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Phosphatidylserine 図

22 査読済み研究からの図表

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Figure 1. Western blot analyses of protein markers in fractions 1–6 from NSL, PD and PDi brain cortices. Equal amounts of total protein were used for NSL, PD and iPD samples. Standard molecular weight values are indicated (left).
Figure 1 Photograph

Western blot analyses of protein markers across density gradient fractions from control, Parkinson's disease, and incidental PD brain cortices reveal altered lipid raft protein distribution.

Severe alterations in lipid composition of frontal cortex lipid rafts from Parkinson's …

Figure 2
Figure 2 Chart

Lipid composition analyses comparing raft and non-raft fractions between control and Parkinson's disease frontal cortex samples show significant alterations in cholesterol and sphingolipid content.

Severe alterations in lipid composition of frontal cortex lipid rafts from Parkinson's …

Figure 4. (A) Comparative analyses of main lipid classes and fatty acid contents and relevant indices between control and PD frontal cortex gray matter. Results are expressed as percent of change versus NSL group. Eight cases were analyzed in each group.
Figure 3 Chart

Comparative analyses of main lipid classes and fatty acid content between control and PD frontal cortex gray matter reveal disease-associated shifts in polyunsaturated fatty acid profiles and raft lipid indices.

Severe alterations in lipid composition of frontal cortex lipid rafts from Parkinson's …

Figure 1. Structure of PKCa C2 domain bound to Ca2+-POPSPIP2 in a quaternary complex. The C2 molecule is shown in green. The three calcium ions are shown in yellow spheres, one of them bridging the protein with phosphatidylserine (PS) at the tip of the do
Figure 1 Diagram

The crystal structure of the PKCα C2 domain bound to calcium, phosphatidylserine, and PIP2 in a quaternary complex is rendered, showing the spatial arrangement of lipid-binding sites.

Phosphatidylinositol 4,5-bisphosphate decreases the concentration of Ca2+, phosphatidylserine and diacylglycerol required for …

Figure 2. The dependence of PKCa activity on Ca2+ concentration. The molar ratios of the lipid components of the vesicles used to activate the enzyme are shown. Ca2+ concentration was 200 mmol. SD calculated from 3 independent experiments. doi:10.1371/jou
Figure 2 Chart

PKCα enzymatic activity is plotted as a function of calcium concentration, demonstrating how PIP2 reduces the calcium requirement for maximal kinase activation.

Phosphatidylinositol 4,5-bisphosphate decreases the concentration of Ca2+, phosphatidylserine and diacylglycerol required for …

Figure 3. The dependence of PKCa activity on the POPS molar percentage in the vesicles. The molar ratios of the lipid components of the vesicles used to activate the enzyme are shown. Ca2+ concentration was 200 mmol. SD calculated from 3 independent exper
Figure 3 Chart

The dependence of PKCα activity on phosphatidylserine (POPS) concentration in lipid vesicles reveals that PIP2 lowers the threshold of phosphatidylserine needed for enzyme activation.

Phosphatidylinositol 4,5-bisphosphate decreases the concentration of Ca2+, phosphatidylserine and diacylglycerol required for …

Figure 4. The dependence of PKCa activity on the DOG molar percentage in the lipid vesicles. The molar ratios of the lipid components of the vesicles used to activate the enzyme are shown. Ca2+ concentration was 200 mmol. SD calculated from 3 independent
Figure 4 Chart

PKCα activity is shown as a function of diacylglycerol (DOG) molar percentage in lipid vesicles, illustrating the cofactor requirements for kinase activation.

Phosphatidylinositol 4,5-bisphosphate decreases the concentration of Ca2+, phosphatidylserine and diacylglycerol required for …

Figure 5. The dependence of PKCa activity on the PIP2 molar percentage in the lipid vesicles. The molar ratios of the lipid components of the vesicles used to activate the enzyme are shown. Ca2+ concentration was 200 mmol. SD calculated from 3 independent
Figure 5 Chart

The relationship between PIP2 concentration and PKCα activity demonstrates that increasing PIP2 in lipid vesicles progressively enhances kinase activation efficiency.

Phosphatidylinositol 4,5-bisphosphate decreases the concentration of Ca2+, phosphatidylserine and diacylglycerol required for …

Figure 1. Correlations between PLA2 activity and GPs- LOAD demonstrated no significant correlation between PLA2 activity and PC in NP (a). However, PLA2 positively correlated with PC in NP in OD samples (ρ = 0.81, p < 0.03) (b). PLA2 activity in CSF fr
Figure 5 Chart

Correlation analysis between PLA2 activity and glycerophospholipid levels in Alzheimer's disease patients reveals no significant association, suggesting independent dysregulation pathways.

