Oxygen Isotope Effect Resulting from Polaron-induced Superconductivity in Cuprates

The planar oxygen isotope effect coefficient measured as a function of hole doping in the Pr- and La-doped YBa2Cu3O7 (YBCO) and the Ni-doped La1.85Sr0.15CuO4 (LSCO) superconductors quantitatively and qualitatively follows the form originally proposed by Kresin and Wolf, which was derived for polarons perpendicular to the superconducting planes. Interestingly, the inverse oxygen isotope effect coefficient at the pseudogap temperature also follows the same formula. These findings allow the conclusion that the superconductivity in YBCO and LSCO results from polarons or rather bipolarons in the CuO2 plane. The original formula, proposed for the perpendicular direction only, is obviously more generally valid and accounts for the superconductivity in the CuO2 planes.Comment: Dedicated to Alex M\"uller on the occasion of his 90th birthda

Role of Synucleins in Alzheimer’s Disease

Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the most common causes of dementia and movement disorders in the elderly. While progressive accumulation of oligomeric amyloid-β protein (Aβ) has been identified as one of the central toxic events in AD leading to synaptic dysfunction, accumulation of α-synuclein (α-syn) resulting in the formation of oligomers has been linked to PD. Most of the studies in AD have been focused on investigating the role of Aβ and Tau; however, recent studies suggest that α-syn might also play a role in the pathogenesis of AD. For example, fragments of α-syn can associate with amyloid plaques and Aβ promotes the aggregation of α-syn in vivo and worsens the deficits in α-syn tg mice. Moreover, α-syn has also been shown to accumulate in limbic regions in AD, Down’s syndrome, and familial AD cases. Aβ and α-syn might directly interact under pathological conditions leading to the formation of toxic oligomers and nanopores that increase intracellular calcium. The interactions between Aβ and α-syn might also result in oxidative stress, lysosomal leakage, and mitochondrial dysfunction. Thus, better understanding the steps involved in the process of Aβ and α-syn aggregation is important in order to develop intervention strategies that might prevent or reverse the accumulation of toxic proteins in AD