Lower Vitamin B12 Level at Multiple System Atrophy Diagnosis Is Associated With Shorter Survival

Wan

et al. 2023

Front. Aging Neurosci.

AimThere is increasing evidence suggesting that vitamins may play important roles in the pathogenesis of multiple system atrophy (MSA). The purpose of this study was to detect the changes of serum vitamin levels and investigate their correlation with disease severity in MSA patients.MethodsIn this cross-sectional study, 244 MSA patients, 200 Parkinson’s disease (PD) patients and 244 age-gender matched healthy controls were recruited. Serum vitamin levels were measured, including vitamin A, B1, B2, B9 (folate), B12, C, D, and E. Relevant clinical scales were used to assess the disease severity of MSA patients.ResultsCompared with the healthy controls, decreased serum folate levels and increased serum vitamin A and C levels were detected in MSA patients. Similar differences were also observed in the gender-based subgroup analysis. There were no differences detected between MSA and PD patients. In MSA patients, significant correlation was found between vitamin A, folate, or vitamin C and relevant clinical scales or laboratory findings. In addition, ROC analysis showed potential diagnostic value of the combination of vitamin A, folate, and vitamin C in distinguishing MSA patients from healthy controls.ConclusionThere were significant changes in the blood vitamin spectrums of MSA patients, suggesting that dysregulation of vitamins homeostasis might play an important role in the pathogenesis of MSA.

Section: Discussionmentioning

confidence: 90%

Serum vitamin levels in multiple system atrophy: A case-control study

Wan

et al. 2023

Front. Aging Neurosci.

“…37 A natural history study showed that low vitamin B12 levels (< 367 ng/L) were associated with shorter survival (hazard ratio, 1.8; 95% confidence interval, 1.3-2.7), increased frequency of falls within three years of onset, and a lower body mass index, suggesting a potential new target for therapeutic intervention. 14 Another retrospective natural history study revealed that patients with MSA treated with SSRIs showed a better prognosis than untreated patients. 38 Fluoxetine, a second-generation antidepressant categorized as an SSRI, did not affect the primary endpoint.…”

Section: Disease-modifying Therapies and Other Treatmentmentioning

confidence: 99%

“…Other treatments, such as the mammalian target of rapamycin inhibitor sirolimus, which induces autophagy, were ineffective after 48 weeks of treatment [ 37 ]. A natural history study showed that low vitamin B12 levels (< 367 ng/L) were associated with shorter survival (hazard ratio, 1.8; 95% confidence interval, 1.3–2.7), increased frequency of falls within three years of onset, and a lower body mass index, suggesting a potential new target for therapeutic intervention [ 14 ].…”

Section: Disease-modifying Therapies and Other Treatmentmentioning

confidence: 99%

“…However, notable advancements have been achieved in the development of antibody therapies against α-synuclein, 9 multitargeted diseasemodifying therapies, including mesenchymal stem cell (MSC)mediated neuroinflammation treatments, and other symptomatic treatments, such as selective serotonin reuptake inhibitors (SSRIs). [10][11][12][13][14] In 2022, the Movement Disorder Society (MDS) proposed new diagnostic criteria to develop disease-modifying therapies and promote clinical trials of MSA, 15 which was the first time that it had been revised since the second consensus was proposed in 2008. Additionally, novel biomarkers for diagnosis and progres-sion have been identified from brain imaging, and blood and cerebrospinal fluid (CSF) data have been reported.…”

Section: Introductionmentioning

confidence: 99%

“…Symptomatic treatment has limited efficacy in MSA, and no treatments suppress or alleviate disease progression. However, notable advancements have been achieved in the development of antibody therapies against α-synuclein [ 9 ], multitargeted disease-modifying therapies, including mesenchymal stem cell (MSC)-mediated neuroinflammation treatments, and other symptomatic treatments, such as selective serotonin reuptake inhibitors (SSRIs) [ 10 - 14 ].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Multiple System Atrophy: Advances in Diagnosis and Therapy

Watanabe

Shima

Mizutani

et al. 2023

JMD

This review summarizes improvements in understanding the pathophysiology and early clinical symptoms of multiple system atrophy (MSA) and advancements in diagnostic methods and disease-modifying therapies for the condition. In 2022, the Movement Disorder Society proposed new diagnostic criteria to develop disease-modifying therapies and promote clinical trials of MSA since the second consensus was proposed in 2008. Regarding pathogenesis, cutting-edge findings have accumulated on the interactions of α-synuclein, neuroinflammation, and oligodendroglia with neurons. In neuroimaging, introducing artificial intelligence, machine learning, and deep learning has notably improved diagnostic accuracy and individual analyses. Advancements in treatment have also been achieved, including immunotherapy therapy against α-synuclein and serotonin-targeted and mesenchymal stem cell therapies, which are thought to affect several aspects of the disease, including neuroinflammation. The accelerated progress in clarifying the pathogenesis of MSA over the past few years and the development of diagnostic techniques for detecting early-stage MSA are expected to facilitate the development of disease-modifying therapies for one of the most intractable neurodegenerative diseases.

Parkinson's disease and vitamins: a focus on vitamin B12

Rekik,

Santoro,

Poplawska-Domaszewicz

et al. 2024

J Neural Transm

Parkinson’s disease (PD) has been linked to a vast array of vitamins among which vitamin B12 (Vit B12) is the most relevant and often investigated specially in the context of intrajejunal levodopa infusion therapy. Vit B12 deficiency, itself, has been reported to cause acute parkinsonism. Nevertheless, concrete mechanisms through which B12 deficiency interacts with PD in terms of pathophysiology, clinical manifestation and progression remains unclear. Recent studies have suggested that Vit B12 deficiency along with the induced hyperhomocysteinemia are correlated with specific PD phenotypes characterized with early postural instability and falls and more rapid motor progression, cognitive impairment, visual hallucinations and autonomic dysfunction. Specific clinical features such as polyneuropathy have also been linked to Vit B12 deficiency specifically in context of intrajejunal levodopa therapy. In this review, we explore the link between Vit B12 and PD in terms of physiopathology regarding dysfunctional neural pathways, neuropathological processes as well as reviewing the major clinical traits of Vit B12 deficiency in PD and Levodopa-mediated neuropathy. Finally, we provide an overview of the therapeutic effect of Vit B12 supplementation in PD and posit a practical guideline for Vit B12 testing and supplementation.