The 4+ Benefits Of Peptide 6 (P6)
Back to Research Library
Alzheimer's

The 4+ Benefits Of Peptide 6 (P6)

||4 min read|7 likes

Peptide 6 is a peptide that can enhance neurogenesis and help with many neurocognitive disorders. 

 
 

Basics

Peptide 6 (P6) is a small molecule that is based off of ciliary neurotropic factor (CNTF), with neurogenic and neurotrophic properties in mouse models of Alzheimer's, traumatic brain injuries, autism spectrum disorders, and down syndrome. R

Benefits

1. Helps With Neurogenesis

 
 

In mice, P6 increases neurogenesis in the brain (partially through inhibiting LIF, which is known to inhibit neurogenesis). R

Hippocampal neuronal loss accompanies >80% of fatal tramautic brain injuries (TBI) and cell death in the hippocampus can be observed up to 12 months following TBI. R

In mice that had TBI, 30-day administration of P6 prevented neuronal loss in the hippocampus. R

2. Helps With Alzheimer's Disease

Neuronal loss in CA1 and parietal cortex are common problems with Alzheimer's Disease (AD), increasing tau and amyloid beta. R

In mice with TBI-induced tau and amyloid beta, P6 prevented neuronal loss in the CA1 and parietal cortex. R

It also helped restore dendritic and synaptic density in those areas (via Peptide 6's ability to inhibit LIF activity). R

In mice with AD, P6 restored cognition by enhancing neurogenesis and neuronal plasticity. R

In the JD Guide

Chapter 11

Neuroinflammation and Cognitive Dysfunction

Brain fog has a mechanism. Neuroinflammation driven by activated microglia and blood-brain barrier breakdown creates measurable cognitive dysfunction. Chapter 11 covers the research and the protocol to reverse it.

Pro members reading this now
Read it in Pro

In another study, cerebrolysin (CBL), P6 and 6A all potentiate neurogenesis in the mice with AβPP. R

3. Helps With Autism Spectrum Disorders

 
 

Autism spectrum disorders (ASD) is a neurodevelopmental disorder characterized clinically by impairments in social interaction and verbal and non-verbal communication skills as well as restricted interests and repetitive behavior. R

In rats that were given sera (blood) from ASD children, P6 was able to prevent cell death and oxidative stress. R

It also rescued rat pups from developmental delays that are normally caused by ASD children's sera. R

In these mice, P6 was able to increase social exploration, grooming, and vocaalization (such as USVs). R

P6 also increased blood levels of BDNF and CNTF, helping protect against neurodegeneration and neuroinflammation . R

4. Helps With Down Syndrome

Down syndrome (DS) is caused by the triplication of È240 proteincoding genes on chromosome 21 and is the most prevalent form of developmental disability. R

The DS brain exhibits degeneration of cortical neurons, profound dendritic and synaptic abnormalities, and a hypocellular hippocampus and cerebral cortex.

In mice with DS, P6 helped improve cognitive function and reduced memory impairment through increased hippocampal growth. R

Mechanism Of Action

P6 works similarly to CNTF, but is much smaller and has less side effects. R

An even smaller version of P6 is Peptide 021 (P21). R

Adding an adamantylated glycine group to P6 to enhance its blood brain barrier (BBB) permeability makes P21. R

P6 inhibits leukemia inhibitory factor (LIF) activity and CNTF/JAK/STAT3 signaling. R

LIF is known to inhibit neurogenesis and promote self-renewal of the early, mostly gliagenic, progenitor cells. R

It also increases EGR-1 gene expression in the brain. R

It has a plasma half-life of over 6 hours. R

P6:

  • Easily crosses BBB R
  • Increases AMPA receptor expression R
  • Increases BDNF expression R
  • Increases CNTF expression R
  • Increases MAP2 expression R
  • Increases PSD95 expression R

Caveats

P6 is a research chemical and most studies on it has only been done in animal models. R

P6 doesn't appear to have the common side effects of CNTF, such as anorexia, skeletal muscle loss, hyperalgesia, severe cramps, and muscle pain. R

More Research

  • Peptide 6-treated I2NTF-CTF rats showed a significant increase in dendritic and synaptic density as reflected by increased expression of synapsin I, synaptophysin and MAP2, especially in the pyramidal neurons of CA1 and CA3 of the hippocampus. R
JG

Jacob Gordon

INHC, FMT-C

Board Certified Health Coach

I spent years battling unexplained chronic illness before discovering biohacking, epigenetics, and functional medicine. Now I share that research at MyBioHack to help others find their own answers.

Book a Consultation

Related Protocols & Supplements

Deep-dive chapters and recommended supplements for this topic

Protocols from Jacob's Junction Dysfunction guideView Full Guide

What's Working For You?

What supplements or protocols have you tried for this topic? Share what's working. Unlock the full community archive with Pro.

Sign in to share your stack