What is it about?

The aggregation of amyloid-β42 (Aβ42) constitutes one of the major pathogenic events in Alzheimer's disease (AD), and the study of regional cerebral blood flow (rCBF), using single photon emission computed tomography (SPECT), aids the diagnosis of AD. In this study, we evaluated whether there was a correlation between rCBF in brain regions and plasma levels of Aβ1-42 in AD. 29 patients (mean age 71 ± 9) with a diagnosis of AD who fulfilled NINCDS-ADRDA criteria with a mean Mini-Mental Status Examination score of 15 ± 9 and 16 normal controls (mean age 64 ± 8) underwent SPECT brain imaging with hexamethylpropylene amine oxime, and semiquantitative analysis of rCBF was performed. Plasma samples were collected the same day of the SPECT and plasma Aβ1-42 measured by ELISA. A significant reduction of rCBF was observed in most regions in AD compared to controls, whereas mean plasma Aβ42 did not differ between the two groups. There was no correlation between rCBF in any region and plasma Aβ42 nor any correlations between gender, age, and severity with plasma levels of Aβ42. Since rCBF is coupled to neuronal activity, we conclude that plasma Aβ1-42 concentration is independent of neuronal function in every single region of the brain.

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Why is it important?

There is no correlation between rCBF in any region of the brain and plasma Aβ42 nor any correlations between gender, age, and severity with plasma levels of Aβ42. Since rCBF is coupled to neuronal activity, we conclude that plasma Aβ1-42 concentration is independent of neuronal function in every single region of the brain.

Perspectives

The accumulation of the β- Amyloid in the brain in Alzheimer's disease is the result of the mitochondrial dysfunction rather than of the vascular factor.

Professor Stavros J Baloyannis or Balogiannis or Balojannis or Baloyiannis or Mpalogiannis
Aristotle University of Thessaloniki

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This page is a summary of: Plasma Levels of Amyloid β1-42 Are Independent of Neuronal Function in Alzheimer's Disease, Journal of Alzheimer’s Disease, June 2009, IOS Press,
DOI: 10.3233/jad-2009-1056.
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