Cognitive Decline and Neurodegenerative Conditions Cognitive decline and neurodegenerative conditions show substantial preclinical evidence across multiple pathologies: Stroke models: BPC-157 given during reperfusion counteracted neuronal damage and produced full functional recovery in spatial memory, motor coordination, and balance tests Parkinsons models: MPTP-induced models showed reduced motor symptoms (tremor, rigidity, akinesia), protection of nigrostriatal dopaminergic neurons, and near-complete prevention of mortality Multiple sclerosis models: Cuprizone-induced demyelination resulted in significantly less brain damage and reduced clinical abnormalities when BPC-157 was given in drinking water or intragastrically Traumatic brain injury: Falling weight model studies demonstrated reduced hemorrhage, decreased brain lacerations and edema, and improved early outcomes These diverse models share common mechanisms

History [edit] Descriptions of deficiency effects [edit] Between 1849 and 1887, Thomas Addison described a case of pernicious anemia, William Osler and William Gardner first described a case of neuropathy, Hayem described large red cells in the peripheral blood in this condition, which he called "giant blood corpuscles" (now called macrocytes), Paul Ehrlich identified megaloblasts in the bone marrow, and Ludwig Lichtheim described a case of myelopathy

The intranasal GHK-Cu treatment was found to delay cognitive impairment, reduce amyloid plaques, and lower inflammation levels in the frontal cortex and hippocampus .37 Randomized controlled trials in human patients are needed to confirm the benefit of GHK-Cu for cognitive decline and Alzheimers disease as well as to evaluate safe and effective human dosing (the human dose equivalent of 15mg/kg in mice would be ~1.2mg/kg, though data on this or any other dosing nasally in humans is not currently available), but preliminary animal trials are promising
Improving nutritional quality of rice for human health
Peptides serve as delivery tags for CRISPR components, directing edits to targeted germ cell populations
Abstract Apical periodontitis (AP) is a biofilm-associated disease initiated by the invasion of dental pulp by microorganisms from the oral cavity