25 research outputs found
The effects of long-term saturated fat enriched diets on the brain lipidome
The brain is highly enriched in lipids, where they influence neurotransmission, synaptic plasticity and inflammation. Non-pathological modulation of the brain lipidome has not been previously reported and few studies have investigated the interplay between plasma lipid homeostasis relative to cerebral lipids. This study explored whether changes in plasma lipids induced by chronic consumption of a well-tolerated diet enriched in saturated fatty acids (SFA) was associated with parallel changes in cerebral lipid homeostasis. Male C57Bl/6 mice were fed regular chow or the SFA diet for six months. Plasma, hippocampus (HPF) and cerebral cortex (CTX) lipids were analysed by LC-ESI-MS/MS. A total of 348 lipid species were determined, comprising 25 lipid classes. The general abundance of HPF and CTX lipids was comparable in SFA fed mice versus controls, despite substantial differences in plasma lipid-class abundance. However, significant differences in 50 specific lipid species were identified as a consequence of SFA treatment, restricted to phosphatidylcholine (PC), phosphatidylethanolamine (PE), alkyl-PC, alkenyl-PC, alkyl-PE, alkenyl-PE, cholesterol ester (CE), diacylglycerol (DG), phosphatidylinositol (PI) and phosphatidylserine (PS) classes. Partial least squares regression of the HPF/CTX lipidome versus plasma lipidome revealed the plasma lipidome could account for a substantial proportion of variation. The findings demonstrate that cerebral abundance of specific lipid species is strongly associated with plasma lipid homeostasis
ΠΠ΅ΡΠΎΠ΄ΠΎΠ»ΠΎΠ³ΠΈΡ ΡΠΈΠ½ΡΠ΅Π·Π° Π°ΡΡ ΠΈΡΠ΅ΠΊΡΡΡΡ ΠΏΡΠΎΠ³ΡΠ°ΠΌΠΌΠ½ΠΎ-ΡΠ΅Ρ Π½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΊΠΎΠΌΠΏΠ»Π΅ΠΊΡΠ° Π°Π²ΡΠΎΠΌΠ°ΡΠΈΠ·ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΡΠΈΡΡΠ΅ΠΌΡ ΠΌΠΎΠ½ΠΈΡΠΎΡΠΈΠ½Π³Π° ΠΎΠ±ΡΡΠ°Π½ΠΎΠ²ΠΊΠΈ
ΠΡΠ΅Π΄Π»ΠΎΠΆΠ΅Π½ ΠΏΠΎΠ΄Ρ
ΠΎΠ΄ ΠΊ ΠΏΡΠΎΠ΅ΠΊΡΠΈΡΠΎΠ²Π°Π½ΠΈΡ Π°ΡΡ
ΠΈΡΠ΅ΠΊΡΡΡΡ ΠΏΡΠΎΠ³ΡΠ°ΠΌΠΌΠ½ΠΎ-ΡΠ΅Ρ
Π½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΊΠΎΠΌΠΏΠ»Π΅ΠΊΡΠ° Π°Π²ΡΠΎΠΌΠ°ΡΠΈΠ·ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΡΠΈΡΡΠ΅ΠΌΡ ΠΌΠΎΠ½ΠΈΡΠΎΡΠΈΠ½Π³Π° ΠΎΠ±ΡΡΠ°Π½ΠΎΠ²ΠΊΠΈ Π² ΡΠ΅Π°Π»ΡΠ½ΠΎΠΌ Π²ΡΠ΅ΠΌΠ΅Π½ΠΈ, ΠΎΡΠ½ΠΎΠ²Π°Π½Π½ΡΠΉ Π½Π° ΠΊΠ»Π°ΡΡΠΈΡΠΈΠΊΠ°ΡΠΈΠΈ ΡΠ΅ΡΠ°Π΅ΠΌΡΡ
ΡΡΠ½ΠΊΡΠΈΠΎΠ½Π°Π»ΡΠ½ΡΡ
Π·Π°Π΄Π°Ρ Π½Π° ΠΎΡΠ½ΠΎΠ²Π΅ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ² ΠΊΠ»Π°ΡΡΠ΅ΡΠ½ΠΎΠ³ΠΎ Π°Π½Π°Π»ΠΈΠ·Π° ΠΈ Π²ΡΠ±ΡΠ°Π½Π½ΠΎΠ³ΠΎ ΠΌΠ½ΠΎΠΆΠ΅ΡΡΠ²Π° ΠΏΡΠΈΠ·Π½Π°ΠΊΠΎΠ² ΠΏΠΎΠ΄ΠΎΠ±ΠΈΡ. Π Π°Π·ΡΠ°Π±ΠΎΡΠ°Π½Π½ΡΠΉ ΠΏΠΎΠ΄Ρ
ΠΎΠ΄ ΠΏΠΎΠ·Π²ΠΎΠ»ΡΠ΅Ρ ΠΈΠ· ΠΌΠ½ΠΎΠΆΠ΅ΡΡΠ²Π° ΡΡΠ½ΠΊΡΠΈΠΉ ΡΠΈΡΡΠ΅ΠΌΡ Π²ΡΠ΄Π΅Π»ΠΈΡΡ ΠΏΠΎΠ΄ΠΎΠ±Π½ΡΠ΅ (ΠΏΠΎ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½Π½ΡΠΌ ΠΏΡΠΈΠ·Π½Π°ΠΊΠ°ΠΌ) ΠΈ ΠΎΠ±ΡΠ΅Π΄ΠΈΠ½ΠΈΡΡ ΠΈΡ
Π² Π°ΡΡ
ΠΈΡΠ΅ΠΊΡΡΡΠ½ΡΠ΅ ΠΊΠΎΠΌΠΏΠΎΠ½Π΅Π½ΡΡ (ΡΠ½ΠΈΡΠΈΡΠΈΡΠΎΠ²Π°Π½Π½ΡΠ΅ ΡΡΠ½ΠΊΡΠΈΠΎΠ½Π°Π»ΡΠ½ΡΠ΅ ΠΌΠΎΠ΄ΡΠ»ΠΈ).ΠΠ°ΠΏΡΠΎΠΏΠΎΠ½ΠΎΠ²Π°Π½ΠΎ ΠΏΡΠ΄Ρ
