Amyloid beta may be an early transient pathological event
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The accumulation of beta-amyloid (Abeta) plaques and neurofibrillary tangles consisting of hyperphosphorylated tau protein are pathological features of Alzheimer's disease (AD) commonly modeled in mice using known human familial mutations; however, the loss of neurons also found to occur in AD is rarely observed in such models. The mechanism of neuron degeneration remains unclear but is of great interest as it is very likely an important factor for the onset of adverse memory deficits occurring in individuals with AD. The role of Abeta in the neuronal degeneration is a matter of controversial debates. In the present study we investigated the impact of extracellular plaque Abeta versus intraneuronal Abeta on neuronal cell death. The thalamus and the frontal cortex of the APP/PS1KI mouse model were chosen for stereological quantification representing regions with plaques only (thalamus) or plaques as well as intraneuronal Abeta (frontal cortex). A loss of neurons was found in the frontal cortex at the age of 6 months coinciding with the decrease of intraneuronal immunoreactivity, suggesting that the neurons with early intraneuronal Abeta accumulation were lost. Strikingly, no neuron loss was observed in the thalamus despite the development of abundant plaque pathology with levels comparable to the frontal cortex. This study suggests that plaques have no effect on neuron death whereas accumulation of intraneuronal Abeta may be an early transient pathological event leading to neuron loss in AD. Acta Neuropathol. 2008 Oct 31
The accumulation of beta-amyloid (Abeta) plaques and neurofibrillary tangles consisting of hyperphosphorylated tau protein are pathological features of Alzheimer's disease (AD) commonly modeled in mice using known human familial mutations; however, the loss of neurons also found to occur in AD is rarely observed in such models. The mechanism of neuron degeneration remains unclear but is of great interest as it is very likely an important factor for the onset of adverse memory deficits occurring in individuals with AD. The role of Abeta in the neuronal degeneration is a matter of controversial debates. In the present study we investigated the impact of extracellular plaque Abeta versus intraneuronal Abeta on neuronal cell death. The thalamus and the frontal cortex of the APP/PS1KI mouse model were chosen for stereological quantification representing regions with plaques only (thalamus) or plaques as well as intraneuronal Abeta (frontal cortex). A loss of neurons was found in the frontal cortex at the age of 6 months coinciding with the decrease of intraneuronal immunoreactivity, suggesting that the neurons with early intraneuronal Abeta accumulation were lost. Strikingly, no neuron loss was observed in the thalamus despite the development of abundant plaque pathology with levels comparable to the frontal cortex. This study suggests that plaques have no effect on neuron death whereas accumulation of intraneuronal Abeta may be an early transient pathological event leading to neuron loss in AD. Acta Neuropathol. 2008 Oct 31
Prebiotic oligofructose passes safety test: study
Consumption of the prebiotic fibre oligofructose at a dietary level of almost 10 per cent is safe, according to a new Anglo-American study. ...http://www.nutraingredients.com
posted by Valery Yermalitsky at
6:52 AM
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