Midlife homocysteine and late-life dementia in women. A prospective population study

Zylberstein, Dimitri; Lissner, Lauren; Björkelund, Cecilia; Mehlig, Kirsten; Thelle, Dag S.; Gustafson, Deborah; Östling, Svante; Wærn, Margda; Guo, Xinxin; Skoog, Ingmar

doi:10.1016/j.neurobiolaging.2009.02.024

Cited by 65 publications

(41 citation statements)

References 43 publications

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“…Several large -scale long follow-up studies have demonstrated an increased risk of AD with high plasma total homocysteine after adjustment of other variables [118,119]. In the Framingham Offspring Study, 2096 participants have been examined seven times for multiple parameters for 30 years followed by a battery of neuropsychological tests, and an inverse association of plasma total homocysteine with multiple cognitive domains has been noted in subjects above 60 years or above [120].…”

Section: Hyperhomocysteinemiamentioning

confidence: 99%

Metabolic Risk Factors of Sporadic Alzheimer's Disease: Implications in the Pathology, Pathogenesis and Treatment

Chakrabarti¹,

Khemka²,

Banerjee³

et al. 2015

Aging and disease

107

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Alzheimer's disease (AD), the major cause of dementia among the elderly world-wide, manifests in familial and sporadic forms, and the latter variety accounts for the majority of the patients affected by this disease. The etiopathogenesis of sporadic AD is complex and uncertain. The autopsy studies of AD brain have provided limited understanding of the antemortem pathogenesis of the disease. Experimental AD research with transgenic animal or various cell based models has so far failed to explain the complex and varied spectrum of AD dementia. The review, therefore, emphasizes the importance of AD related risk factors, especially those with metabolic implications, identified from various epidemiological studies, in providing clues to the pathogenesis of this complex disorder. Several metabolic risk factors of AD like hypercholesterolemia, hyperhomocysteinemia and type 2 diabetes have been studied extensively both in epidemiology and experimental research, while much less is known about the role of adipokines, proinflammatory cytokines and vitamin D in this context. Moreover, the results from many of these studies have shown a degree of variability which has hindered our understanding of the role of AD related risk factors in the disease progression. The review also encompasses the recent recommendations regarding clinical and neuropathological diagnosis of AD and brings out the inherent uncertainty and ambiguity in this area which may have a distinct impact on the outcome of various population-based studies on AD-related risk factors.

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Section: Hyperhomocysteinemiamentioning

confidence: 99%

Metabolic Risk Factors of Sporadic Alzheimer's Disease: Implications in the Pathology, Pathogenesis and Treatment

Chakrabarti¹,

Khemka²,

Banerjee³

et al. 2015

Aging and disease

107

View full text Add to dashboard Cite

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“…Another study showed that HHcy treatment with B-vitamins for 2 years improved cognition more in milder severity patients [7]. The most extreme example of the impact of severity on HHcy response was reported among asymptomatic, untreated HHcy females in midlife; their late life ADRD risk assessed 35 years later was increased by 1.7-fold [46]. CFLN management of HHcy in cognitively impaired patients significantly reduced rate of hippocampal and cortical atrophy, and significantly reduced rate of forebrain parenchymal atrophy in CVD.…”

Section: Study Limitationsmentioning

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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“…Although homocysteine is an established risk factor for cardiovascular disease, its role in dementia has been controversial [30]. High homocysteine concentrations in mid-life is an independent risk factor for the development of late-life AD in women [31]. Although these epidemiological studies do not explain how pre-existing or co-morbid vascular disease precisely impacts on processes that lead to neurodegeneration characteristic of AD they collectively demonstrate that there is a clear link between vascular disease and an increased burden of AD (Table 2).…”

Section: Vascular Disease As Risk Factor For Increasing Clinically DImentioning

confidence: 99%

Does vascular pathology contribute to Alzheimer changes?

Kalaria

Akinyemi

Ihara

2012

Journal of the Neurological Sciences

212

170

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Midlife homocysteine and late-life dementia in women. A prospective population study

Cited by 65 publications

References 43 publications

Metabolic Risk Factors of Sporadic Alzheimer's Disease: Implications in the Pathology, Pathogenesis and Treatment

Metabolic Risk Factors of Sporadic Alzheimer's Disease: Implications in the Pathology, Pathogenesis and Treatment

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

Does vascular pathology contribute to Alzheimer changes?

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