niacinamide has been researched along with Alzheimer Disease in 38 studies
nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.
Alzheimer Disease: A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)
| Excerpt | Relevance | Reference |
|---|---|---|
| " The likely involvement of the kinase pathway is implicated in the unique effects of nicotinamide riboside in raising tissue NAD concentrations in rodents and for potent effects in eliciting insulin sensitivity, mitochondrial biogenesis, and enhancement of sirtuin functions." | 4.89 | Nicotinamide riboside, a trace nutrient in foods, is a vitamin B3 with effects on energy metabolism and neuroprotection. ( Chi, Y; Sauve, AA, 2013) |
| "Familial forms of Alzheimer's disease associated with the accumulation of a toxic form of amyloid-β (Aβ) peptides are linked to mitochondrial impairment." | 1.62 | Parp mutations protect from mitochondrial toxicity in Alzheimer's disease. ( Celardo, I; Fedele, G; Loh, SHY; Martins, LM; Yu, Y, 2021) |
| "oral, in the early stage of Alzheimer's disease." | 1.48 | Nicotinamide loaded functionalized solid lipid nanoparticles improves cognition in Alzheimer's disease animal model by reducing Tau hyperphosphorylation. ( Akbari Javar, H; Amini, A; Baha'addini Beigi Zarandi, BF; Dinarvand, R; Montaseri, H; Vakilinezhad, MA, 2018) |
| "Alzheimer's disease is a common and devastating disease characterized by aggregation of the amyloid-β peptide." | 1.46 | Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity. ( Auwerx, J; Beck, JS; Counts, SE; D'Amico, D; Mouchiroud, L; Moullan, N; Potenza, F; Rietsch, S; Romani, M; Schmid, AW; Sorrentino, V; Zhang, H, 2017) |
| "The underlying mechanisms of Alzheimer's Disease (AD) are still unclear." | 1.40 | Nicotinamide treatment reduces the levels of oxidative stress, apoptosis, and PARP-1 activity in Aβ(1-42)-induced rat model of Alzheimer's disease. ( Kanit, L; Koylu, E; Turunc Bayrakdar, E; Uyanikgil, Y; Yalcin, A, 2014) |
| "Currently available treatment used in Alzheimer's disease is based on acetylcholinesterase inhibitors, e." | 1.39 | Synthesis and biological activity of new donepezil-hydrazinonicotinamide hybrids. ( Mikiciuk-Olasik, E; Szymański, P; Zurek, E, 2013) |
| "Memory loss is the signature feature of Alzheimer's disease, and therapies that prevent or delay its onset are urgently needed." | 1.35 | Nicotinamide restores cognition in Alzheimer's disease transgenic mice via a mechanism involving sirtuin inhibition and selective reduction of Thr231-phosphotau. ( Green, KN; LaFerla, FM; Martinez-Coria, H; Schreiber, SS; Steffan, JS; Sun, X; Thompson, LM, 2008) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 1 (2.63) | 18.7374 |
| 1990's | 1 (2.63) | 18.2507 |
| 2000's | 4 (10.53) | 29.6817 |
| 2010's | 20 (52.63) | 24.3611 |
| 2020's | 12 (31.58) | 2.80 |
| Authors | Studies |
|---|---|
| Kumar, R | 1 |
| Nigam, L | 1 |
| Singh, AP | 1 |
| Singh, K | 1 |
| Subbarao, N | 1 |
| Dey, S | 1 |
| Larrick, JW | 1 |
| Mendelsohn, AR | 1 |
| Ryu, WI | 1 |
| Shen, M | 1 |
| Lee, Y | 1 |
| Healy, RA | 1 |
| Bormann, MK | 1 |
| Cohen, BM | 1 |
| Sonntag, KC | 1 |
| Fathi, M | 1 |
| Vakili, K | 1 |
| Yaghoobpoor, S | 1 |
| Tavasol, A | 1 |
| Jazi, K | 1 |
| Hajibeygi, R | 1 |
| Shool, S | 1 |
| Sodeifian, F | 1 |
| Klegeris, A | 1 |
| McElhinney, A | 1 |
| Tavirani, MR | 1 |
| Sayehmiri, F | 1 |
| Kim, H | 1 |
| Kim, B | 1 |
| Kim, HS | 1 |
| Cho, JY | 1 |
| Zhao, N | 1 |
| Xia, J | 1 |
| Xu, B | 1 |
| Braidy, N | 1 |
| Liu, Y | 1 |
| Hacioglu, C | 1 |
| Kar, F | 1 |
| Kanbak, G | 1 |
| Zhong, Y | 1 |
| Yang, S | 1 |
| Cui, J | 1 |
| Wang, J | 2 |
