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== Synopsis ==
== Synopsis ==
Hacking retrograde anandamide signaling
=== Brainstorming ===
* Key concept 1: Retrograde anandamide trafficking with dopamine conjugate of DHA may induce selective GPCR receptor heteromerization.
* Key concept 2: Microglial Neuroprotection!
* Key concept 3: CREB phosphorylation
* Key concept 4: BDNF expression, a biomarker for learning-dependent synapse formation. (synaptogenesis) <cite>Parkhurst-2013</cite>


* Stimulation of endocannabinoid transport with polyunsaturated (22:6n-3) fatty acids (DHA, EPA) to target [https://en.wikipedia.org/wiki/Major_depressive_disorder major depressive disorders] (MDD) , epilepsy, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), posttraumatic stress disorder (PTSD), Parkinson's disease (PD), and Alzheimer's disease (AD).
=== Synaptogenic endocannabinoids ===
* Distribution of endocannabinoid-dependent activity (LTP, synaptogenesis) in the hippocampus promoting brain-derived neurotrophic factor (BDNF) expression, a biological marker for learning-dependent synapse formation. [https://www.ncbi.nlm.nih.gov/pubmed/21035522 PMID] [https://www.ncbi.nlm.nih.gov/pubmed/24360280 PMID]
* Intracellular CB1/BDNF signaling mediate on-demand neuroprotection on excitatory (glutamatergic) synapses and in particular astrocytes. <cite>Marsicano-2003</cite>
* Intracellular CB1 signaling mediate on-demand neuroprotection on excitatory (glutamatergic) synapses, and in particular astrocytes. [https://www.ncbi.nlm.nih.gov/pubmed/21376829 PMID] [https://www.ncbi.nlm.nih.gov/pubmed/14526074 PMID]
* DHA supplementation improves mitochondrial function and neuronal survival (homeostasis). <cite>Stanley-2012</cite>
** DHA supplementation improves mitochondrial function and neuronal survival. [https://www.ncbi.nlm.nih.gov/pubmed/22248591 PMID]
* Anti-proliferative effects of DHEA on prostate cancer cell lines. <cite>Website2</cite>
* Identification of a functional GPR40-GPR55 receptor heteromer with potent anti-inflammatory, antiglutamatergic and neuroprotective properties.
=== Microglial activation ===
** Anti-proliferative effects of DHEA on prostate cancer cell lines. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2930808/ PMC]
* Inhibitory effect of the CB2 receptor on monocyte subpopulations and microglial activation. <cite>Martin-Moreno-2011</cite>
** A synaptogenic endocannabinoid promoting synaptogenesis.
** Anti-inflammatory role of anandamide and 2-AG signaling in LPS-stimulated microglial activation of endogenous CB2 receptor. <cite>Website1</cite>
** Antioxidant (cytoprotective) properties of GPR40-GPR55 heteromer.
** '''Neuroprotection by inhibition of microglial activation.''' <cite>Obregon-2005</cite>
* Effects of the endothelial CB2 receptor persistent activation on monocyte subpopulations/microglial activation [https://www.ncbi.nlm.nih.gov/pubmed/21350020 PMID]
** Anti-inflammatory role of anandamide and 2-AG signaling in LPS-stimulated microglial activation of endogenous CB2 receptor. [http://www.hindawi.com/journals/np/2015/130639/ Link]
** Neuroprotection by inhibition of microglial activation. [https://www.ncbi.nlm.nih.gov/pubmed/19805493 PMID] [https://www.ncbi.nlm.nih.gov/pubmed/16343349 PMID]
** CB2 stimulation is proneurogenic on adult hippocampal neurogenesis [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2435344/ PMC]
** CB2 stimulation is proneurogenic on adult hippocampal neurogenesis [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2435344/ PMC]
* Caffeine is a adenosine antagonist which mediate CB1 receptor activation in the hippocampus [https://www.ncbi.nlm.nih.gov/pubmed/26065937 PMID] [https://www.ncbi.nlm.nih.gov/pubmed/20573894 PMID]
* Caffeine is a adenosine antagonist which potentiate CB1 receptor transactivation in the hippocampus [https://www.ncbi.nlm.nih.gov/pubmed/26065937 PMID] [https://www.ncbi.nlm.nih.gov/pubmed/20573894 PMID]
 
