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These findings [5] suggested that there is a PKA-dependent phase of LTP intermediate to E-LTP and L-LTP, which was called intermediate LTP (I-LTP). In the transgenic mice, on the other hand, LTP induced by two trains decayed faster than in wild-type mice, implying that excessive calcineurin activity suppresses both I-LTP and L-LTP.
HEPPS (EPPS) is a buffering agent used in biology and biochemistry.The pKa of HEPPS is 8.00. It is ones of Good's buffers. [1]Research on mice with Alzheimer's disease-like amyloid beta plaques has shown that HEPPS can cause the plaques to break up, reversing some of the symptoms in the mice.
Brain Aβ is elevated in people with sporadic Alzheimer's disease. Aβ is the main constituent of brain parenchymal and vascular amyloid; it contributes to cerebrovascular lesions and is neurotoxic. [ 33 ] [ 34 ] [ 35 ] It is unresolved how Aβ accumulates in the central nervous system and subsequently initiates the disease of cells.
In cell biology, protein kinase A (PKA) is a family of serine-threonine kinase [1] whose activity is dependent on cellular levels of cyclic AMP (cAMP). PKA is also known as cAMP-dependent protein kinase (EC 2.7.11.11). PKA has several functions in the cell, including regulation of glycogen, sugar, and lipid metabolism.
It also acts on the brain's cholinergic system; [4] Amyloid β containing pyroglutamic acid is increased in Alzheimer's disease; this may be part of the disease process. [5] Increased levels of pyroglutamic acid in the blood, leading to excess in the urine ( 5-oxoprolinuria ), can occur following paracetamol overdose , as well as in certain ...
Two molecular mechanisms for synaptic plasticity involve the NMDA and AMPA glutamate receptors. Opening of NMDA channels (which relates to the level of cellular depolarization) leads to a rise in post-synaptic Ca 2+ concentration and this has been linked to long-term potentiation, LTP (as well as to protein kinase activation); strong depolarization of the post-synaptic cell completely ...
Zhenyu Yue's research has primarily concentrated on the molecular and cellular mechanisms underlying neurodegenerative diseases, with a particular focus on Parkinson’s disease and Alzheimer’s disease. [9] One of the notable areas of Yue's research involves the study of autophagy, a cellular process that degrades and recycles cellular ...
CREB proteins are activated by phosphorylation from various kinases, including PKA, and Ca 2+ /calmodulin-dependent protein kinases on the Serine 133 residue. [7] When activated, CREB protein recruits other transcriptional coactivators to bind to CRE promoter 5’ upstream region.
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