Hyperhomocysteinemia influenced malnutrition in Parkinson’s disease patients

Tomić, Svetlana; Pekić, Vlasta; Popijać, Željka; Pučić, Tomislav; Vinkovic, Marta Petek; Kuric, Tihana Gilman; Popović, Zvonimir

doi:10.1007/s10072-018-3480-5

Cited by 13 publications

(12 citation statements)

References 33 publications

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“…Third, in the present study, lower numbers of regular exercise habits were observed in the malnutrition-risk group relative to the normal-nutrition group. However, regular physical activity could decrease the homocysteine levels [ 49 ], which are significantly associated with nutritional status in PD patients [ 50 ]. In addition, increasing levodopa (L-dopa) equivalent daily dosages were associated with an increasing probability of malnutritional risk in PD patients [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

Nutritional Status Associated with Molecular Biomarkers, Physiological Indices, and Clinical Severity in Parkinson’s Disease Patients

Lin

Chang

Chen

et al. 2020

IJERPH

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This study is intended to explore the associations between nutritional status and molecular biomarkers and the clinical severity of Parkinson’s disease (PD), as well as to examine the differences in related factors between PD patients with normal nutrition and those with at risk for malnutrition. A cross-sectional assessment of 82 consecutive outpatients with PD was conducted using the mini nutritional assessment (MNA), Unified Parkinson’s Disease Rating Scale (UPDRS), and the Hoehn and Yahr scale to determine the nutritional status, the clinical severity of PD, and the stage of the disease. Recordings of blood samples collected after 12 h of overnight fasting were also assessed in terms of serum levels of glycated hemoglobin (HbA1c), blood urea nitrogen (BUN), creatinine, cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), hemoglobin (Hgb), folate, and vitamin B12. All participants were divided into normal nutrition and malnutrition risk groups via the MNA scores to compare the above-mentioned parameters. The results showed that the total MNA score was significantly correlated with some parts of the UPDRS scale (e.g., Sections 1 and 2) and the levels of HbAlc in PD patients and those with risk for malnutrition, with significantly lower weight and body mass index (BMI), and with lower levels of Hgb and HDL. Higher levels of cholesterol were observed in the malnutrition risk group as compared with the normal nutrition group. The findings suggest that the clinical severity of PD is associated with nutritional status. Body weight, BMI, and the levels of Hgb, cholesterol, and HDL could be, at least partially, important biological markers to monitor malnutrition and the progression of the disease.

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Section: Discussionmentioning

confidence: 99%

Nutritional Status Associated with Molecular Biomarkers, Physiological Indices, and Clinical Severity in Parkinson’s Disease Patients

Lin

Chang

Chen

et al. 2020

IJERPH

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“…1 Many risk factors may lead to depressive disorders, such as gender, age, co-occurrence with other mental disorders, cardiovascular disease and increased chemical compounds that perturb neurotransmitters. [3][4][5] Homocysteine is an α-amino acid derived from heating methionine with sulphuric acid, 6 and the chemical structure of homocysteine is similar to cysteine. 7 Elevated plasma homocysteine, also known as hyperhomocysteinaemia, may be a risk factor for cardiovascular diseases, Parkinson's disease and cognitive impairment.…”

Section: Introductionmentioning

confidence: 99%

“…[8][9][10][11] It is also associated with neurodegenerative and psychiatric disorders, such as Alzheimer's disease, schizophrenia and anxiety. 12,13 Hyperhomocysteinaemia can be caused by impaired renal function, smoking, lack of physical activity, high blood pressure and hyperlipidaemia since some lipid-lowering drugs might also have an effect on homocysteine levels, 6,12,14 whilst excessive alcohol intake, high coffee intake and vitamin B12 and folate deficiency may increase the risk of hyperhomocysteinaemia. 6 Accordingly, supplementation with either folic acid or vitamin B12 has been proposed for the treatment of hyperhomocysteinaemia.…”

Section: Introductionmentioning

confidence: 99%

“…12,13 Hyperhomocysteinaemia can be caused by impaired renal function, smoking, lack of physical activity, high blood pressure and hyperlipidaemia since some lipid-lowering drugs might also have an effect on homocysteine levels, 6,12,14 whilst excessive alcohol intake, high coffee intake and vitamin B12 and folate deficiency may increase the risk of hyperhomocysteinaemia. 6 Accordingly, supplementation with either folic acid or vitamin B12 has been proposed for the treatment of hyperhomocysteinaemia. 15 Hyperhomocysteinaemia can interfere with neurological functions in various ways 10 ; indeed, excitotoxicity, DNA damage, oxidative stress and inflammation caused by hyperhomocysteinaemia may lead to abnormal neurological functions.…”

Section: Introductionmentioning

confidence: 99%

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The association between serum homocysteine and depression: A systematic review and meta‐analysis of observational studies

