Elevating bdnf levels as treatment for pws hypothesis

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note that this page was not created nor endorsed by PWSmom.

BDNF contributes to neuroplasticity, to problem solving as evident in rats: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4388634/
Lack of BDNF is related to insomnia and sleep deprivation https://www.ncbi.nlm.nih.gov/pubmed/26758201?fbclid=IwAR1fdjSZZHi_GxZkmceCHfXd3BMsNEARLPzIUwe9TIvTySBYIhpxLc4irCM

BDNF deficiency in PWS: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2928902/
from this article : 'bdnf knockout mice also exhibit hyperphagia and obesity. reversible with bdnf administration ... '
and from the conclusion paragraph : 'If larger studies confirm a connection between BDNF and PWS, therapeutic interventions aimed at modulating BDNF/TrkB signaling may ameliorate some of the behavioral abnormalities. For example, TrkB agonists may be of benefit, as may early behavioral therapy, because early-life environmental factors have been shown in rodents to alter Bdnf promoter DNA methylation and cause lifelong changes in Bdnf expression'


Interesting, that a TrkB-agonist called N-Acetylserotonin (a.k.a NAS a.k.a. normelatonin) wikipedia page says this : 'naturally occurring chemical precursor and intermediate in the endogenous production of melatonin from serotonin'
NAS is also a melatonin precursor and is a intermediate in the generation of melatonin from serotonin. The interesting anecdote here is that NAS is related to the sleep inducting melatonin.
related read: https://www.nature.com/articles/s41583-018-0088-y?WT.feed_name=subjects_neurology
and from it:
'A double-blind placebo-controlled study of 125 children and adolescents (2–17.5 years of age) supports the use of melatonin supplementation to treat sleep disturbances associated with ASD and may lead to other therapeutic approaches targeting circadian rhythms and sleep issues, as well as other symptoms of ASD.
Other neurodevelopmental disorders, such as PWS and SMS, are linked more directly to dysfunctional circadian rhythm pathways. ... and it is due to a paternal deficiency of the 15q11–13 locus. PWS is also accompanied by shorter sleep duration and excessive daytime sleepiness. The 15q11–13 locus contains several clusters of genes encoding small nucleolar RNAs (snoRNAs), including SNORD116, which is expressed in the brain of mice and humans. In mice, paternal deletion of Snord116 increases the expression of several genes specifically during the light phase, including Ube3a, which encodes ubiquitin ligase E3A (UBE3A)116. UBE3A targets the circadian transcription factor BMAL1 for proteasomal degradation and thus is crucial for maintaining the pace of molecular clock timing. UBE3A belongs to a cluster of imprinted genes also within the 15q11–13 locus '

related read: snord116 and circadian clock - https://www.nature.com/articles/s41467-018-03676-0?fbclid=IwAR0vULnhR2CTnOuY5tufV5bv8vv9VczZcEt671dEnfKh0p-U_BxNLbmhZSA


BDNF deficiency in PWS : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5896230/


All the above provide a hint that elevating BDNF levels can be considered a treatment to PWS.