5 RESULTS
COMMENT In their recent article, Liu et al provided clear evidence that abnormal hyperphospharylation of tau protein may be induced by decreased 0-GlcNAcylation subsequent to a deficient glucose metabolism in Alzheimer disease (AD) brain. Experimentally, the ...
COMMENT The paper from Kahn and coworkers is interesting and deserves greater attention. The expanded life expectancy due to leanness caused by a selective loss of insulin signalling in adipose tissue may point to an active metabolic role of that tissue. In this ...
COMMENT Alzheimer Disease and brain insulin metabolism may be assumed to be tightly coupled. 1. Both insulin binding to its receptor and receptor autophosphorylation were found to be reduced by Ab40 and Ab42, and this effect was mediated via a decrease in the ...
COMMENT "A central issue in medicine is the grouping of disorders on the basis of their etiology, yet one common clinico-pathologic feature of diseases does not indicate a common etiology. Therefore, from a nosological point of view, Alzheimer's disease ...
COMMENT On Insulin and Neuronal Plasticity Functionally, synaptic plasticity forms the most important site of neuronal plasticiy. Recent evidence suggests that both activity and plasticity of synapses depend on biochemical stimuli induced by the expression of the ...