Lipid Metabolism in Late-Onset Alzheimer's Disease Differs from Patients Presenting with Other …

Fig 1. The possible mechanisms of action of compound nutrients. Ach: acetylcholine; cAMP: Cycilic adenosine monophospate; APP: amyloid precursor protein-presenilin; Aβ: anti-β-amyloid; GSH-PX: glutathione peroxidase; SOD: superoxide dismutase; TChE: total
Figure 4 Diagram

A schematic diagram illustrates the proposed mechanisms by which the compound nutrient mixture may protect against Alzheimer's pathology, including acetylcholine and cAMP signaling.

Protective Effects of Dietary Supplementation with a Combination of Nutrients in a …

There was no significant difference in the daily food intake across groups (LG, 3.39 ± 0.18 g; HG, 3.34 ± 0.22 g; MG, 3.63 ± 0.26 g; NG, 3.51 ± 0.23 g), and over time, the body weights of all the mice (regardless of group affiliation) were similar up to 9
Figure 5 Chart

Daily food intake across groups confirms consistent consumption, with no significant differences between the low, high, and model groups during the study.

Protective Effects of Dietary Supplementation with a Combination of Nutrients in a …

Figure 6
Figure 6 Chart

Biochemical markers of oxidative stress and antioxidant capacity in brain tissue are compared across treatment groups, showing dose-dependent protective effects.

Protective Effects of Dietary Supplementation with a Combination of Nutrients in a …

Fig 4. Results from Morris water maze tests. (A) The average incubation period from the first to fifth day for the four groups. After 3 months and 7 months of intervention, the mice in HG and NG spent much less time searching for new (reversal) hidden pla
Figure 7 Chart

Morris water maze test results reveal that nutrient-supplemented APP-PSN mice demonstrate shorter escape latency and improved spatial memory compared to untreated transgenic controls.

Protective Effects of Dietary Supplementation with a Combination of Nutrients in a …

Fig 5. Immunofluorescence staining with rabbit anti-Aβ1–42 and HE dyeing of the temporal cortex and hippocampus of APP/PSN mice. (1) LG and HG: APP/PSN (Fig 5A) mice with 7 months of intervention; MG: APP/PSN (Fig 5B) mice without intervention and their w
Figure 8 Micrograph

Immunofluorescence staining of amyloid-beta plaques in the temporal cortex and hippocampus shows reduced plaque burden in nutrient-treated APP-PSN transgenic mice.

Protective Effects of Dietary Supplementation with a Combination of Nutrients in a …

Figure 1. Flow-chart.
Figure 1

Figure 1. Flow-chart.

Exploring the Efficacy and Safety of Nutritional Supplements in Alzheimer's Disease.

Figure 2
Figure 2

Exploring the Efficacy and Safety of Nutritional Supplements in Alzheimer's Disease.

Figure 4
Figure 4

Concentration of Phosphatidylserine Influence Rates of Insulin Aggregation and Toxicity of Amyloid …

Figure 1. Increase in the concentration of PS in the lipid mixtures increases the aggregation rate of insulin. Averages of triplicates of ThT aggregation kinetics of insulin (Ins) in the lipid-free environment (red), insulin in the presence of LUVs of PC/
Figure 6

Figure 1. Increase in the concentration of PS in the lipid mixtures increases the aggregation rate of insulin. Averages of triplicates of ThT aggregation kinetics of insulin (Ins) in the …

Concentration of Phosphatidylserine Influence Rates of Insulin Aggregation and Toxicity of Amyloid …

Figure 7
Figure 7

Concentration of Phosphatidylserine Influence Rates of Insulin Aggregation and Toxicity of Amyloid …

Figure 4. AFM-IR spectra acquired from insulin (Ins) fibrils grown in the lipid-free environment (red), insulin in the presence of LUVs of PC/PE/PS (40:40:20) (yellow), PC/PE/PS (30:40:30) (green), PC/ PE/PS (20:40:40) (blue), and PC/PE/PS (30:30:40) (pur
Figure 8

Figure 4. AFM-IR spectra acquired from insulin (Ins) fibrils grown in the lipid-free environment (red), insulin in the presence of LUVs of PC/PE/PS (40:40:20) (yellow), PC/PE/PS (30:40:30) (green), PC/ PE/PS …

Concentration of Phosphatidylserine Influence Rates of Insulin Aggregation and Toxicity of Amyloid …

Figure 9
Figure 9

Concentration of Phosphatidylserine Influence Rates of Insulin Aggregation and Toxicity of Amyloid …

Figure 10
Figure 10

Concentration of Phosphatidylserine Influence Rates of Insulin Aggregation and Toxicity of Amyloid …