==References==
<biblio>
#Parkhurst-2013 https://www.ncbi.nlm.nih.gov/pubmed/24360280
//Microglia promote learning-dependent synapse formation through brain-derived neurotrophic factor.
#Marsicano-2003 https://www.ncbi.nlm.nih.gov/pubmed/14526074
//CB1 cannabinoid receptors and on-demand defense against excitotoxicity.
#Stanley-2012 https://www.ncbi.nlm.nih.gov/pubmed/22248591
//Update on lipids and mitochondrial function: impact of dietary n-3 polyunsaturated fatty acids.
#Martin-Moreno-2011 https://www.ncbi.nlm.nih.gov/pubmed/21350020
//Cannabidiol and other cannabinoids reduce microglial activation in vitro and in vivo: relevance to Alzheimer's disease.
#Obregon-2005 https://www.ncbi.nlm.nih.gov/pubmed/16343349
//Stimulation of cannabinoid receptor 2 (CB2) suppresses microglial activation.
#Website1 http://www.hindawi.com/journals/np/2015/130639/
#Website2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2930808/
</biblio>

Latest revision as of 14:58, 2 October 2018

Synopsis

Hacking retrograde anandamide signaling

Brainstorming

  • Key concept 1: Retrograde anandamide trafficking with dopamine conjugate of DHA may induce selective GPCR receptor heteromerization.
  • Key concept 2: Microglial Neuroprotection!
  • Key concept 3: CREB phosphorylation
  • Key concept 4: BDNF expression, a biomarker for learning-dependent synapse formation. (synaptogenesis) [1]

Synaptogenic endocannabinoids

  • Intracellular CB1/BDNF signaling mediate on-demand neuroprotection on excitatory (glutamatergic) synapses and in particular astrocytes. [2]
  • DHA supplementation improves mitochondrial function and neuronal survival (homeostasis). [3]
  • Anti-proliferative effects of DHEA on prostate cancer cell lines. [4]

Microglial activation

  • Inhibitory effect of the CB2 receptor on monocyte subpopulations and microglial activation. [5]
    • Anti-inflammatory role of anandamide and 2-AG signaling in LPS-stimulated microglial activation of endogenous CB2 receptor. [6]
    • Neuroprotection by inhibition of microglial activation. [7]
    • CB2 stimulation is proneurogenic on adult hippocampal neurogenesis PMC
  • Caffeine is a adenosine antagonist which potentiate CB1 receptor transactivation in the hippocampus PMID PMID

References

  1. https://www.ncbi.nlm.nih.gov/pubmed/24360280

    [Parkhurst-2013]

    Microglia promote learning-dependent synapse formation through brain-derived neurotrophic factor.

  2. https://www.ncbi.nlm.nih.gov/pubmed/14526074

    [Marsicano-2003]

    CB1 cannabinoid receptors and on-demand defense against excitotoxicity.

  3. https://www.ncbi.nlm.nih.gov/pubmed/22248591

    [Stanley-2012]

    Update on lipids and mitochondrial function: impact of dietary n-3 polyunsaturated fatty acids.

  4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2930808/

    [Website2]

  5. https://www.ncbi.nlm.nih.gov/pubmed/21350020

    [Martin-Moreno-2011]

    Cannabidiol and other cannabinoids reduce microglial activation in vitro and in vivo: relevance to Alzheimer's disease.

  6. http://www.hindawi.com/journals/np/2015/130639/

    [Website1]

  7. https://www.ncbi.nlm.nih.gov/pubmed/16343349

    [Obregon-2005]

    Stimulation of cannabinoid receptor 2 (CB2) suppresses microglial activation.

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