| Li, L | 1 |
| Chen, Y | 1 |
| Chen, J | 1 |
| Feng, P | 1 |
| Huang, S | 1 |
| Li, H | 1 |
| Han, Y | 1 |
| Tang, G | 1 |
| Hu, K | 1 |
| Willyard, C | 1 |
| Hosseini, L | 1 |
| Mahmoudi, J | 1 |
| Pashazadeh, F | 1 |
| Salehi-Pourmehr, H | 1 |
| Sadigh-Eteghad, S | 1 |
| Yu, Y | 1 |
| Fedele, G | 1 |
| Celardo, I | 1 |
| Loh, SHY | 1 |
| Martins, LM | 1 |
| Jiang, X | 1 |
| Liu, C | 1 |
| Zou, M | 1 |
| Xie, H | 1 |
| Lin, T | 1 |
| Lyu, W | 1 |
| Xu, J | 1 |
| Li, Y | 1 |
| Feng, F | 1 |
| Sun, H | 1 |
| Liu, W | 1 |
| Kling, A | 1 |
| Jantos, K | 1 |
| Mack, H | 1 |
| Hornberger, W | 1 |
| Drescher, K | 1 |
| Nimmrich, V | 1 |
| Relo, A | 1 |
| Wicke, K | 1 |
| Hutchins, CW | 1 |
| Lao, Y | 1 |
| Marsh, K | 1 |
| Moeller, A | 1 |
| Czarnecka, K | 1 |
| Girek, M | 1 |
| Maciejewska, K | 1 |
| Skibiński, R | 1 |
| Jończyk, J | 1 |
| Bajda, M | 1 |
| Kabziński, J | 1 |
| Sołowiej, P | 1 |
| Majsterek, I | 1 |
| Szymański, P | 3 |
| Sorrentino, V | 1 |
| Romani, M | 1 |
| Mouchiroud, L | 1 |
| Beck, JS | 1 |
| Zhang, H | 1 |
| D'Amico, D | 1 |
| Moullan, N | 1 |
| Potenza, F | 1 |
| Schmid, AW | 1 |
| Rietsch, S | 1 |
| Counts, SE | 1 |
| Auwerx, J | 1 |
| Vakilinezhad, MA | 1 |
| Amini, A | 1 |
| Akbari Javar, H | 1 |
| Baha'addini Beigi Zarandi, BF | 1 |
| Montaseri, H | 1 |
| Dinarvand, R | 1 |
| Xie, X | 1 |
| Gao, Y | 1 |
| Zeng, M | 1 |
| Wang, Y | 1 |
| Wei, TF | 1 |
| Lu, YB | 1 |
| Zhang, WP | 1 |
| Esteves, AR | 1 |
| Filipe, F | 1 |
| Magalhães, JD | 1 |
| Silva, DF | 1 |
| Cardoso, SM | 1 |
| Zurek, E | 2 |
| Mikiciuk-Olasik, E | 2 |
| Ghosh, D | 2 |
| LeVault, KR | 2 |
| Brewer, GJ | 2 |
| Chi, Y | 1 |
| Sauve, AA | 2 |
| Turunc Bayrakdar, E | 1 |
| Uyanikgil, Y | 2 |
| Kanit, L | 2 |
| Koylu, E | 2 |
| Yalcin, A | 2 |
| Bayrakdar, ET | 1 |
| Armagan, G | 1 |
| Schou, M | 1 |
| Varnäs, K | 1 |
| Jureus, A | 1 |
| Ahlgren, C | 1 |
| Malmquist, J | 1 |
| Häggkvist, J | 1 |
| Tari, L | 1 |
| Wesolowski, SS | 1 |
| Throner, SR | 1 |
| Brown, DG | 1 |
| Nilsson, M | 1 |
| Johnström, P | 1 |
| Finnema, SJ | 1 |
| Nakao, R | 1 |
| Amini, N | 1 |
| Takano, A | 1 |
| Farde, L | 1 |
| Wolak, N | 1 |
| Zawrotniak, M | 1 |
| Gogol, M | 1 |
| Kozik, A | 1 |
| Rapala-Kozik, M | 1 |
| Lethbridge, NL | 1 |
| Chazot, PL | 1 |
| Gao, M | 1 |
| Wang, M | 1 |
| Zheng, QH | 1 |
| Green, KN | 1 |
| Steffan, JS | 1 |
| Martinez-Coria, H | 1 |
| Sun, X | 1 |
| Schreiber, SS | 1 |
| Thompson, LM | 1 |
| LaFerla, FM | 1 |
| Medhurst, AD | 2 |
| Roberts, JC | 2 |
| Lee, J | 1 |
| Chen, CP | 1 |
| Brown, SH | 1 |
| Roman, S | 1 |
| Lai, MK | 1 |
| Thurairatnam, S | 1 |
| Barnett, AJ | 1 |
| Liu, D | 1 |
| Pitta, M | 1 |
| Jiang, H | 1 |
| Lee, JH | 1 |
| Zhang, G | 1 |
| Chen, X | 1 |
| Kawamoto, EM | 1 |
| Mattson, MP | 1 |
| Gong, B | 1 |
| Pan, Y | 1 |
| Vempati, P | 1 |
| Zhao, W | 1 |
| Knable, L | 1 |
| Ho, L | 1 |
| Sastre, M | 1 |
| Ono, K | 1 |
| Pasinetti, GM | 1 |
| Atkins, AR | 1 |
| Beresford, IJ | 1 |
| Brackenborough, K | 1 |
| Briggs, MA | 1 |
| Calver, AR | 1 |
| Cilia, J | 1 |
| Cluderay, JE | 1 |
| Crook, B | 1 |
| Davis, JB | 1 |
| Davis, RK | 1 |
| Davis, RP | 1 |
| Dawson, LA | 1 |
| Foley, AG | 1 |
| Gartlon, J | 1 |
| Gonzalez, MI | 1 |
| Heslop, T | 1 |
| Hirst, WD | 1 |
| Jennings, C | 1 |
| Jones, DN | 1 |
| Lacroix, LP | 1 |
| Martyn, A | 1 |
| Ociepka, S | 1 |
| Ray, A | 1 |
| Regan, CM | 1 |
| Schogger, J | 1 |
| Southam, E | 1 |
| Stean, TO | 1 |
| Trail, BK | 1 |
| Upton, N | 1 |
| Wadsworth, G | 1 |
| Wald, JA | 1 |
| White, T | 1 |
| Witherington, J | 1 |
| Woolley, ML | 1 |
| Worby, A | 1 |
| Wilson, DM | 1 |
| Hankes, LV | 1 |
