
| Roberson, ED | 1 |
| Scearce-Levie, K | 1 |
| Palop, JJ | 1 |
| Yan, F | 1 |
| Cheng, IH | 1 |
| Wu, T | 1 |
| Gerstein, H | 1 |
| Yu, GQ | 1 |
| Mucke, L | 1 |
| Goodnick, P | 1 |
| Gershon, S | 1 |
| Panegyres, PK | 1 |
| Murphy, DE | 1 |
| Boast, CA | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Phase 2a Levetiracetam Trial for AD-Associated Network Hyperexcitability[NCT02002819] | Phase 2 | 34 participants (Actual) | Interventional | 2014-10-16 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Alzheimer's Disease Assessment Scale - Cognitive Subscale (ADAS-cog) - The ADAS-cog rating instrument (Rosen et al. 1984) will be used to evaluate the global cognitive functioning. The ADAS-cog is a 70-point scale that includes an assessment of verbal memory, language, orientation, reasoning, and praxis.The score is derived from adding point values from each of its subsections. The higher your score on the ADAS-cog, the better you do. (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | score on a scale (Mean) |
|---|---|
| Levetiracetam (Epileptiform Activity) | -1.0 |
| Placebo (Epileptiform Activity) | 1.5 |
Blood samples intended for Quest Diagnostics LEV and prolactin serum levels (one 6 mL tube) will be processed in the following manner, as outlined in the Quest Diagnostics lab manual. The whole blood will be allowed to clot for 60 minutes and centrifuged at 2200 - 2500 revolutions per minute (RPM) for at least 15 minutes. The resulting serum will be split into 2 cryovials which will be stored at -20°C and immediately shipped for external assessment of LEV and prolactin levels. Prolactin will be assessed via immunoassay. The concentration of LEV in serum will be measured using validated liquid chromatography/tandem mass spectrometry (LC/MS-MS) methods. (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | ng/mL (Mean) |
|---|---|
| Levetiracetam | 0.1 |
| Placebo | 0.2 |
Alzheimer's Disease Assessment Scale - Cognitive Subscale (ADAS-cog) - The ADAS-cog rating instrument (Rosen et al. 1984) will be used to evaluate the global cognitive functioning. The ADAS-cog is a 70-point scale that includes an assessment of verbal memory, language, orientation, reasoning, and praxis.The score is derived from adding point values from each of its subsections. The higher your score on the ADAS-cog, the better you do. (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | score on a scale (Mean) |
|---|---|
| Levetiracetam | -0.2 |
| Placebo | 0.8 |
Alzheimer's Disease Cooperative Study Activities of Daily Living Scale (ADCS-ADL) - The ADCS-ADL rating instrument (Galasko et al. 1997) will be used to evaluate functional capacity. The ADCS-ADL is a caregiver rated questionnaire. Scores on the 24-item ADCS-ADL range from 0 to 78. A higher score indicates less severity while a lower score indicates greater severity. (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | score on a scale (Mean) |
|---|---|
| Levetiracetam | 0.4 |
| Placebo | 0.3 |
ADCS-Clinical Global Impression of Change (ADCS-CGIC) - The ADCS-CGIC is a seven-point scale that gives a global rating of change from baseline (Schneider et al. 1997). The baseline and follow up assessments are based on interviews with the subject and the informant. The ADCS-CGIC is a clinician-rated measure of: global severity at baseline scored from 1 (normal, not at all ill) to 7 (among the most extremely ill patients); and global change at follow-up scored from 1 (marked improvement) to 7 (marked worsening), where 4 indicates no change. (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | score on a scale (Mean) |
|---|---|
| Levetiracetam | 4.0 |
| Placebo | 4.0 |
Neuropsychiatric Inventory (NPI) - The NPI (Cummings et al. 1994) will be used to evaluate the severity of behavioral symptoms. The severity scale has scores ranging from 1 to 3 points (1=mild; 2=moderate; and 3=severe) and the scale for assessing caregiver distress has scores ranging from 0 to 5 points (0=no distress; 1=minimal distress; 2=mild distress; 3=moderate distress; 4=severe distress; and 5=extreme distress). (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | score on a scale (Mean) |
|---|---|
| Levetiracetam | -0.8 |
| Placebo | 0.2 |
A 20-minute computer-based virtual navigation test will be used to assess how well a subject can navigate a virtual community to reach a goal destination. The subjects will then be measured on their ability to accurately navigate the virtual community after a period of a few hours. The subject's performance after the study treatment will be compared with results from a baseline assessment done before the study treatment, using statistical tests to assess whether there was any significant change. (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | correct turns (Mean) |
|---|---|
| No Epileptiform Activity | -6.0 |
| Epileptic Activity | 17.4 |
"Epileptiform activity will be measured using a 1-hr resting magnetoencephalogram/electroencephalogram (M/EEG). M/EEG can detect abnormal epileptiform findings called spikes. The M/EEG will be read by an epileptologist with specialized training to assess whether there are any spikes. If spikes are observed during the M/EEG they will be counted to determine their frequency (e.g., 5 spikes per 1 hour recording). The frequency of spikes will then be compared to baseline values from before beginning the study treatment, using statistical tests to determine if the frequency changed with treatment." (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | Epileptiform events (Mean) |
