The Role and Mechanisms of Action of Catechins in Neurodegenerative Diseases.

The prevalence, incidence and mortality rates of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease are gradually increasing. New approaches are being developed to manage the progression and treatment of neurodegenerative diseases. Catechins, polyphenolic compounds, are key compounds that demonstrate therapeutic effects with their properties such as antioxidant, anti-inflammatory, anti-apoptotic properties in the prevention and treatment of neurodegenerative diseases. The therapeutic effects of catechins have been exhaustively studied in human and animal models. Catechins can have anti-inflammatory effects by suppressing inflammatory pathways and cytokines, as well as antioxidant effects such as chelating metal ions and scavenging radicals. They might reduce phosphorylation of tau proteins, aggregation of amyloid-beta and apoptotic proteins release. They can also decrease alpha-synuclein accumulation and increase dopamine levels. With all these effects, they can have an effect on neurodegenerative diseases. This review points to the potential mechanisms of catechins in neurodegenerative diseases, based on their findings in the literature review.Key teaching pointsCatechins can reduce amyloid-ß plaque aggregation and tau phosphorylation.Catechins can decrease alfa-synuclein levels.Catechins can protect neuronal cells with their anti-apoptotic effect.More comprehensive studies are needed to clarify this issue.

The correlation of uric acid levels with biochemical parameters and dietary factors in individuals with asymptomatic hyperuricemia and gouty arthritis.

Diet may play an important role in the development of asymptomatic hyperuricemia (ASH) and gouty arthritis (GOUT). However, the association between dietary factors and hyperuricemia remains unclear. Serum uric acid levels are affected by dietary factors. This study aimed to evaluate the correlation of uric acid levels with biochemical parameters and dietary factors in individuals with ASH and GOUT. This study was conducted in 145 individuals with ASH and GOUT. General characteristics of individuals were collected via face-to-face interviews. Food frequency questionnaire was used to obtain energy, macro- and micronutrients intakes. Biochemical parameters were obtained from patient files. The incidence of gout was higher in men comparing to women. Individuals in the GOUT group consumed more alcohol and higher serum levels of vitamin B12, C-reactive protein (CRP), triglyceride, and uric acid. Individuals in the GOUT group had higher intakes of energy, protein, carbohydrate, fat, fructose, vitamin C, and vitamin B12. Triglyceride, uric acid, CRP, vitamin B12, and homeostatic model assessment of insulin resistance were found to be affected by high uric acid levels. Dietary factors can pose a risk for health problems in addition to GOUT and ASH, such as cardiovascular disease, diabetes, and obesity.

Neuroprotective effects of catechins in an experimental Parkinson's disease model and SK-N-AS cells: evaluation of cell viability, anti-inflammatory and anti-apoptotic effects.

OBJECTIVES: The aim of the study was to establish an in vitro Parkinson's disease (PD) model and to investigate the cell viability, anti-inflammatory, anti-apoptotic and neuroprotective effects of catechin and EGCG in SK-N-AS and in vitro PD model cells. METHOD: SK-N-AS human neuroblastoma cells were used. To develop an in vitro PD model, SK-N-AS cells were exposed to 6-hydroxydopamine. Model control was performed after ELISA analysis of dopamine and α-synuclein levels in the culture medium. Catechin and EGCG were administered to SK-N-AS and in vitro PD model cells. Cell viability was measured using MTT assay and trypan blue staining. Anti-inflammatory and anti-apoptotic activities of catechin and EGCG were investigated by indirect immunocytochemistry using anti-TNF-α, anti-IL-1ß and anti-caspase-3. RESULTS: After 24 hours of 6-hydroxydopamine administration at 50 µM, higher αlfa-synuclein and lower dopamine levels were found in PD model than SK-N-AS cells. Cell viability was similar between SK-N-AS and in vitro PD model cells. Treatment with both bioactive components increased cell viability of in vitro PD model cells. Caspase-3 immunoreactivity was significantly reduced in SK-N-AS and PD model cells after EGCG administration, while it was decreased only in PD model cells after catechin administration. IL-1ß staining intensity weakened after catechin administration in PD model cells, after EGCG administration in SK-N-AS cells. TNF-α staining intensity was similar in both cells. CONCLUSION: Catechin and EGCG increased cell viability in PD model neuron cells. Both components showed anti-apoptotic and anti-inflammatory effects. Catechin may be more effective in preventing damage to neurons PD.