| Coenen, HH | 1 |
| Rota, E | 1 |
| Langen, KJ | 1 |
| Herzog, H | 1 |
| Wutz, W | 1 |
| Stoecklin, G | 1 |
| Feinendegen, LE | 1 |
| Blass, JP | 1 |
| Gleason, P | 1 |
| Brush, D | 1 |
| DiPonte, P | 1 |
| Thaler, H | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Validation of an Enzymatic Assay for Quantification of Nicotinamide Adenine Dinucleotide in Blood Plasma After Ingestion of the Vitamin B3 Variant Nicotinamide Riboside: a Randomized Controlled Trial[NCT06005350] | 54 participants (Anticipated) | Interventional | 2023-11-01 | Recruiting | |||
| Nicotinamide Riboside (NR) in Paclitaxel-induced Peripheral Neuropathy[NCT03642990] | Phase 2 | 5 participants (Actual) | Interventional | 2019-11-08 | Terminated (stopped due to Enrollment challenges) | ||
| A Double-Blind-Randomized, Placebo-Controlled Adaptive Design Trial of Nicotinamide in Mild Cognitive Impairment Due to Alzheimer's Disease and Mild Alzheimer's Disease Dementia[NCT03061474] | Phase 2 | 46 participants (Actual) | Interventional | 2017-07-12 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Difference in Score on the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - neurotoxicity questionnaire at the end of treatment; i.e. Score at screening - score at end of treatment. This questionnaire asks 11 questions that are specific to chemotherapy-induced peripheral neuropathies. Maximum score is 44, minimum score is 0. Positive differences indicate a decrease in neuropathy. Negative differences indicate a worsening of neuropathy. Zero means unchanged. (NCT03642990)
Timeframe: 4 weeks
| Intervention | units on a scale (Median) |
|---|---|
| NIAGEN®) | 7 |
Exploratory analysis of ability of the clinical version of the Total Neuropathy Score questionnaire to detect changes in CIPN severity over time. Unlike the CTCAE or the FACT&GOG-NTX questionnaires, the TNS is a patient reported outcome measure. HIghest score (worse neuropathy is 24, lowest score is 0. Outcome assessed difference between end of treatment and screening. A positive number indicates improvement in neuropathy (NCT03642990)
Timeframe: 4 weeks
| Intervention | score on a scale (Median) |
|---|---|
| NIAGEN®) | 2 |
Count the number of (i.e. the incidence) of dose reduction events due to neuropathy (each occasion of dose reduction is a separate event); (NCT03642990)
Timeframe: 3 weeks
| Intervention | event (Number) |
|---|---|
| NIAGEN®) | 0 |
"The primary outcome variable is defined as no worsening of the grade of peripheral sensory neuropathy as scored according to the Common Terminology Criteria for Adverse Events (CTCAE) version 4.03 guidelines. Per the CTCAE a score of 1 would be assigned in the instance of parethesias or a loss of deep tendon reflexes. A score of 2 would be assigned in the instance of moderate symptoms that limit instrumental activities of daily living. A score of 3 would be assigned in the instance of severe symptoms that limit self-care activities of daily living. Because the outcome measure is defined as no worsening of the grade, it was recorded as either yes( i.e. it worsened) or no (i.e. it did not worsen)." (NCT03642990)
Timeframe: approximately 4 weeks
| Intervention | Participants (Count of Participants) |
|---|---|
| NIAGEN®) | 3 |
Quantitate the percentage of patients that experience a dose reduction of paclitaxel or nab-paclitaxel therapy due to neuropathy. (NCT03642990)
Timeframe: 3 weeks
| Intervention | Participants (Count of Participants) |
|---|---|
| NIAGEN®) | 0 |
