Keine Ansammlung von Amyloidplaques im Hirn und eine gute Funktion der Mitochondrien ebendort im hohen Alter, das ist schon was! Carnosin!
The pathogenic road map leading to Alzheimer's disease (AD) is still not completely understood; however, a large body of studies in the last few years supports the idea that beside the classic hallmarks of the disease, namely the accumulation of amyloid-β (Aβ) and neurofibrillary tangles, other factors significantly contribute to the initiation and the progression of the disease. Among them, mitochondria failure, an unbalanced neuronal redox state, and the dyshomeostasis of endogenous metals like copper, iron, and zinc have all been reported to play an important role in exacerbating AD pathology. Given these factors, the endogenous peptide carnosine may be potentially beneficial in the treatment of AD because of its free-radical scavenger and metal chelating properties.
In this study, we explored the effect of L-carnosine supplementation in the 3xTg-AD mouse, an animal model of AD that shows both Aβ- and tau-dependent pathology.
We found that carnosine supplementation in 3xTg-AD mice promotes a strong reduction in the hippocampal intraneuronal accumulation of Aβ and completely rescues AD and aging-related mitochondrial dysfunctions. No effects were found on tau pathology and we only observed a trend toward the amelioration of cognitive deficits.
Conclusions and Significance
Our data indicate that carnosine can be part of a combined therapeutic approach for the treatment of AD.
Mitochondrien in Hirnmzellen wurden wieder funktionstüchtiog wie eh und je:
Data from these experiments indicate that, compared to control mice, hippocampal mitochondria of untreated 3xTg-AD mice show a strong deregulation in the activity of complexes I, II, and IV (Fig. 4A–B). Interestingly, carnosine-fed 3xTg-AD mice exhibited a complete recovery of all these deficits and in the case of complexes II and IV the activity was actually significantly higher compared to mitochondria of control animals (Figure 4A–B). Analysis of mitochondrial activity in the cortex revealed that untreated 3xTg-AD mice showed a dramatic decline in the activity of complex I and, to a lesser extent, of complex IV (Figure 4C–D). Similarly to what was found in the hippocampus, carnosine treatment promoted a complete recovery of all these cortical deficits.
PS: wer rechnet das mal in eine Humandosis um: "Mice...were treated with 10 mM L-Carnosine (Sigma-Aldrich) in standard tap water"