Abbreviations AGEs: Advanced glycation end products AMPK: Adenosine monophosphate-activated protein kinase Akt: Serine/threonine kinase 1 CHCHD2 : Coiled-Coil-Helix-Coiled-Coil-Helix Domain Containing 2 CSF: Cerebrospinal fluid ER: Estrogen receptor FDG-PET: Fluorodeoxyglucose positron emission Tomography FOXO: Forkhead box O G6PD: Glucose-6-phosphate dehydrogenase GAPDH: Glyceraldehyde-3-phosphate dehydrogenase GLUT: Glucose transporters GLP-1: Glucagon-like peptide-1 GLP-1 RA: GLP-1 receptor agonist HIF1: Hypoxia-inducible factor-1 iRBD: Idiopathic rapid eye movement sleep behavior disorder KGDHC: -Ketoglutarate dehydrogenase complex LRRK2 : Leucine-rich repeat kinase2 mTOR: Mammalian target of rapamycin MPTP: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine MPP + : 1-Methyl-4-phenylpyridinium NADPH: Nicotinamide adenine dinucleotide phosphate NOX2: NADPH oxidase 2 OXPHOS: Oxidative phosphorylation PD: Parkinson's disease PDSP: PD specific pattern PDD: PD dementia PGK1: Phosphoglycerate kinase 1 PPP: Pentose phosphate pathway PQ: Paraquat PINK1 : PTEN induced putative kinase 1 ROS: Reactive oxygen species SGLT: Sodium-glucose cotransporter SN: Substantia nigra T2DM: Type 2 diabetes mellitus TCA: Tricarboxylic acid TRAP1: Tumor necrosis factor receptor associated protein 1 VH: Visual hallucinations 6-OHDA: 6-Hydroxydopamine References Bloem BR, Okun MS, Klein C
In preclinical research models, exposure to GHK-Cu has been associated with altered gene expression patterns and modulation of signalling pathways related to extracellular matrix dynamics, oxidative stress response, and cellular turnover
( d-e ) Western blotting for total and phospho (p-)ERK1/2 levels in ( d ) SLC31A1-KO or ( e ) BCS treated SEM, NALM6, REH or MOLT16 cells
Transcriptional up-regulation of the mouse cytosolic glutathione peroxidase gene in erythroid cells is due to a tissue-specific 3 enhancer containing functionally important CACC/GT motifs and binding sites for GATA and Ets transcription factors
For parthanatos, DNA damage caused by mitochondrial impairment activates poly(ADP-ribose) polymerase 1 (PARP1), and excessive production of poly(ADP-ribose) (PAR) leads to NAD+ depletion and mitochondrial function collapse, ultimately inducing parthanatos [42]
Influenza antiviral medications: Summary for clinicians . Centers for Disease Control and Prevention
