Database Query Results : Vitamin A, Retinoic Acid, ,

VitA,RetA, Vitamin A, Retinoic Acid: Click to Expand ⟱
Features:
Retinoic acid is a naturally occurring derivative of vitamin A (retinol).

Retinoic acid is produced in the body from dietary vitamin A. Vitamin A can be ingested in two primary forms:
• Preformed vitamin A (retinol and its esters) found in animal products like liver, dairy, and fish.
• Provitamin A carotenoids (such as beta-carotene) found in colorful fruits and vegetables. Once ingested, these compounds are converted into retinol, which can then be oxidized to retinal and further oxidized to retinoic acid.

All-trans retinoic acid (ATRA) is a key component in the treatment of acute promyelocytic leukemia (APL). In APL, ATRA induces the differentiation of malignant promyelocytes into mature granulocytes, leading to clinical remission.

-Retinoic acid can have antioxidant properties
-High levels of retinoic acid have been associated with increased ROS production and oxidative stress
-The potential prooxidant action may contribute to its anti-cancer effects by inducing oxidative damage in cancer cells, thereby enhancing apoptosis.
Scientific Papers found: Click to Expand⟱
3863- RES,  MEL,  VitA,RetA,    Target Enzymes Considered for the Treatment of Alzheimer's Disease and Parkinson's Disease
- Review, AD, NA - Review, Park, NA
*ADAM10↑, resveratrol, with a polyphenol framework found in grape skin, peanut, and pomegranates, has been reported to be applied for the treatment of ND to enhance ADAM10 expression indirectly.
*ADAM10↑, In short, ADAM10 activity could be elevated by biological molecules such as XBP-1, SOX-2, PAX2, and melatonin.
*ADAM10↑, Small molecules such as bryostatin-1, retinoic acid, acitretin, Am80, and phlogacantholide C and multiple natural products (i.e., resveratrol, gemfibrozil, and etazolate) have been reported as upregulators of ADAM10.

4313- VitA,RetA,    Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology
- Review, AD, NA
*neuroP↑, deficiency impairs memory and learning in AD. RA acts as a neuroprotective agent by regulating gene expression, and neuronal survival
memory↑,
*Inflam↓, VA deficiency is also associated with elevated inflammatory cytokines, promoting neuroinflammation involved in AD progression
*neuroG↑, RA also stimulates adult neurogenesis, potentially influencing cognition in AD [17].
*cognitive↑,
*Aβ↓, It also influences Aβ clearance and tau phosphorylation, key pathological features of AD [19].
p‑tau↓,
*BACE↓, VA deficiency enhances BACE1 activity, increasing Aβ production and promoting neurotic plaque formation, a hallmark of AD pathology [21]


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Results for Effect on Cancer/Diseased Cells:
memory↑,1,   p‑tau↓,1,  
Total Targets: 2

Results for Effect on Normal Cells:
ADAM10↑,3,   Aβ↓,1,   BACE↓,1,   cognitive↑,1,   Inflam↓,1,   neuroG↑,1,   neuroP↑,1,  
Total Targets: 7

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