| Source: |
| Type: |
| Advanced Glycation End Products (AGEs) are highly reactive compounds formed when proteins or lipids become non-enzymatically glycated after exposure to sugars. AGEs accumulate with age and are implicated in various chronic diseases—including Alzheimer’s disease (AD). -AGEs bind to Aβ peptides, increasing aggregation and plaque stability. -AGEs activate kinases like GSK-3β and p38 MAPK, promoting tau phosphorylation. -Human brains with AD show increased AGE-modified proteins and elevated RAGE expression. -Blocking RAGE or reducing AGEs slows cognitive decline and pathology in mice. Strategies to Reduce AGE Burden -Low-AGE cooking (steaming, boiling), Mediterranean diet - reduce processed meats, sugary baked goods, and fried foods. |
| 4529- | MAG, | Effectiveness of Magnolol, a Lignan from Magnolia Bark, in Diabetes, Its Complications and Comorbidities—A Review |
| - | Review, | Diabetic, | NA |
| 4311- | VitB1/Thiamine, | Benfotiamine treatment activates the Nrf2/ARE pathway and is neuroprotective in a transgenic mouse model of tauopathy |
| - | in-vivo, | AD, | NA |
| 4312- | VitB1/Thiamine, | Pharmacological thiamine levels as a therapeutic approach in Alzheimer's disease |
| - | Review, | AD, | 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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:1375 State#:% Dir#:%
wNotes=0 sortOrder:rid,rpid