Moradi

Lotfi

Armin

et al. 2021

Eur J Clin Investigation

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Background: Hyperhomocysteinaemia is known to interfere with neurological functions; however, there is a controversy regarding the relationship between homocysteine and depression. Materials and methods: Science Direct, MEDLINE and ISI Web of Science were searched to find relevant articles, published up to August 2020. Studies were included if they compared homocysteine levels in healthy subjects with subjects with depression. Also, articles that reported the association between hyperhomocysteinaemia and risk of depression were included. Odds ratios of depression and means of homocysteine were used to ascertain the overall effect size. Results: Homocysteine level was higher in subjects with depression in comparison with healthy controls (weight mean difference = 2.53 µmol/L, 95% confidence interval: 1.77, 3.30), and the depression diagnostic tool was a source of heterogeneity.Homocysteine level was significantly higher in subjects with depression in studies that used Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-IV), Geriatric Depression Scale (GDS), Zung Self-Rating Depression Scale (ZDRS) and Beck Depression Index II (BDI-II) as depression diagnostic tools. Also, participants with hyperhomocysteinaemia had a higher chance of depression (Pooled risk = 1.34, 95% confidence interval: 1.19, 1.52), where the depression diagnostic tool was a source of heterogeneity. In contrast to ZDRS and Patient Health Questionnaire (PHQ) subgroups, hyperhomocysteinaemia yielded a significantly higher risk of depression in DSM-IV, GDS and 'other' subgroups. Conclusion: Homocysteinemia level is higher in individuals with depression.However, the depression diagnostic tool used is instrumental in influencing their association, and thus, future studies should focus on the tools for depression assessment.

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“…Homocysteine (Hcy) is a non-protein amino acid, formed by methionine (Met) derived from the diet and secreted during metabolism 1 . An elevated level of Hcy in the blood results in hyperhomocysteinemia (HHcy) and is closely associated with some neurodegenerative diseases, including dementia, Alzheimer's disease and Parkinson's disease 2 - 5 . The deleterious influences of HHcy have also been reported in the developing central nervous system (CNS) 1 , 6 .…”

Section: Introductionmentioning

confidence: 99%

Homocysteine aggravates DNA damage by impairing the FA/Brca1 Pathway in NE4C murine neural stem cells

et al. 2020

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There is existing evidence that elevated homocysteine (Hcy) levels are risk factors for some neurodegenerative disorders. The pathogenesis of neurological diseases could be contributed to excessive cell dysfunction and death caused by defective DNA damage response (DDR) and accumulated DNA damage. Hcy is a neurotoxic amino acid and acts as a DNA damage inducer. However, it is not clear whether Hcy participates in the DDR. To investigate the effects of Hcy on DNA damage and the DDR, we employed mitomycin C (MMC) to cause DNA damage in NE4C murine neural stem cells (NSCs). Compared to treatment with MMC alone, we found that co-treatment with MMC and Hcy worsened DNA damage and increased death in NE4C cells. Intriguingly, in this DNA damage model mimicked by MMC, immunoblotting results showed that the monoubiquitination levels of Fanconi anemia complementation group I (Fanci) and Fanconi anemia complementation group D2 (Fancd2) were decreased to about 60.3% and 55.7% by supplementing cell culture medium with Hcy, indicating Hcy inactivates the function of Fanci and Fancd2 in DNA damage conditions. Given Breast Cancer 1 (BRCA1) is an important downstream of FANCD2, we next detected the interaction between Fancd2 and Brca1 in NE4C cells. Compared to treatment with MMC alone, the Fancd2-Brca1 interaction and the amount of Brca1 on chromatin were decreased when cells were co-exposed to MMC and Hcy, suggesting Hcy could impair the Fanconi anemia (FA)/Brca1 pathway. Taken together, our study demonstrates that Hcy may enhance cell death, which contributes to the accumulation of DNA damage and promotion of hypersensitivity to cytotoxicity by impairing the FA/Brca1 pathway in murine NSCs in the presence of DNA damage.

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Hyperhomocysteinemia influenced malnutrition in Parkinson’s disease patients

Abstract: PD patients are at a risk of hyperhomocysteinemia. Regular physical activity decreases Hcy level, whereas poor motor function increases it. There is correlation between Hcy level and malnutrition in PD patients.

Cited by 13 publications

References 33 publications

Nutritional Status Associated with Molecular Biomarkers, Physiological Indices, and Clinical Severity in Parkinson’s Disease Patients

Nutritional Status Associated with Molecular Biomarkers, Physiological Indices, and Clinical Severity in Parkinson’s Disease Patients

The association between serum homocysteine and depression: A systematic review and meta‐analysis of observational studies

Homocysteine aggravates DNA damage by impairing the FA/Brca1 Pathway in NE4C murine neural stem cells

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