Serum Folate, Homocysteine, Brain Atrophy, and Auto-CM System: The Treviso Dementia (TREDEM) Study

Gallucci, Maurizio; Zanardo, Andrea; Bendini, Matteo; Paola, Francesco Di; Boldrini, Paolo; Grossi, Enzo

doi:10.3233/jad-130956

Cited by 30 publications

(32 citation statements)

References 28 publications

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“…The present study used doses of L-methylfolate and B12 that were respectively 10 and 4 times larger than the folate and B12 doses used in other regional brain volumetric studies of HHcy treatment with B vitamins [6,7,44]. Whether such dosing difference could significantly affect regional brain atrophy rates in HHcy-treated patients is not known and should be studied.…”

Section: Study Limitationsmentioning

confidence: 99%

“…Compared to subjects with normal homocysteine levels, HHcy also associates with poorer cognitive performance [5], and with relatively greater regional brain atrophy [6] and ischemic lesions (i.e., white matter hyperintensities, ischemia, or infarcts) [7]. Furthermore, the odds of brain atrophy are up to 10 times higher in HHcy patients than in those with normal homocysteine levels [8], and high, compared to normal, baseline homocysteine levels predicts moderate-severe whole brain atrophy 5 years later [9].…”

Section: Introductionmentioning

confidence: 99%

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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: Study Limitationsmentioning

confidence: 99%

Section: Introductionmentioning

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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“…46 Low concentrations of folate and high levels of homocysteine in the blood are related to MaND, Alzheimer's disease, and poor cognitive function in older adults. [47][48][49][50][51][52][53][54] In the TREDEM (Treviso Dementia) study carried out in Treviso, Italy, 55 close associations were found between low serum folate levels and severe cortical-subcortical atrophy along with severe hippocampal atrophy measured by the width of the temporal horns of the lateral ventricles. The Nun Study 37 and the Rotterdam Scan Study 56 showed a similar correlation between low serum folate levels and high brain cortical atrophy.…”

Section: Diet and Nutritionmentioning

confidence: 99%

Collaborative Management of Neurocognitive Disorders in Primary Care: Explorations of an Attempt at Culture Change

Mehl‐Madrona

Mainguy

2017

TPJ

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Introduction: Minor neurocognitive disorder (MiND; previously mild cognitive impairment) is a transitional zone between normal cognitive function and early stages of major neurocognitive disorder (previously called dementia). Of people with MiND, 5% to 10% progress to major neurocognitive disorder. Simple interventions such as memory activities, balance exercises, and anti-inflammatory diets have been shown to improve cognitive ability. Also, education and support in group settings have proved beneficial for patients with MiND.Design: Survey evaluation of outcomes of geriatric consultation and prospective educational study. Main Outcome Measures:We collaborated with an academic training program to introduce into primary care the ideas of educational activities and participation in group medical care for people with MiND. Educational programs were developed and presented to family medicine residents and practicing physicians, and their knowledge was assessed before and after education.Results: Two group programs were implemented: one at our hospital and one at a local skilled nursing facility. These were initially envisioned as time-limited, but participants insisted on their continuance. Thirty-two different patients attended the groups for at least six sessions. Participants enthusiastically reported positive change on qualitative interviews and showed improvement in cognition, balance, and self-esteem. Family medicine residents and practicing physicians both shifted toward lifestyle medicine and significantly changed their views on the efficacy of treatments. Despite these activities, community physicians making referrals for geriatric consultations did not change their discussions with patients and families about exercise, diet, cognitive enhancement, and socialization for MiND.Conclusion: Group visits that emphasized support for increased exercise, improved diet, more movement and balance, and cognitive enhancement appear to please and benefit patients with MiND. Physicians are more open to these approaches with training after initial skepticism. A struggle exists to convince the profession that lifestyle change may be beneficial in MiND.

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“…The major neuropathological features of AD are amyloid-β peptide aggregation and tau hyperphosphorylation in the hippocampus and cortex, along with brain atrophy and cognitive decline [17]. An elevated concentration of Hcy is associated with a serious decrease of volume in the hippocampus in a group of old outpatients [16]. Several potential mechanisms underlying the deleterious effect of Hcy in the brain have been proposed.…”

Section: Introductionmentioning

confidence: 99%

Monoacylglycerol lipase inhibitor protects primary cultured neurons against homocysteine-induced impairments in rat caudate nucleus through COX-2 signaling

Dong

Zou

et al. 2015

Life Sciences

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Serum Folate, Homocysteine, Brain Atrophy, and Auto-CM System: The Treviso Dementia (TREDEM) Study

Cited by 30 publications

References 28 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

Collaborative Management of Neurocognitive Disorders in Primary Care: Explorations of an Attempt at Culture Change

Monoacylglycerol lipase inhibitor protects primary cultured neurons against homocysteine-induced impairments in rat caudate nucleus through COX-2 signaling

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