What is behind Brain Aging & Neuroprotection
Insulin-like growth factor-1 — the dermal-papilla growth factor that drives follicle proliferation and prolongs anagen (the active growth phase). Evidence A — Human trial evidence.
Memory and focus neurotransmitter. Evidence A — Human trial evidence.
The transcription factor that commands the body's own antioxidant and detoxification arsenal. Evidence A — Human trial evidence.
The master inflammatory switch — indispensable to defend against threat, corrosive when it never stands down. Evidence B — Preclinical.
Mitochondrial energy (ATP) output. Evidence A — Human trial evidence.
The cystine–glutamate exchange that supplies antioxidant building blocks while tuning excitatory neurotransmission. Evidence A — Human trial evidence.
The cell's self-cleaning and recycling program — it digests worn proteins and organelles and renews the interior. Evidence A — Human trial evidence.
The lipid sheath that insulates nerve fibers, setting the speed and precision of neural signaling. Evidence A — Human trial evidence.
A sensor of cellular stress that ignites inflammation driven by damage rather than by germs. Evidence A — Human trial evidence.
The whole apparatus of thinking: taking information in, holding it, working with it, and getting it back out. Evidence A — Human trial evidence.
Evidence on these pathways
Autophagy → Proteostasis. “We show that HPK-1 fortifies proteostasis and extends longevity by an additional independent mechanism: induction of autophagy.” — The homeodomain-interacting protein kinase HPK-1 preserves protein homeostasis and longevity through master regulatory control of the HSF-1 chaperone network and TORC1-restricted autophagy in Caenorhabditis elegans. PLoS Genetics; 2017; volume 13; page/elocation not printed on either retrieved record. doi:10.1371/journal.pgen.1007038
Myelin → Perceptual-Motor Function. “We concluded that new oligodendrocytes contribute to both early and late stages of motor skill learning.” — Rapid production of new oligodendrocytes is required in the earliest stages of motor-skill learning. Nature Neuroscience, 2016, 19(9), 1210-1217. doi:10.1038/nn.4351 | PMID 27455109
NF-κB → CD38 NADase. “Regulation of CD38 expression in HASM cells involves the transcription factor NF-κB, and glucocorticoids inhibit this expression through NF-κB-dependent and -independent mechanisms.” — Regulation of the cd38 promoter in human airway smooth muscle cells by TNF-α and dexamethasone. Respiratory Research, 2008, vol 9, 26. doi:10.1186/1465-9921-9-26
NF-κB → COX-2 Induction. “Moreover, the nuclear factor kappa B (NF-κB) inhibitor BAY11‐7085 or the TLR4 neutralizing antibody markedly blocked PM2.5-induced IL-6 and COX-2 expression.” — PM2.5 exposure upregulates pro-inflammatory protein expression in human microglial cells via oxidant stress and TLR4/NF-κB pathway. Ecotoxicology and Environmental Safety, 2024, vol 277, article 116386. doi:10.1016/j.ecoenv.2024.116386
Formulas that act on these pathways
Acts on 4 of these pathways: Nrf2, NF-κB, Cystine–Glutamate Antiporter, Myelin.
Acts on 4 of these pathways: Nrf2, NF-κB, Autophagy, Myelin.
Acts on 4 of these pathways: Nrf2, NF-κB, Cystine–Glutamate Antiporter, Autophagy.
Acts on 4 of these pathways: Nrf2, NF-κB, Cystine–Glutamate Antiporter, Myelin.
Acts on 3 of these pathways: Nrf2, NF-κB, Autophagy.
What this page does not claim
This page names the pathways involved and the published evidence on each. It does not claim that any formula treats, cures or prevents Brain Aging & Neuroprotection. A pathway opens here only on graded, published evidence, under a standard fixed before the evidence was gathered, and every figure above carries its grade.
These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.