LAUSR

Peter Riederer was always a bridge builder between basic and applied neuroscience. Thus, he is a frontrunner in what we nowadays call translational research. We have the privilege to discuss in brief 14 manuscripts on the basic mechanism of Parkinson’s disease (PD) and Alzheimer’s disease (AD) from friends of Peter Riederer (Name of communicating author, Country). We are impressed that this work is reflecting wide international collaboration of Peter since the manuscripts were submitted from all over the world. Richard M Kostrzewa (United States) describes a real classical animal model of PD, i.e. rats with neonatal application of 6-Hydroxydopamine (n6-OHDA) which results in destruction of dopaminergic neurons and thus imitating motor and non-motor abnormalities similar to the ones in Parkinson’s disease. It is fair to say that this is standard model for PD and helped to get important insights into the basic mechanisms of cell death of dopaminergic neurons in the substantia nigra. Peter Riederer used the model for various publications to address iron metabolism in PD and to study treatment with sarizotan or COMT-inhibitors in such lesioned rats. Young J Oh et al. (Korea) report that RNF-166, a novel RING (Really Interesting New Gene) type 3-kinase, plays a dual role for Lys63-linked ubiquitination and sumoylation of its target proteins such as signal-regulating kinase 1 (ASK1). The results suggest that RING-type E3 ligases may play essential roles in cell survival and death in PD and AD. Lutz Frölich et al. (Germany) discuss an emerging framework in which ApoE4, the strongest risk factor for Alzheimer’s disease, is associated with amyloid and tau pathology at specific time points in AD pathogenesis. The authors investigated the associations between ApoE4 with CSF Aβ42, total tau (t-tau), phospho-tau181 (p-tau) and the progression of decline in a large cohort of mild cognitive impairment (MCI) subjects, both progressors to AD and other dementias as well as non-progressors. Peter Riederer has contributed numerous papers in this field and it is great to see how his many former co-workers continued to work in this important field. Wolf-Dieter Rausch et al. (Austria) present a review on tyrosine hydroxylase in PD. Tyrosine hydroxylase is the ratelimiting enzyme for dopamine biosynthesis, and decreases in transcript, protein and activity in dopaminergic neurons due to neurodegeneration. The authors describe in detail the relation of tyrosine hydroxylase with various endogenous and exogenous factors. This contribution is based on many landmark papers by Peter Riederer. Kay Double et al. (Australia) report on the history of iron in PD and related disorders, from the first observations in early twentieth century to recent efforts that view extrapyramidal iron as a novel therapeutic target and diagnostic indicator. Together with Professor Moussa Youdim Peter Riederer has extensively contributed to the iron story in neurodegenerative diseases and this explains that young scientists even from Australia joined his group. Kurt A. Jellinger (Austria) presents an update on the heterogeneity of AD spectrum. Based on multiple scientific approach, Jellinger shows tha AD is a heterogeneous and multifunctional disorder with selective vulnerability of different brain networks which implies that precision medicine will be needed to address the right targets in individual subjects with so-called AD. Kurt Jellinger and Peter Riederer have published together since 1978 and as a doyen of neuropathology Kurt Jellinger has often stimulated the doyen of neurometabolism and neurotransmitter knowledge. Carsten Scheller et al. (Germany) report on plasma autoantibodies to Glial Fibrillary Acidic Protein (GFAD) which show correlation to the dissemination of PD pathology described by Heiko Braak. Tissue homogenates from different brain regions (DM, SN, MC, HC, FC) from PD * Toshiharu Nagatsu [email protected]; [email protected]