Gradual alteration of mitochondrial structure and function by &#946;-amyloids: importance of membrane viscosity changes, energy deprivation, ROS production and cytochrome c release.

A. L. E. A. R. D. I., Am; B. E. N. A. R. D. G, A. U. G. E. R. E. A. U. O; Malgat,; Talbot, Jc; M. A. Z. A. T., Jp; Letellier, T; DACHARY P. R. I. G. E. N. T., J; Solaini, Giancarlo; R. O. S. S. I. G. N. O. L. R.,

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Intracellular amyloid beta-peptide (Abeta) accumulation is considered to be a key pathogenic factor in sporadic Alzheimer's disease (AD), but the mechanisms by which it triggers neuronal dysfunction remain unclear. We hypothesized that gradual mitochondrial dysfunction could play a central role in both initiation and progression of sporadic AD. Thus, we analyzed changes in mitochondrial structure and function following direct exposure to increasing concentrations of Abeta(1-42) and Abeta(25-35) in order to look more closely at the relationships between mitochondrial membrane viscosity, ATP synthesis, ROS production, and cytochrome c release. Our results show the accumulation of monomeric Abeta within rat brain and muscle mitochondria. Subsequently, we observed four different and additive modes of action of Abeta, which were concentration dependent: (i) an increase in mitochondrial membrane viscosity with a concomitant decrease in ATP/O, (ii) respiratory chain complexes inhibition, (iii) a potentialization of ROS production, and (iv) cytochrome c release.

Titolo:	Gradual alteration of mitochondrial structure and function by β-amyloids: importance of membrane viscosity changes, energy deprivation, ROS production and cytochrome c release.
Autore/i:	A.L.E.A.R.D.I. AM; B.E.N.A.R.D. G, A.U.G.E.R.E.A.U. O; MALGAT; TALBOT JC; M.A.Z.A.T. JP; LETELLIER T; DACHARY P.R.I.G.E.N.T. J; SOLAINI, GIANCARLO; R.O.S.S.I.G.N.O.L. R.
Autore/i Unibo:	A.L.E.A.R.D.I. AM B.E.N.A.R.D. G, A.U.G.E.R.E.A.U. O MALGAT TALBOT JC M.A.Z.A.T. JP LETELLIER T DACHARY P.R.I.G.E.N.T. J SOLAINI, GIANCARLO R.O.S.S.I.G.N.O.L. R. mostra contributor esterni nascondi contributor esterni
Anno:	2005
Rivista:	JOURNAL OF BIOENERGETICS AND BIOMEMBRANES
Abstract:	Intracellular amyloid beta-peptide (Abeta) accumulation is considered to be a key pathogenic factor in sporadic Alzheimer's disease (AD), but the mechanisms by which it triggers neuronal dysfunction remain unclear. We hypothesized that gradual mitochondrial dysfunction could play a central role in both initiation and progression of sporadic AD. Thus, we analyzed changes in mitochondrial structure and function following direct exposure to increasing concentrations of Abeta(1-42) and Abeta(25-35) in order to look more closely at the relationships between mitochondrial membrane viscosity, ATP synthesis, ROS production, and cytochrome c release. Our results show the accumulation of monomeric Abeta within rat brain and muscle mitochondria. Subsequently, we observed four different and additive modes of action of Abeta, which were concentration dependent: (i) an increase in mitochondrial membrane viscosity with a concomitant decrease in ATP/O, (ii) respiratory chain complexes inhibition, (iii) a potentialization of ROS production, and (iv) cytochrome c release.
Data prodotto definitivo in UGOV:	2005-10-17 11:50:39
Appare nelle tipologie:	1.01 Articolo in rivista

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