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The phosphatase and tensin homologue deleted on chromosome ten (PTEN) dephosphorylates the protein kinase Akt (also known as protein kinase B). Mice null for PTEN develop neuron-selective neurodegeneration, with tau deposition in neurons. We generated mice null for phosphatase and tensin homologue deleted on chromosome ten gene 2 (PTEN2), an isoform of PTEN which lacks PTEN’s lipid phosphatase activity. Our results showed that the PTEN2 isoform, like PTEN, co-localizes to neurofibrillary tangles, but is not associated with other phospho-tau epitopes. Neuronal loss induced by PTEN2 overexpression was accompanied by tau pathology in neocortex and hippocampus in cell culture. Furthermore, PTEN2 overexpression in mice caused neuron loss in neocortex and hippocampus, with tau pathology in cells and tau-positive thread-like inclusions, but without microglia or astrocyte response. Our findings support a role for PTEN2 in the pathogenesis of Alzheimer’s disease-related tauopathy.Myocardial metabolism during oral glucose tolerance test in patients with ischaemic heart disease.
Metabolic adaptations, especially in non-anaerobic metabolism, are observed in the myocardium during insulin resistance. The aim of the present study was to test the influence of an oral glucose load, together with glucose infusion, on systemic and myocardial metabolism in patients with ischaemic heart disease (IHD). We studied patients with angiographically verified IHD (mean age 58 +/- 3 years) and control subjects (mean age 51 +/- 3
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