Alzheimerin taudissa aivosolut k?rvistelev?t energian puutteessa, koska niiden mahdollisuus k?ytt?? glukoosia energian (ATP:n) tuotannossa on heikentynyt. Glukoosia korvaamaan k?ytet??n b-hydroxybutyraattia, jota tuotetaan maksassa naist? keskipitkist? rasvoista (MCFA).
Samalla ainakin yhdess? jenkkilehdess? seurataan tilanteen kehittymist? perheess? jossa l??k?rivaimo l?ysi miehelle dementia l??kkeeksi kookos?ljyn vahvistettuna MCFA-liuoksella. Miehen tila oli parantunut.
Seuraavaksi asiaa leptiinist? liittyen AD:hen:
Leptin regulates tau phosphorylation and amyloid through AMPK in neuronal cells
Leptin, which serves as a lipid-modulating hormone to control metabolic energy availability, is decreased in Alzheimer?s disease (AD) patients, and serum levels are inversely correlated to severity of dementia...Direct stimulation of AMPK with the cell-permeable activator, 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR), replicated leptin?s effects and conversely, Compound C, an inhibitor of AMPK, blocked leptin?s action. The data implicate that AMPK is a key regulator of both AD-related pathways.
Ja toinen juttu ketogeenisen vaikutuksesta neuronien toimintaan ja apoptoosiin:
Ketogenic diet attenuates kainic acid-induced hippocampal cell death by decreasing AMPK/ACC pathway activity and HSP70
These results indicate that the KD promotes neuroprotective effects through suppression of the AMPK cascade and that HSP70 is involved in neuronal cell death or oxidative stress.
After animals receive a KD, large amounts of acetyl-CoA are generated, leading to the synthesis in the liver of three ketone body species: -hydroxybutyrate, acetoacetate, and acetone. These metabolites enter the brain through the blood?brain barrier (BBB). Under normal diet conditions
utilization of ketone bodies in adult brain is minimal. However, ketone bodies partly replace glucose as fuel for the brain during KD consumption. Theses ketone bodies are converted to acetyl-CoA by several enzymes and then enter the Krebs cycle within mitochondria, leading to the production of ATP. Our results indicate that ACC phosphorylation in the hippocampus was increased after KA treatment, consistent with the stimulatory effect of KA on AMPK activity.
Aika mielenkiintoisia juttuja eik? kovasti l?ydy tukea Puskan rasvalinjalle n?ist? jutuista. N?m? tukevat aika hyvin sairaustilastoja joten onhan t?ss? ihan "mielenkiintoista" seurata miten teoria ja k?yt?nt? kohtaa....
