A Phase II Randomized Clinical Trial of a Nutritional Formulation for Cognition and Mood in Alzheimer's Disease

Remington, Ruth; Bechtel, Cynthia; Larsen, David A.; Samar, Annemarie; Doshanjh, Laura; Fishman, Paul S.; Luo, Yuan; Smyers, Kathleen; Page, Robert G.; Morrell, Christopher H.; Shea, Thomas B.

doi:10.3233/jad-142499

Cited by 106 publications

(96 citation statements)

References 35 publications

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“…A phase II, double blind, randomized trial of 106 AD patients compared cognitive and symptom severity outcomes for placebo versus treatment consisting of folate, alpha-tocopherol, S-adenosyl methioinine, acetyl-Lcarnitine, and NAC, for 3 or 6 months, followed by open-label treatment for 6 months. There was statistically significant improvement at 3 months in a constructional praxis task (Clox), and in overall dementia severity (Dementia Severity Scale), plus no decline below baseline for all subjects during six months of the open-label phase [37]. Eighty-one US soldiers actively deployed in Iraq, who had suffered mild TBI due to blast exposure in the field, were randomized to NAC or placebo and treated for 7 days.…”

Section: Other Possible Mechanisms Underlying Cfln Treatment Effect Ementioning

confidence: 99%

CerefolinNAC Therapy of Hyperhomocysteinemia Delays Cortical and White Matter Atrophy in Alzheimer’s Disease and Cerebrovascular Disease

Shankle¹,

Hara²,

Barrentine

et al. 2016

JAD

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Abstract. We examined whether using a medical food therapy for hyperhomocysteinemia (HHcy) in patients with Alzheimer's disease (AD) or cognitive impairment due to cerebrovascular disease (CVD) with Cerefolin ® /CerefolinNAC ® (CFLN: Lmethylfolate, methylcobalamin, and N-acetyl-cysteine) slowed regional brain atrophy. Thirty HHcy patients with AD and related disorders (ADRD) received CFLN (HHcy+CFLN: duration [ ± σ] = 18.6 ± 16.1 months); a sub-sample of this group did not receive CFLN for varying periods of time (HHcy+NoCFLN: duration [ ± σ] = 12.6 ± 5.6 months). Thirtyseven NoHHcy patients with ADRD did not receive CFLN (NoHHcy+NoCFLN: duration [ ± σ] = 13.3 ± 17.7 months). No participant took supplemental B vitamins. Regional brain volumes were measured at baseline and end of study, and covariate-adjusted rates of hippocampal, cortical, and forebrain parenchymal (includes white matter) atrophy were predicted. The HHcy+CFLN group's hippocampal and cortical atrophy adjusted rates were 4.25 and 11.2 times slower than those of the NoHHcy+NoCFLN group (p < 0.024). The HHcy+CFLN group's forebrain parenchyma atrophy rate was significantly slower only for CVD; the rate of slowing was proportional to the degree of homocysteine lowering (p < 0.0001). CFLN was associated with significantly slowed hippocampal and cortical atrophy rates in ADRD patients with HHcy, and forebrain parenchymal atrophy rates in CVD patients with HHcy. The present results should be further validated.

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Section: Other Possible Mechanisms Underlying Cfln Treatment Effect Ementioning

confidence: 99%

CerefolinNAC Therapy of Hyperhomocysteinemia Delays Cortical and White Matter Atrophy in Alzheimer’s Disease and Cerebrovascular Disease

Shankle¹,

Hara²,

Barrentine

et al. 2016

JAD

View full text Add to dashboard Cite

show abstract

“…Those with genetically lower levels of an enzyme necessary for folate metabolism (methylenetetrahydrofolate reductase) were more prone to develop Alzheimer's disease than were individuals with adequate enzyme activity (108). Supplements with a combination of vitamins show promise for treating Alzheimer's disease (110,111), but confirmation with well-constructed randomized clinical trials is needed (73,79).…”