Paclitaxel levels in plasma were measured ~30 min after each infusion of taxane. This was undertaken to ascertain whether NIAGEN altered plasma levels of paclitaxel because increases or decreases in plasma levels of paclitaxel by itself could lead to an apparent worsening or improvement, respectively, in CIPN and confound interpretation of NIAGEN's effect. (NCT03642990)
Timeframe: up to 3 weeks
| Intervention | ng/ml (Median) |
|---|---|
| NIAGEN®) | 810 |
Quantitate the total cumulative dose of paclitaxel administered over the 12 weeks. (NCT03642990)
Timeframe: 3 weeks
| Intervention | mg/M^2 (Number) |
|---|---|
| NIAGEN®) | 200 |
The ADCS-ADL-MCI is a measure of patient functional performance in Alzheimer's Disease and Mild Cognitive Impairment trials. The informant-based questionnaire assesses conduct of basic and instrumental Activities of Daily Living (ADLs). A total of 24 ADLs are evaluated. Scores range from 0 to 53, with higher scores representing more maintained function. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | score on a scale (Mean) |
|---|---|
| Nicotinamide | -4.05 |
| Placebo | -1.39 |
ADAS-Cog13 is a structured scale that evaluates memory (immediate and delayed word recall; immediate word recognition), receptive and expressive language, orientation, ideational praxis (preparing a letter for mailing), constructional praxis (copying figures), and attention (number cancellation). Ratings of spoken language, language comprehension, word finding difficulty, and ability to remember test instructions also are obtained. Range: 0-85; higher scores indicate greater impairment. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | score on a scale (Mean) |
|---|---|
| Nicotinamide | 3.2 |
| Placebo | 5.16 |
CDR-SB is a composite rating of cognition and everyday function which incorporates both informant input and direct assessment of performance. It assesses through semi-structured interview three cognitive domains (memory, orientation, and judgement/problem solving) and three everyday functional domains (community affairs, home and hobbies, personal care). Level of impairment in each of the six domains is rated from none (score=0) to severe (score=3). The six domain scores are then summed to create the CDR-SB. Range 0-18; higher scores indicate greater impairment. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | score on a scale (Mean) |
|---|---|
| Nicotinamide | 0.76 |
| Placebo | 2.18 |
Change in key peptide in cerebrospinal fluid (CSF) from baseline to 48 weeks. Lower ab40 is associated with a greater probability of fibrillar amyloid burden in the brain. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | pg/ml (Mean) |
|---|---|
| Nicotinamide | 2307 |
| Placebo | 1961.1 |
Change in key peptide in cerebrospinal fluid (CSF) from baseline to 48 weeks. Lower ab42 is associated with a greater probability of fibrillar amyloid burden in the brain. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | pg/ml (Mean) |
|---|---|
| Nicotinamide | 127.74 |
| Placebo | 113.79 |
Change in key peptide in cerebrospinal fluid (CSF) from baseline to 48 weeks. Higher total value is associated with greater severity of Alzheimer's disease pathology. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | pg/ml (Mean) |
|---|---|
| Nicotinamide | -0.41 |
| Placebo | -10.43 |
Change in key peptide in cerebrospinal fluid (CSF) from baseline to 48 weeks. Higher phosphorylated tau (p-tau) is associated with a severity of Alzheimer's disease pathology. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | pg/ml (Mean) |
|---|---|
| Nicotinamide | 4.71 |
| Placebo | 2.28 |
Average within-subject change in electrocardiogram QT interval. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | ms (Mean) |
