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fredag 2 december 2016

Brichos Chaperone estää katalyyttisen ketjun

http://www.nature.com/nsmb/journal/v22/n3/fig_tab/nsmb.2971_F6.html
Tämä on mielestäni  täsmöäterapiaa, muta asiaa tehostaisi, jos  kehon fosfaattitasapinokin selvitettäisiin, munuaisetn fosfaatin käsittelykapasiteetti jne.   Aivoautonomian ja muun kehoaition fosfaaattiaineenvaihdunta- onko siinä jokin  huonompi edellytys  normaaliuteen aivoautonomian puolella ja miten siitä saa käsityksen, onhan siellä fosfolipidien  remodellingprosessi menossa aina ja  kalvosignaalijärjestelmätkin toimivat  fosfaattiverkostossa, varsinkin harmaassa aivokuoressa- jos fosfaatia ei saada pois ( IP6 muodossaan esim)  se luonollseisti saostuu jonnekin mikä on primääristi  vitaalia, mutta sekundaaristi hivuttavaa.

Figure 6: Brichos inhibits the catalytic cycle that generates toxic ​Aβ42 oligomers.

From A molecular chaperone breaks the catalytic cycle that generates toxic Aβ oligomers

Nature Structural & Molecular Biology
22,
207–213
doi:10.1038/nsmb.2971
Received
Accepted
Published online

torsdag 1 december 2016

APP:n AV:n hyperfosforyloitunut tila patologiassa

 Löysin artikkelin josas puututaan tähän hyperfosforylaatioon  Bricho chaperoni-terapialla.
katselin tri Samuel Cohenin you tube videon Cambridgesta . Se tuli kun selasin BACE1 entsyymiaihetta filmi filmiltä.
http://www.cam.ac.uk/research/news/molecular-inhibitor-breaks-cycle-that-leads-to-alzheimers



https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3739963/

VIII. Protein Phosphatase-Directed Therapeutics for the Prevention and Treatment of Alzheimer’s Disease

According to the National Institute on Aging, there are more than 5 million Americans who suffer from AD. Yet, despite a desperate need, development of an effective treatment for AD has been a major challenge. Four drugs are currently approved by the FDA to treat cognitive deficits in AD. Three of them are acetylcholinesterase inhibitors, which combat the loss of acetylcholine caused by the death of cholinergic neurons, while the other is a noncompetitive NMDA receptor antagonist, which inhibits overactivation of NMDA receptors by glutamate.1 None of these drugs halts progression of the disease. Significant effort has been put into development of inhibitors of Aβ production.233 However, targeting γ-secretase with nonselective γ-secretase inhibitors has deleterious effects on health, likely because γ-secretase also cleaves other substrates, such as Notch, which are essential for normal biological function.234 This limitation is highlighted by the recent failure of the γ-secretase inhibitor semagacestat in Phase III clinical trials.235 Given the lack of available drugs to treat AD, it is imperative to identify novel molecular processes that might be amenable to targeting through new drugs. Protein phosphatases, including PP2A, and STEP may be potential therapeutic targets for AD. It may also be possible to use a strategy that would combine one or more regulator of a protein phosphatase with kinase inhibitors that would provide a complementary approach to control of, for example, hyperphosphorylation of tau.

PS: Kappale on pitkä ja siinä on paljon asiaa. hyperfosforylaatiossa on yksi  seikka mitä voisi myös ottaa pinsettiin: orgaanisen ja epäorgaanisen  fosfaatin suhde kehossa, sillä siinäkin on moduloimisen varaa  dietääriä tietä.-   Tämä suhde on  nykyaikana käänteinen verrattuna  entisaikojen ravinnon  aiheuttamaan  fosfaattisuhtgeeseen.