Section: Folatementioning

confidence: 99%

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2017

Cereal Foods World

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“…Recently clinical trial of a nutritional formula contains α-tocopherol showed no significant improvement in cognitive performances [120] . Albarracin et al (2012) [121] have also reviewed the effect of natural antioxidants in neurodegenerative diseases.…”

Section: Evidences For the Beneficial Use Of Antioxidants In Neurodegmentioning

confidence: 99%

“…Frank et al (2012) [121] have reviewed the role of tocotrienols as neuroprotective dietary factors but still the information is scarce. Epidemiological studies have reported that vitamin E (ortocopherol) can prevent the AD pathology however, prospective, randomized studies have not been convincingly able to demonstrate the clinical efficacy [122] .…”

Section: Evidences For the Beneficial Use Of Antioxidants In Neurodegmentioning

confidence: 99%

Antioxidants as a preventive therapeutic option for age related neurodegenerative diseases

Singh

2015

Ther Targets Neurol Dis

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Neurodegenerative diseases: an overview -Neurodegenerative disease term illustrate a range of conditions in which primarily neurons get affected or die. Neurons are the building blocks of the central and peripheral nervous system. Neurons could not reproduce or replace themselves with age therefore, when they get damaged or die they cannot be replaced and lead to specific neurodegenerative disease. Few evidences for the presence of stem cells are reported [1] but still it is not understood whether damaged neuron could regenerate or not. The Parkinson's, Alzheimer's, and Huntington's diseases are the most prevalent age related neurodegenerative diseases of central nervous system involving death of specific neuronal population. The treatment of these neurodegenerative diseases might involve the re-supplementation of specific neuronal population with the help of stem cells but researchers and clinicians did not get noticeable success in this approach yet. Millions of people each year are getting affected by these neurodegenerative diseases and the incidences are increasing further significantly with the extended life expectancy. It has been reported by World Health Organisation (2006) that the number of older people of more than 65 years age are expected to increase to approximately 1 billion in 2030 worldwide. Developing countries like India and China will see the largest increase in numbers of aged persons. Therefore the percentage of aged population in developing countries would increase from 59% to 71% worldwide [2] . Since occurrence of most of the neurodegenerative Advances in our understanding for neurodegenerative mechanisms have increased significantly in last few decades. But still no novel disease modifying therapy has been developed which could prevent the disease progression and drawn our attention towards the development of new alternative therapy. The major obstacle for the development of disease therapy is incomplete knowledge about neurodegenerative mechanisms. Due to the insufficient information about neurodegenerative mechanisms no standard diagnostic tests for the detection of neurodegenerative disease could be develop to date, causes delayed diagnosis and disease worsening. So far the exploratory reports and clinical data have suggested the involvement of oxidative stress, mitochondrial impairment and apoptosis as major neurodegenerative mechanisms. Investigations have elicited that once initiated the degeneration of neurons could not be arrested therefore in the scarcity of curative therapy we should approach for the preventive neurodegenerative therapy. Since oxidative stress has noteworthy involvement in neuronal death solely, and in connection to other death pathways therefore, antioxidants as preventive therapeutics might provide beneficial effects in age related neurodegenerative diseases. With this hypothesis in this review we are discussing about the use of antioxidants as a preventive treatment of neurodegenerative diseases. Such therapies may work in the preventive phase or in curati...

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A Phase II Randomized Clinical Trial of a Nutritional Formulation for Cognition and Mood in Alzheimer's Disease

Abstract: These findings extend phase I studies where NF maintained or improved cognitive performance and mood/behavior.

Cited by 106 publications

References 35 publications

CerefolinNAC Therapy of Hyperhomocysteinemia Delays Cortical and White Matter Atrophy in Alzheimer’s Disease and Cerebrovascular Disease

CerefolinNAC Therapy of Hyperhomocysteinemia Delays Cortical and White Matter Atrophy in Alzheimer’s Disease and Cerebrovascular Disease

Full Issue PDF

Antioxidants as a preventive therapeutic option for age related neurodegenerative diseases

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