|---|---|
| Nicotinamide | 6.41 |
| Placebo | 2.1 |
Change in ratio of key peptides in cerebrospinal fluid (CSF) from baseline to 48 weeks. A lower ab40/tau ratio is associated with a higher risk of dementia. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | ratio (Mean) |
|---|---|
| Nicotinamide | -0.02 |
| Placebo | -0.02 |
Change in ratio of key peptides in cerebrospinal fluid (CSF) from baseline to 48 weeks. A lower ab42/tau ratio is associated with a higher risk of dementia. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | ratio (Mean) |
|---|---|
| Nicotinamide | -0.46 |
| Placebo | -0.5 |
Change in CSF total tau in individuals with mild Alzheimer's disease (AD) dementia or Mild Cognitive Impairment due to AD. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | pg/ml (Mean) |
|---|---|
| Nicotinamide | -8.42 |
| Placebo | -60.47 |
Count of treatment emergent adverse events (TEAEs) over the duration of the study period (baseline to 48 weeks). (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | events (Number) |
|---|---|
| Nicotinamide | 79 |
| Placebo | 71 |
Count of participants experiencing at least one electrocardiogram (ECG) abnormality. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | Participants (Count of Participants) |
|---|---|
| Nicotinamide | 24 |
| Placebo | 20 |
Count of participants experiencing at least one electrocardiogram (ECG) QT interval abnormality. Abnormal defined as above 460 for men and above 470 for women. (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | Participants (Count of Participants) |
|---|---|
| Nicotinamide | 2 |
| Placebo | 1 |
"The Columbia-Suicide Severity Rating Scale (C-SSRS) captures the occurrence, severity, and frequency of suicide-related thoughts and behaviors during the corresponding assessment period. The scale includes suggested questions to elicit the type of information needed to determine if a suicide-related thought or behavior occurred. The number and proportion of subjects with treatment emergent Suicidal ideation or behavior during the study period of (baseline to week 48) will be reported overall and by study arm. Treatment emergent suicidal ideation or behavior is defined as a yes answer at any time during treatment to any one of the questions in the ten suicidal ideation and behavior categories (Categories 1- 10) on the C-SSRS. Self-injurious behavior without suicidal intent, while assessed on the C-SSRS, does not form part of this outcome." (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | events (Number) | |
|---|---|---|
| Baseline Number of abnormal C-SSRS events | Post-baseline number of abnormal C-SSRS events | |
| Nicotinamide | 0 | 1 |
| Placebo | 3 | 3 |
Count of treatment emergent adverse events (TEAEs) over the duration of the study period (baseline to 48 weeks). (NCT03061474)
Timeframe: Baseline to 48 weeks
| Intervention | events (Number) | |||
|---|---|---|---|---|
| Mild | Moderate | Severe | Total | |
| Nicotinamide | 49 | 27 | 3 | 79 |
| Placebo | 38 | 31 | 2 | 71 |
Body Mass Index (BMI) was recorded at every study visit (screening, baseline, week 12, week 24, and week 48) (NCT03061474)
Timeframe: Screening through end of study (week 48)
| Intervention | kg/m^2 (Mean) | ||||
|---|---|---|---|---|---|
| Screening Visit | Baseline Visit | Week 12 Visit | Week 24 Visit | Week 48 Visit | |
| Nicotinamide | 26.35 | 26.33 | 26.42 | 26.52 | 26.24 |
| Placebo | 24.09 | 24.85 | 24.72 | 25.08 | 24.68 |
Diastolic blood pressure was recorded at every study visit (screening, baseline, week 12, week 24, and week 48) (NCT03061474)
