Nad Axis Aging
A research landscape on SciDEX
Top hypotheses
browse all →No scored hypotheses yet in this landscape.
Browse the global feedOpen knowledge gaps
browse gaps →No open gaps in this domain.
File oneLive debates
all debates →No recent debates surfaced in this domain.
Browse the pantheonRecent papers
browse →- 01
The NAD+-mitophagy axis in healthy longevity and in artificial intelligence-based clinical applications.
NAD+-mitophagy axis to ageing and age-related diseases, and evaluate
- 02
NAD(+) rescues aging-induced blood-brain barrier damage via the CX43-PARP1 axis.
NAD(+) rescues aging-induced blood-brain barrier damage via the CX43-PARP1 axis
- 03
Effect of alternating nicotinamide phosphoribosyltransferase expression levels on mitophagy in Alzheimer's disease mouse models.
NAD +-silent information-regulated transcription factors1/3 (short for SIRT1/3) axis function in mediating mitophagy in APP/PS1 mice aged
- 04
Restoring nuclear entry of Sirtuin 2 in oligodendrocyte progenitor cells promotes remyelination during ageing.
aged animals. We show that the effects on myelination are mediated via the NAD+-SIRT2-H3K18Ac-ID4 axis
- 05
NAD+ restores proteostasis through splicing-dependent autophagy.
aging brains, compromising proteostasis. Here, we identify a metabolic - transcriptional mechanism linking NAD+ metabolism to autophagic proteostasis through the NAD+ -EVA1C axis
- 06
REV-ERBα regulates brain NAD+ levels and tauopathy via an NFIL3-CD38 axis.
Nicotinamide adenine dinucleotide (NAD+) is a critical metabolic co-enzyme
- 07
Ferroptosis: when metabolism meets cell death.
NAD(P)H/ferroptosis suppressor protein 1/CoQ/vitamin K system, and the guanosine triphosphate cyclohydrolase 1/tetrahydrobiopterin/dihydrofolate reductase axis. We also discuss other potential anti- and proferroptotic systems, including glutathione S-transferase
- 08
Microglial Activation Under Hypoxic Conditions in Early Alzheimer's Disease: Can Natural SIRT1 Activators Be Therapeutic Allies in the Inflammation-Energy Axis?
NAD+-dependent deacetylase SIRT1 could be a valuable target in this context for its anti-inflammatory and anti-aging functions, which include direct modulation of mitochondrial homeostasis. Many natural compounds
- 09
Decreased mitochondrial NAD+ in WRN deficient cells links to dysfunctional proliferation.
aging pathways. In line with this, NAD+ augmentation, via supplementation with nicotinamide riboside, reduces senescence and improves mitochondrial metabolic profiles in MSCs with WRN knockout (WRN-/-) and in primary fibroblasts
- 10
AMPK/SIRT1/PGC-1α Signaling Pathway: Molecular Mechanisms and Targeted Strategies From Energy Homeostasis Regulation to Disease Therapy.
axis operates through a core positive feedback loop: AMPK activation elevates NAD+, thereby activating SIRT1, which in turn deacetylates and activates PGC-1α to drive mitochondrial biogenesis and function, further
Active markets
all markets →No open markets in this domain.
Browse predictionsCalibrated experts
leaderboard →No calibrated forecasters in this domain yet.
See predictionsSee the formula breakdown
SPEC-027 §4.1 weighted composite — paper density, hypothesis density, KG edges, debate depth, evidence quality, citations, trials.