ΡΠ΄ Π΄ΠΎ ΠΏΡΠΎΠ΅ΠΊΡΡΠ²Π°Π½Π½Ρ Π°ΡΡ
ΡΡΠ΅ΠΊΡΡΡΠΈ ΡΠ΅Π½ΡΡΡ ΠΎΠ±ΡΠΎΠ±ΠΊΠΈ ΡΠ½ΡΠΎΡΠΌΠ°ΡΡΡ Π°Π²ΡΠΎΠΌΠ°ΡΠΈΠ·ΠΎΠ²Π°Π½ΠΎΡ ΡΠΈΡΡΠ΅ΠΌΠΈ ΠΌΠΎΠ½ΡΡΠΎΡΠΈΠ½Π³Ρ ΡΠ΅ΡΠ΅Π΄ΠΎΠ²ΠΈΡΠ° Π² ΡΠ΅Π°Π»ΡΠ½ΠΎΠΌΡ ΡΠ°ΡΡ, ΡΠΎ Π·Π°ΡΠ½ΠΎΠ²Π°Π½ΠΈΠΉ Π½Π° ΠΊΠ»Π°ΡΠΈΡΡΠΊΠ°ΡΡΡ ΡΡΠ½ΠΊΡΡΠΎΠ½Π°Π»ΡΠ½ΠΈΡ
Π·Π°Π΄Π°Ρ Π½Π° ΠΏΡΠ΄ΡΡΠ°Π²Ρ ΠΌΠ΅ΡΠΎΠ΄ΡΠ² ΠΊΠ»Π°ΡΡΠ΅ΡΠ½ΠΎΠ³ΠΎ Π°Π½Π°Π»ΡΠ·Ρ Ρ ΠΎΠ±ΡΠ°Π½ΠΎΡ ΠΌΠ½ΠΎΠΆΠΈΠ½ΠΈ ΠΎΠ·Π½Π°ΠΊ ΡΡ
ΠΎΠΆΠΎΡΡΡ. Π ΠΎΠ·ΡΠΎΠ±Π»Π΅Π½ΠΈΠΉ ΠΏΡΠ΄Ρ
ΡΠ΄ Π΄ΠΎΠ·Π²ΠΎΠ»ΡΡ Π²ΠΈΠ±ΡΠ°ΡΠΈ ΡΠ· ΠΌΠ½ΠΎΠΆΠΈΠ½ΠΈ ΡΡΠ½ΠΊΡΡΠΉ ΡΠΈΡΡΠ΅ΠΌΠΈ ΡΡ
ΠΎΠΆΡ (Π·Π° ΠΏΠ΅Π²Π½ΠΈΠΌΠΈ ΠΎΠ·Π½Π°ΠΊΠ°ΠΌΠΈ) Ρ ΠΏΠΎΡΠ΄Π½Π°ΡΠΈ ΡΡ
Π² Π°ΡΡ
ΡΡΠ΅ΠΊΡΡΡΠ½Ρ ΠΊΠΎΠΌΠΏΠΎΠ½Π΅Π½ΡΠΈ (ΡΠ½ΡΡΡΠΊΠΎΠ²Π°Π½Ρ ΡΡΠ½ΠΊΡΡΠΎΠ½Π°Π»ΡΠ½Ρ ΠΌΠΎΠ΄ΡΠ»Ρ).The approach to designing architecture of the information processing complex of the automated real time conditions monitoring system based on classification of functional tasks on the basis of methods of cluster analysis and the chosen set of similarity attributes is offered. The developed approach allows to allocate from a set of functions the systems similar (on certain attributes) and to unite them in architectural components (unified functional modules)
The airbag problem-a potential culprit for bench-to-bedside translational efforts: relevance for Alzheimer's disease
For the last 20Β years, the "amyloid cascade hypothesis" has dominated research aimed at understanding, preventing, and curing Alzheimer's disease (AD). During that time researchers have acquired an enormous amount of data and have been successful, more than 300 times, in curing the disease in animal model systems by treatments aimed at clearing amyloid deposits. However, to date similar strategies have not been successful in human AD patients. Hence, before rushing into further clinical trials with compounds that aim at lowering amyloid-beta (AΞ²) levels in increasingly younger people, it would be of highest priority to re-assess the initial assumption that accumulation of AΞ² in the brain is the primary pathological event driving AD. Here we question this assumption by highlighting experimental evidence in support of the alternative hypothesis suggesting that APP and AΞ² are part of a neuronal stress/injury system, which is up-regulated to counteract inflammation/oxidative stress-associated neurodegeneration that could be triggered by a brain injury, chronic infections, or a systemic disease. In AD, this protective program may be overridden by genetic and other risk factors, or its maintenance may become dysregulated during aging. Here, we provide a hypothetical example of a hypothesis-driven correlation between car accidents and airbag release in analogy to the evolution of the amyloid focus and as a way to offer a potential explanation for the failure of the AD field to translate the success of amyloid-related therapeutic strategies in experimental models to the clinic