Timeframe: Screening through end of study (week 48)
| Intervention | mm Hg (Mean) | ||||
|---|---|---|---|---|---|
| Screening Visit | Baseline Visit | Week 12 Visit | Week 24 Visit | Week 48 Visit | |
| Nicotinamide | 75.42 | 74.21 | 72.45 | 75.2 | 71.9 |
| Placebo | 71.32 | 70.45 | 71.4 | 71.4 | 69.74 |
Pulse rate was recorded at every study visit (screening, baseline, week 12, week 24, and week 48) (NCT03061474)
Timeframe: Screening through end of study (week 48)
| Intervention | bpm (Mean) | ||||
|---|---|---|---|---|---|
| Screening Visit | Baseline Visit | Week 12 Visit | Week 24 Visit | Week 48 Visit | |
| Nicotinamide | 56.42 | 59.33 | 58.86 | 58.6 | 59.57 |
| Placebo | 62.5 | 64.91 | 63.45 | 62.26 | 64.84 |
Systolic blood pressure was recorded at every study visit (screening, baseline, week 12, week 24, and week 48) (NCT03061474)
Timeframe: Screening through end of study (week 48)
| Intervention | mm Hg (Mean) | ||||
|---|---|---|---|---|---|
| Screening Visit | Baseline Visit | Week 12 Visit | Week 24 Visit | Week 48 Visit | |
| Nicotinamide | 134.67 | 137.42 | 133.36 | 130.4 | 129.43 |
| Placebo | 126.09 | 125.41 | 128.05 | 130.16 | 129.37 |
Weight in kg was recorded at every study visit (screening, baseline, week 12, week 24, and week 48) (NCT03061474)
Timeframe: Screening through end of study (week 48)
| Intervention | kg (Mean) | ||||
|---|---|---|---|---|---|
| Screening Visit | Baseline Visit | Week 12 Visit | Week 24 Visit | Week 48 Visit | |
| Nicotinamide | 76.39 | 76.29 | 77.27 | 76.88 | 76.43 |
| Placebo | 68.11 | 70.05 | 69.36 | 72.22 | 70.27 |
6 reviews available for niacinamide and Alzheimer Disease
| Article | Year |
|---|---|
Dynamic changes in metabolites of the kynurenine pathway in Alzheimer's disease, Parkinson's disease, and Huntington's disease: A systematic Review and meta-analysis.
Topics: 3-Hydroxyanthranilic Acid; Adenosine; Alzheimer Disease; Humans; Huntington Disease; Hydroxyindoleac | 2022 |
Can nicotinamide riboside protect against cognitive impairment?
Topics: Alzheimer Disease; Amyloid Precursor Protein Secretases; Animals; Aspartic Acid Endopeptidases; Brai | 2020 |
Protective Effects of Nicotinamide Adenine Dinucleotide and Related Precursors in Alzheimer's Disease: A Systematic Review of Preclinical Studies.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Anti-Inflammatory Agents; Apoptosis; Behavior, An | 2021 |
Nicotinamide riboside, a trace nutrient in foods, is a vitamin B3 with effects on energy metabolism and neuroprotection.
Topics: Alzheimer Disease; Animals; Brain; Disease Models, Animal; Energy Metabolism; Humans; Insulin Resist | 2013 |
Nicotinamide riboside, a trace nutrient in foods, is a vitamin B3 with effects on energy metabolism and neuroprotection.
Topics: Alzheimer Disease; Animals; Brain; Disease Models, Animal; Energy Metabolism; Humans; Insulin Resist | 2013 |
Nicotinamide riboside, a trace nutrient in foods, is a vitamin B3 with effects on energy metabolism and neuroprotection.
Topics: Alzheimer Disease; Animals; Brain; Disease Models, Animal; Energy Metabolism; Humans; Insulin Resist | 2013 |
Nicotinamide riboside, a trace nutrient in foods, is a vitamin B3 with effects on energy metabolism and neuroprotection.
Topics: Alzheimer Disease; Animals; Brain; Disease Models, Animal; Energy Metabolism; Humans; Insulin Resist | 2013 |
Vitamins B1, B2, B3 and B9 - Occurrence, Biosynthesis Pathways and Functions in Human Nutrition.
Topics: Alzheimer Disease; Biological Availability; Dietary Supplements; Folic Acid; Humans; Metabolic Disea | 2017 |
Hematopoietic prostaglandin D synthase inhibitors.