|---|---|
| Levetiracetam | -0.1 |
| Placebo | -0.2 |
Changes in executive function were measured using the NIH EXAMINER, a 1-hour computer-based battery of various executive function tasks. The subject's performance after the study treatment will be compared with results from a baseline assessment done before the study treatment, using statistical tests to assess whether there was any significant change. The Examiner assessment consists of the following scales: antisaccade , set shifting , flanker task, dot counting, spatial 1-back, category fluency, and letter fluency. Scores for this task have an indefinite range. Higher scores however do indicate better performance. Scores for this scale were generated using item response theory. For this study, scores with SEs greater than 0.55 were classified as unreliable and excluded from analysis. Composite scores from 2 participants were excluded on this basis.The EXAMINER ranges for the participants in the study were -2.59 to 1.33. (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | score on a scale (Mean) |
|---|---|
| Levetiracetam | -0.06 |
| Placebo | -0.14 |
Stroop Test - The Stroop Test (Stroop 1935) will be used to assess executive functions including selective attention, cognitive flexibility and processing speed. Subtasks include Stroop color naming and Stroop interference naming, and each subtask is restricted to 1 minute. The minimum score is 0 and the maximum score is 126. The higher the score the better a participant does. (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | score on a scale (Mean) |
|---|---|
| Levetiracetam | 1.5 |
| Placebo | -1.4 |
Clinical Dementia Rating Sum of Boxes (CDR-SOB) - The CDR will be used as a global measure of dementia severity (Morris 1993). The CDR consists of questions addressed to the caregiver/informant. The lowest score one can receive is a 0 and the highest is a 3. Score is measured by getting the mean of the individual scores in each category. Lower scores equate to less dementia severity. (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | score on a scale (Mean) |
|---|---|
| Levetiracetam | 0.1 |
| Placebo | 0.1 |
Changes in executive function will be measured using the NIH EXAMINER, a 1-hour computer-based battery of various executive function tasks. The subject's performance after the study treatment will be compared with results from a baseline assessment done before the study treatment, using statistical tests to assess whether there was any significant change. The Examiner assessment consists of the following scales: NIH EXAMINER - antisaccade , NIH EXAMINER - set shifting , NIH EXAMINER - flanker task, NIH EXAMINER - dot counting, NIH EXAMINER - spatial 1-back, NIH EXAMINER - category fluency, and NIH EXAMINER - letter fluency. Scores for this task have an indefinite range. Higher scores however do indicate better performance. Scores for this scale were generated using item response theory (Kramer et al. J Int Neuropsychol Soc. 2014;20(1):11-19. doi:10.1017/S1355617713001094). (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | score on a scale (Mean) |
|---|---|
| No Epileptiform Activity | -0.01 |
| Epileptiform Activity | 0.22 |
The One Day Fluctuation Assessment Scale will be used to quantitate fluctuations of dementia symptoms (Walker et al. 2000). The One Day Fluctuation Assessment Scale has a score range of 0-21 points,with higher scores indicatingmore fluctuations. (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | score on a scale (Mean) |
|---|---|
| Levetiracetam | 0.3 |
| Placebo | -0.4 |
Two standardized methods will be used to quantitate fluctuations of dementia symptoms: The Clinician Assessment of Fluctuation and the One Day Fluctuation Assessment Scale (Walker et al. 2000). : The Clinician Assessment of Fluctuation (score range,0-12 points, with higher scores indicating more fluctuations),26 the One Day Fluctuation Assessment Scale (score range,0-21 points, with higher scores indicatingmore fluctuations). (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | score on a scale (Mean) |
|---|---|
| Levetiracetam | 0.9 |
| Placebo | 0.1 |
Stroop Test - The Stroop Test (Stroop 1935) will be used to assess executive functions including selective attention, cognitive flexibility and processing speed. Subtasks include Stroop color naming and Stroop interference naming, and each subtask is restricted to 1 minute. The minimum score is 0 and the maximum score is 126. The higher the score the better a participant does. The mean below represents the average change in score between the timepoints for all participants. (NCT02002819)
Timeframe: Difference between weeks 0-4 (Baseline) and weeks 8-12 (Treatment)
| Intervention | score on a scale (Mean) |
|---|---|
| Levetiracetam (Epileptiform Activity) | 4.7 |
| Placebo (Epileptiform Activity) | -2.6 |
1 review available for pentylenetetrazole and Acute Confusional Senile Dementia
| Article | Year |
|---|---|
Chemotherapy of cognitive disorders in geriatric subjects.
