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| Acer okamotoanum - Acer okamotoanum Extract Alternative Names: Acer okamotoanum, Ulleungdo maple Type: Botanical extract / flavonoid-rich plant product Source: Acer okamotoanum is a maple species native to Korea, particularly Ulleung Island. Experimental studies have used leaf extracts and solvent fractions, including flavonoid-rich ethyl acetate fractions. Active Constituents: Reported constituents include isoquercitrin, quercitrin, afzelin, and other phenolic and flavonoid compounds. Function: Acer okamotoanum extracts exhibit antioxidant, anti-inflammatory, cytoprotective, and neuroprotective activities. Experimental studies show reductions in reactive oxygen species, lipid peroxidation, inflammatory signaling, and apoptotic damage, together with preservation of neuronal viability and cellular stress resistance. Alzheimer's Disease: Preclinical evidence suggests potential neuroprotective and cognition-preserving effects. Acer okamotoanum extract has improved learning and memory and reduced oxidative stress in experimental models involving amyloid-β and metabolic stress. Constituents including isoquercitrin, quercitrin, and afzelin may contribute to these effects through antioxidant, anti-inflammatory, and amyloid-related mechanisms. Clinical efficacy for Alzheimer's disease has not been established. |
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| Type: |
| PSEN1 - Presenilin-1 Abbreviation: PSEN1, PS1 Type: Intramembrane aspartyl protease / catalytic subunit of the γ-secretase complex Function: PSEN1 is the principal catalytic component of the γ-secretase complex, which performs intramembrane proteolysis of numerous substrates including amyloid precursor protein (APP) and NOTCH receptors. APP cleavage by PSEN1-containing γ-secretase generates amyloid-β peptides including Aβ40 and Aβ42. PSEN1 also regulates cellular signaling, membrane-protein processing, calcium homeostasis, and neuronal function. Cancer: ↕ Context-dependent. PSEN1-dependent γ-secretase activity can promote oncogenic signaling through cleavage and activation of NOTCH receptors and other substrates. γ-Secretase inhibition can suppress NOTCH-driven proliferation, survival, stemness, and tumor progression in selected cancers, although PSEN1 function varies substantially according to tumor type and substrate context. Alzheimer's Disease: ↕ Pathogenic alteration of PSEN1 function is a major cause of autosomal-dominant early-onset Alzheimer's disease. Disease-causing PSEN1 mutations alter γ-secretase processivity and commonly increase the relative production of longer, aggregation-prone Aβ species, particularly the Aβ42/Aβ40 ratio. Many pathogenic mutations reduce overall γ-secretase cleavage efficiency, so Alzheimer's disease is better characterized by abnormal PSEN1 function than by a simple increase or decrease in PSEN1 expression. |
| 7839- | AO, | ISQ, | The Protective Effects of Acer okamotoanum and Isoquercitrin on Obesity and Amyloidosis in a Mouse Model |
| - | in-vivo, | AD, | NA | - | in-vivo, | Obesity, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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