Topics: Alzheimer Disease; Animals; Asthma; Dermatitis, Atopic; Drug Design; Enzyme Inhibitors; Humans; Intr | 2012 |
1 trial available for niacinamide and Alzheimer Disease
| Article | Year |
|---|---|
Thiamine and Alzheimer's disease. A pilot study.
Topics: Alzheimer Disease; Behavior; Cognition; Double-Blind Method; Humans; Mental Status Schedule; Niacina | 1988 |
31 other studies available for niacinamide and Alzheimer Disease
| Article | Year |
|---|---|
Design, synthesis of allosteric peptide activator for human SIRT1 and its biological evaluation in cellular model of Alzheimer's disease.
Topics: Allosteric Regulation; Alzheimer Disease; Amyloid beta-Peptides; Animals; Cell Death; Cell Line, Tum | 2017 |
Modulation of cGAS-STING Pathway by Nicotinamide Riboside in Alzheimer's Disease.
Topics: Alzheimer Disease; Animals; Humans; Membrane Proteins; Mice; Niacinamide; Nucleotidyltransferases; P | 2021 |
Nicotinamide riboside and caffeine partially restore diminished NAD availability but not altered energy metabolism in Alzheimer's disease.
Topics: Alzheimer Disease; Caffeine; Energy Metabolism; Humans; NAD; Niacinamide; Pyridinium Compounds | 2022 |
Nicotinamide attenuates the decrease in dendritic spine density in hippocampal primary neurons from 5xFAD mice, an Alzheimer's disease animal model.
Topics: Adenosine Monophosphate; Alzheimer Disease; Amyloid beta-Peptides; Animals; Cells, Cultured; Dendrit | 2020 |
Physical exercise may exert its therapeutic influence on Alzheimer's disease through the reversal of mitochondrial dysfunction via SIRT1-FOXO1/3-PINK1-Parkin-mediated mitophagy.
Topics: Adenosine Triphosphate; Alzheimer Disease; Amyloid beta-Peptides; Brain-Derived Neurotrophic Factor; | 2021 |
Ex Vivo Investigation of Bexarotene and Nicotinamide Function as a Protectıve Agent on Rat Synaptosomes Treated with Aβ(1-42).
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Apoptosis; Bexarotene; Brain; Male; Neuroprotecti | 2021 |
Novel
Topics: Alzheimer Disease; Animals; Bipolar Disorder; Blood-Brain Barrier; Brain; Cell Line, Tumor; Diabetes | 2021 |
How gut microbes could drive brain disorders.
Topics: alpha-Synuclein; Alzheimer Disease; Amyotrophic Lateral Sclerosis; Animals; Autism Spectrum Disorder | 2021 |
Parp mutations protect from mitochondrial toxicity in Alzheimer's disease.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Animals, Genetically Modified; Behavior, Animal; | 2021 |
Discovery of 2-(cyclopropanecarboxamido)-N-(5-((1-(4-fluorobenzyl)piperidin-4-yl)methoxy)pyridin-3-yl)isonicotinamide as a potent dual AChE/GSK3β inhibitor for the treatment of Alzheimer's disease: Significantly increasing the level of acetylcholine in th
Topics: Acetylcholine; Acetylcholinesterase; Alzheimer Disease; Animals; Binding Sites; Blood-Brain Barrier; | 2021 |
Discovery of Novel and Highly Selective Inhibitors of Calpain for the Treatment of Alzheimer's Disease: 2-(3-Phenyl-1H-pyrazol-1-yl)-nicotinamides.
Topics: Alzheimer Disease; Aminobutyrates; Animals; Calpain; Cathepsins; Cysteine Proteinase Inhibitors; Dog | 2017 |
New cyclopentaquinoline hybrids with multifunctional capacities for the treatment of Alzheimer's disease.
Topics: Acetylcholinesterase; Alzheimer Disease; Aminoquinolines; Amyloid beta-Peptides; Animals; Butyrylcho | 2017 |
Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Caenorhabditis elegans; Disease Models, Animal; H | 2017 |
Nicotinamide loaded functionalized solid lipid nanoparticles improves cognition in Alzheimer's disease animal model by reducing Tau hyperphosphorylation.
