nervous
Brain / cognition
Cortical and cognitive papers — short peptides written for neural tissue, not a general nootropic aisle.
This chapter is neural tissue: cortex, and the cognitive questions authors attach to it. The Khavinson literature includes cortical extracts and short peptides designed after neural tissue. This hub files those papers. It is not a catalog of every compound sold for “focus.” If the authors did not write the work for brain or cortical tissue, it does not belong here.
Peptide themes that belong on this hub are cortical extracts and short-chain analogs discussed in that lineage (names you will meet include Cortexin, Cortagen, and Pinealon, among others). Themes include neuronal cultures, behavioral models, and clinical communications that name the brain as the target tissue. Vascular papers that mention the brain only in passing stay in Vascular / cardiac unless the authors made cortex the subject.
Read linked studies for the model and the claim size. A cell-culture communication is not a memory trial. A small clinical series is not a guideline. Follow the PMID; do not treat this hub as a protocol for cognition.
Studies
- Short Peptides Protect Fibroblast-Derived Induced Neurons from Age-Related Changes.
In induced cortical neurons transdifferentiated from elderly-donor fibroblasts, EDR, KED, and AEDG increased dendritic arborization; EDR also lowered oxidative DNA damage — culture work, not a patient trial.
- Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer's Disease
An open-access IJMS review hypothesizing that ultrashort peptides could act on Alzheimer-related gene expression via histones, DNA elements, and non-coding RNA — a mechanism essay, not a clinical trial.
- EDR Peptide: Possible Mechanism of Gene Expression and Protein Synthesis Regulation Involved in the Pathogenesis of Alzheimer's Disease
A 2021 open-access review of how the tripeptide EDR has been proposed to touch AD-related gene-expression and protein-synthesis pathways — not a trial, and not evidence that EDR treats Alzheimer’s disease.
- Neuroprotective Effects of Tripeptides-Epigenetic Regulators in Mouse Model of Alzheimer's Disease
In 5xFAD mice, the authors report that KED and EDR lessened dendritic-spine loss; KED 400 µg/kg daily from 2 to 4 months of age only tended to raise a neuroplasticity readout, with docking offered as a mechanistic hypothesis.
- AEDG Peptide (Epitalon) Stimulates Gene Expression and Protein Synthesis during Neurogenesis: Possible Epigenetic Mechanism.
In human gingival mesenchymal stem cells, AEDG (Epitalon) raised nestin, GAP43, β-tubulin III, and doublecortin mRNA and protein; histone docking is offered as a possible epigenetic mechanism, not a clinical result.
- Short peptides stimulate serotonin expression in cells of brain cortex
In aging primary rat cortex cultures, Glu-Asp-Arg and Lys-Glu-Asp increased serotonin immunostaining; molecular docking is offered as a complementary TPH-promoter hypothesis, not a wet-lab binding assay.
- Pinealon increases cell viability by suppression of free radical levels and activating proliferative processes.
In cerebellar granule cells, neutrophils, and PC12 cells, Pinealon (EDR) restricted ROS accumulation and necrotic death in a dose-dependent way; higher concentrations also shifted ERK timing and the cell cycle.