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torsdag 3 oktober 2019

Aivojen alueen lipidistruktuurissa on havaittu AD taudissa varhain kardiolipiinin muutoksia synaptisissa mitokondrioissa.

https://www.ncbi.nlm.nih.gov/pubmed/25182746

Kardiolipiini eroaa  muista fosfolipidirakenteista olennaisesti ja sen toimintapaikka on tosiaankin  vain mitokodnria, jolla on erikoinen kalvorakenne, ulko kalvo ja sisäkalvo ja niitten välille jäänyt  enregiatarkoituksiin tärkeä  tila. Ulkokalvolla ja sisäkalvolla on  erilaiset fosfolipidikoostumat.
KARDIOLIPIINI  on tosi moduli joka on kondensoitu kolmesta  glyserolirungosta. R tarkoittaa rasvahappoa.
Kuva  Bildresultat för Cardiolipin

https://www.ncbi.nlm.nih.gov/pubmed/25627476
 https://link.springer.com/article/10.1007%2Fs10863-015-9607-y

  • Metabolisia mitokondrioita on tutkittu 2014, kardiolipiini, joka on mitokondrain sisäkalvossa.  Kardiolipiinirakenteeseen vaikuttaa ihmisen elintapa ja dieetti ainakin osaltaan,  herediteetti on tietysti  vahvin vaikuttaja. muta ihminen voi  elintavoillaan haitata kardiolipiinirakenteen  pätevyyttä. Ala on yksi linkki, josas on kuvattu mitokondrian ulompaa kaksoislipidikerrosta joka suojaa  sisäossaa, jonka ympärillä on poimuinen lipidikerros, ja siinä sisäkerroksessa on kardiolipiinin sijaintipaikka.  Siihen sisäkerrokseen asettu kellumaan  tämän "energialaitoksen" proteiiniketju, "hengitysketju" , joka  kuljttaa elektroneja ja ottaa vastaan happea, tekee   radikaalimuotoista  happea  ja muodostaa  vesimolekyyliä, metabolista  vettä H2O.  ATP-pakkauksia tekevä järjestelmä sijaitsee myös  siinä.  Tuottuvia protoneja  syötetään kalvovälitilaan ja sieltä ne virtaavat  alas ja  nergia otetaan fosfaattisidoksiin  proiteiinissa : ATP-pakkauksiin.  
  •  Alustana  tälle järjestelmälle täytyy olla  normaalia kardiolipiiniä.

2014 Oct;46(5):447-57. doi: 10.1007/s10863-014-9555-y. Epub 2014 Jun 21.
Impact of high dietary lipid intake and related metabolic disorders on the abundance and acyl composition of the unique mitochondrial phospholipid, cardiolipin.
UMR 866, Dynamique Musculaire et Métabolisme, Centre INRA de Montpellier, 34060, Montpellier,Abstract
Excessive dietary lipid intake, coupled with lack of exercise, are the major causes of the development and progression of metabolic syndrome features e. g. obesity, hepatic steatosis, insulin resistance, type 2 diabetes and cardiovascular diseases. These metabolic diseases are associated with both structural and functional alterations of mitochondria.  
Cardiolipin (CL) is a unique phospholipid that is almost exclusively localized in the mitochondrial inner membrane.

 Cardiolipin is at the heart of mitochondrial metabolism playing a key role in several processes of mitochondrial bioenergetics as well as in mitochondrial membrane stability and dynamics, and in many of the mitochondrial-dependent steps of apoptosis. Indeed, alterations to CL content and acyl chain profile have been associated with mitochondrial dysfunction in multiple tissues in Barth syndrome and in many other physio-pathological conditions. After a brief overview of the biological roles of CL, we highlight the consequences of lipid overload-related nutritional manipulations as well as related metabolic disorders on both CL content and its fatty acid composition in the major metabolic tissues, the heart, muscle and liver. The goal of this review is to fill a void in the CL literature concerning the effects of CL abundance and form that arise following high lipid supplementation and the related metabolic disorders.
[Indexed for MEDLINE]
https://qph.fs.quoracdn.net/main-qimg-17d708fb1ead71db48b33e79ec6a05bf-c 


  •  Viime vuodelta löytyy selvitystä kardiolipidin molekulaarisesta  koostumuskesta. 
https://www.ncbi.nlm.nih.gov/pubmed/29618609
2018 Apr 17;115(16):4158-4163. doi: 10.1073/pnas.1719407115. Epub 2018 Apr 4.

Molecular structural diversity of mitochondrial cardiolipins.Oemer G1, Lackner K1, Muigg K1, Krumschnabel G2, Watschinger K3, Sailer S3, Lindner H4, Gnaiger E2, Wortmann SB5,6, Werner ER3, Zschocke J1, Keller MA7.Abstract

cardiolipin; lipids; mass spectrometry; mathematical modeling; mitochondria
PMID:
29618609
PMCID:
PMC5910844
DOI:
10.1073/pnas.1719407115
[Indexed for MEDLINE]
Free PMC Article
  • ENTÄ SITtEN AIVOJEN mitokondrioitten kardiolipiinin piirteet?
     

    2015;43(4):1375-92. doi: 10.3233/JAD-141002.

    Cardiolipin profile changes are associated to the early synaptic mitochondrial dysfunction in Alzheimer's disease.

    l. Abstract
    Brain mitochondria are fundamental to maintaining healthy functional brains, and their dysfunction is involved in age-related neurodegenerative disorders such as Alzheimer's disease (AD). In this study, we conducted a research on how both non-synaptic and synaptic mitochondrial functions are compromised at an early stage of AD-like pathologies and their correlation with putative changes on membranes lipid profile, using 3 month-old nontransgenic and 3xTg-AD mice, a murine model of experimental AD. Bioenergetic dysfunction in 3xTg-AD brains is evidenced by a decrease of brain ATP levels resulting, essentially, from synaptic mitochondria functionality disruption as indicated by declined respiratory control ratio associated with a 50% decreased complex I activity. Lipidomics studies revealed that synaptic bioenergetic deficit of 3xTg-AD brains is accompanied by alterations in the phospholipid composition of synaptic mitochondrial membranes, detected either in phospholipid class distribution or in the phospholipids molecular profile. Globally, diacyl- and lyso-phosphatidylcholine lipids increase while ethanolamine plasmalogens and cardiolipins content drops in relation to nontransgenic background
     However, the main lipidomic mark of 3xTg-AD brains is that cardiolipin cluster-organized profile is lost in synaptic mitochondria due to a decline of the most representative molecular species.
    In contrast to synaptic mitochondria, results support the idea that non-synaptic mitochondria function is preserved at the age of 3 months. Although the genetically construed 3xTg-AD mouse model does not represent the most prevalent form of AD in humans, the present study provides insights into the earliest biochemical events in AD brain, connecting specific lipidomic changes with synaptic bioenergetic deficit that may contribute to the progressive synapses loss and the neurodegenerative process that characterizes AD. KEYWORDS:
    Alzheimer's disease; brain bioenergetics; cardiolipin; mitochondrial lipidomics.

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