Topics: Alzheimer Disease; Animals; Cell Line; Disease Models, Animal; Drug Carriers; Humans; Injections, In | 2018 |
Nicotinamide ribose ameliorates cognitive impairment of aged and Alzheimer's disease model mice.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animals; Astrocytes; Brain | 2019 |
The Role of Beclin-1 Acetylation on Autophagic Flux in Alzheimer's Disease.
Topics: Acetylation; Aged; Alzheimer Disease; Autophagy; Beclin-1; Cell Survival; E1A-Associated p300 Protei | 2019 |
Synthesis and biological activity of new donepezil-hydrazinonicotinamide hybrids.
Topics: Alzheimer Disease; Butyrylcholinesterase; Cholinesterase Inhibitors; Colorimetry; Donepezil; Indans; | 2013 |
Dual-energy precursor and nuclear erythroid-related factor 2 activator treatment additively improve redox glutathione levels and neuron survival in aging and Alzheimer mouse neurons upstream of reactive oxygen species.
Topics: Aging; Alzheimer Disease; Amyloid beta-Peptides; Animals; Cell Survival; Cells, Cultured; Disease Mo | 2014 |
Nicotinamide treatment reduces the levels of oxidative stress, apoptosis, and PARP-1 activity in Aβ(1-42)-induced rat model of Alzheimer's disease.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Antioxidants; Apoptosis; Apoptosis Regulatory Pro | 2014 |
Ex vivo protective effects of nicotinamide and 3-aminobenzamide on rat synaptosomes treated with Aβ(1-42).
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Benzamides; Brain; Male; Mitochondria; Neurons; N | 2014 |
Discovery and Preclinical Validation of [(11)C]AZ13153556, a Novel Probe for the Histamine Type 3 Receptor.
Topics: Alzheimer Disease; Animals; Autoradiography; Benzamides; Benzazepines; Brain; Carbon Radioisotopes; | 2016 |
Ligand autoradiographical quantification of histamine H
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Autoradiography; Benzazepines; Cerebellar Cortex; Dement | 2016 |
Synthesis of carbon-11-labeled isonicotinamides as new potential PET agents for imaging of GSK-3 enzyme in Alzheimer's disease.
Topics: Alzheimer Disease; Carbon Radioisotopes; Chromatography, High Pressure Liquid; Glycogen Synthase Kin | 2017 |
Nicotinamide restores cognition in Alzheimer's disease transgenic mice via a mechanism involving sirtuin inhibition and selective reduction of Thr231-phosphotau.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animals; Behavior, Animal; | 2008 |
Characterization of histamine H3 receptors in Alzheimer's Disease brain and amyloid over-expressing TASTPM mice.
Topics: Aged; Alzheimer Disease; Amyloid beta-Protein Precursor; Animals; Autoradiography; Benzazepines; Bra | 2009 |
A reversible early oxidized redox state that precedes macromolecular ROS damage in aging nontransgenic and 3xTg-AD mouse neurons.
Topics: Adenine Nucleotides; Aging; Alzheimer Disease; Amyloid beta-Protein Precursor; Animals; Calcium; Cel | 2012 |
Nicotinamide forestalls pathology and cognitive decline in Alzheimer mice: evidence for improved neuronal bioenergetics and autophagy procession.
Topics: Alzheimer Disease; Animals; Autophagy; Cells, Cultured; Cognition Disorders; Disease Models, Animal; | 2013 |
Nicotinamide riboside restores cognition through an upregulation of proliferator-activated receptor-γ coactivator 1α regulated β-secretase 1 degradation and mitochondrial gene expression in Alzheimer's mouse models.
Topics: Alzheimer Disease; Amyloid Precursor Protein Secretases; Animals; Aspartic Acid Endopeptidases; Cell | 2013 |
New tacrine-hydrazinonicotinamide hybrids as acetylcholinesterase inhibitors of potential interest for the early diagnostics of Alzheimer's disease.
Topics: Acetylcholinesterase; Alzheimer Disease; Butyrylcholinesterase; Cholinesterase Inhibitors; Humans; H | 2006 |
GSK189254, a novel H3 receptor antagonist that binds to histamine H3 receptors in Alzheimer's disease brain and improves cognitive performance in preclinical models.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Alzheimer Disease; Animals; Benzazepines; Binding, Compe | 2007 |
Effect of Huntington's and Alzheimer's diseases on the transport of nicotinic acid or nicotinamide across the human blood-brain barrier.
Topics: Alzheimer Disease; Blood-Brain Barrier; Brain; Humans; Huntington Disease; Niacin; Niacinamide; Tomo | 1991 |