1.
Systemic and brain metabolic dysfunction as a new paradigm for approaching Alzheimer's dementia.
Giordano, V, Peluso, G, Iannuccelli, M, Benatti, P, Nicolai, R, Calvani, M
Neurochemical research. 2007;(4-5):555-67
Abstract
Since its definition Alzheimer's disease has been at the centre of consideration for neurologists, psychiatrists, and pathologists. With John P. Blass it has been disclosed a different approach Alzheimer's disease neurodegeneration understanding not only by the means of neurochemistry but also biochemistry opening new scenarios in the direction of a metabolic system degeneration. Nowadays, the understanding of the role of cholesterol, insulin, and adipokines among the others in Alzheimer's disease etiopathogenesis is clarifying approaches valuable not only in preventing the disease but also for its therapy.
2.
[Tubolopaties associated to hypokalemia].
Capasso, G
Giornale italiano di nefrologia : organo ufficiale della Societa italiana di nefrologia. 2004;(1):73-83
Abstract
We have described two clinical cases of two young men affected by hypkalemia associated with metabolic alkalosis. The first patient also presented hypercalciucia, normal magnesemia, defect in renal concentrating ability and increased renin activity; in addition he was affected by congenital sensorineural deafness. The diagnosis of Bartter's syndrome was made and it was confirmed by the gene analysis, which revealed a mutation for the beta-subunit of the ClC chloride channels known as barttin. The second case was characterized by hypocalciuria and hypomagnesemia, polyuria and nicturia. The genetic analysis revealed a mutation for the gene encoding the Na+-Cl(-) cotransporter and the diagnosis of Gitelman's syndrome was formulated. We present experimental and clinical evidence to explain, at the molecular level, the differences in calcium and magnesium homeostatis in the two cases. Moreover, we propose different causes to justify the pathogenesis of hypokalemia and the related metabolic alkalosis.