Topics: Adrenocorticotropic Hormone; Aged; Aging; Alzheimer Disease; Arecoline; Brain Chemistry; Choline; Co | 1984 |
15 other studies available for pentylenetetrazole and Acute Confusional Senile Dementia
| Article | Year |
|---|---|
Topics: Alzheimer Disease; Animals; Anticonvulsants; Cognitive Dysfunction; Disease Models, Animal; Epilepsy | 2023 |
ZOMEC via the p-Akt/Nrf2 Pathway Restored PTZ-Induced Oxidative Stress-Mediated Memory Dysfunction in Mouse Model.
Topics: Alzheimer Disease; Animals; Antioxidants; Catalase; Disease Models, Animal; Glutathione Transferase; | 2022 |
Hyperexcitability and seizures in the THY-Tau22 mouse model of tauopathy.
Topics: Alzheimer Disease; Animals; Disease Models, Animal; Electroencephalography; Mice, Inbred C57BL; Mice | 2020 |
The role of mTORC1 activation in seizure-induced exacerbation of Alzheimer's disease.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Disease Models, Animal; Humans; Mechanistic Targe | 2022 |
Metabolic correction by pyruvate halts acquired epilepsy in multiple rodent models.
Topics: Alzheimer Disease; Animals; Anticonvulsants; Brain; Brain Waves; Drug Evaluation, Preclinical; Epile | 2017 |
Seizure susceptibility in the APP/PS1 mouse model of Alzheimer's disease and relationship with amyloid β plaques.
Topics: Alzheimer Disease; Animals; Benzylamines; Cerebral Cortex; Disease Models, Animal; Disease Susceptib | 2017 |
Tanshinone IIA exhibits anticonvulsant activity in zebrafish and mouse seizure models.
Topics: Abietanes; Alzheimer Disease; Animals; Anticonvulsants; Brain Ischemia; Disease Models, Animal; Dise | 2013 |
Low brain ascorbic acid increases susceptibility to seizures in mouse models of decreased brain ascorbic acid transport and Alzheimer's disease.
Topics: Alzheimer Disease; Amyloid beta-Protein Precursor; Animals; Ascorbic Acid; Ascorbic Acid Deficiency; | 2015 |
Increased Epileptiform EEG Activity and Decreased Seizure Threshold in Arctic APP Transgenic Mouse Model of Alzheimer's Disease.
Topics: Age Factors; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animals; Brai | 2016 |
Alzheimer's disease and Down syndrome rodent models exhibit audiogenic seizures.
Topics: Acoustic Stimulation; Alzheimer Disease; Amyloid beta-Protein Precursor; Animals; Convulsants; Down | 2010 |
Up-regulation of P-glycoprotein reduces intracellular accumulation of beta amyloid: investigation of P-glycoprotein as a novel therapeutic target for Alzheimer's disease.
Topics: Alzheimer Disease; Amyloid beta-Peptides; ATP Binding Cassette Transporter, Subfamily B, Member 1; C | 2011 |
Increased seizure threshold and severity in young transgenic CRND8 mice.
Topics: Alzheimer Disease; Amyloid beta-Protein Precursor; Animals; Disease Models, Animal; Male; Mice; Mice | 2004 |
Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animals; Axons; Convulsant | 2007 |
The effects of excitotoxicity on the expression of the amyloid precursor protein gene in the brain and its modulation by neuroprotective agents.
Topics: Alzheimer Disease; Amyloid beta-Protein Precursor; Animals; Benzofurans; Brain; Dizocilpine Maleate; | 1998 |
Searching for models of Alzheimer's disease: a comparison of four amnestic treatments in two behavioral tasks.
Topics: Acetylcholine; Age Factors; Alzheimer Disease; Animals; Avoidance Learning; Behavior, Animal; Discri | 1985 |