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Research Grants



The Foundation supports research projects, scientific publications, events, and other activities focussing on the age-related neurodegenerative diseases. Our efforts are directed to translational approaches based on expertise in biology, biochemistry and biophysics to provide mechanistic, pharmacological and methodological insights for future clinical translation of novel, more specific and effective strategies for diagnosis, prevention and therapy. Because of the presently rather low profits from the Foundation's assets the scientific members of the Board recommend research projects that deserve to be funded. It is currently not possible to submit grant applications.


Funded since 2012

Prof. Dr. Robert Perneczky, Klinik für Psychiatrie und Psychotherapie, Ludwig-Maximilians-Universität München
1st International Conference on Brain and Cognitive Reserve in Dementia Disorders
New: The high calibre two-day conference at the University of Munich in November 2017 will mainly focus on investigations of the structural and the functional brain mechanismens, which can delay or even prevent dementia onset. Too, research on neuroimaging and biomarkers will be addressed. Aim of the international conference is first of all a gain in knowledge, but also a better network (forum) of the leading scientists in this area of research. About 200 particpants are expected.


Dr. Johannes Levin, Ludwig-Maximilians-Universität, München
Establishment of a cohort of patients with Down syndrome (Trisomy 21) for imaging and biomarker studies
Current: Approximately three out of four patients with Down syndrome develop a dementia from the fifth decade of live onwards. The anatomical distribution of pathological alterations are similar to the ones of patients with Alzheimer disease. Aims of the study are to recruit a cohort of patients with Down syndrome, to clinically evaluate them, to determine if these patients show different cerebrospinal fluid and plasma concentations of the soluble protein TREM2, and to test how these differences are associated. The study is funded with 120 000 € for two years.


Dr. Christel Depienne & Dr. Alexandra Durr, Institut du Cerveau et de la Moelle Epinière, Paris
Identification of genetic, epigenetic and environmental modifiers in hereditary spastic paraplegia
Current: Hereditary spastic paraplegia (HSP) is a neurodegenerative disorder with genetic modulators, but it is likely that non-genetic factots contribute too. Therefore, the aim is the identification of genetic, epigenetic and/or environmental influences that can predict onset, progression and outcome and, thus, lead to the development of new treatments. The study focusses on the gene SPG4-HSP, as in this kind of HSP the development of dementia has been observed. Because of the well-documented progress of the research project the Board approved an extension. The study will be funded with 204.000 € for three years.


Prof. Sascha Weggen, Institut für Neuropathologie, Heinrich-Heine-Universität Düsseldorf
A novel metalloprotease in Abeta peptide generation and Alzheimer's disease
Finished: The effects of ADAMTS4, a metalloprotease, on Abeta generation in primary neurons and in transgenic Alzheimer mouse models are characterized. Aims are to confirm these effects, to investigate a direct interaction between ADAMTS4 and APP (Amyloid Precursor Protein), to compare mRNA and protein expression levels of ADAMTS4 in brain samples from Alzheimer patients and non-demented controls, and to investigate the physiological relevance of ADAMTS4 for brain Abeta levels in vivo. The successful research work offers important insights into the processing of amylodogenic fragments of the APP protein. The study was funded with 81.450 € for 2 years.


Prof. Alexis Brice, Association pour le Développement de la Recherche sur les Maladies Génétiques, Neurologiques et Psychiatriques, Paris
Use of next generation sequencing to improve knowledge of the molecularer bases of spinocerebellar degenerations
Finished: Based on preliminary work the knowledge of the molecular bases of spinocerebellar degenerations was to be improved. The group could - partly in an international cooperation - identify multiple genes, increase the knowledge of the molecular bases of the described diseases by the extension of the phenotype and inheritance modes of known genes and highlight the functional link between lysosomal storage and frequent forms of autosomal recessive spastic paraplegia, thus, opening avenues of research to therapeutic intervention. The study was funded with 129 000 € for two years.

Publications: Novarino G et al. (2014) Exome sequencing links corticospinal motor neuron disease to common neurodegenerative disorders. Science 343(6170):506-11. doi: 10.1126/science.1247363. ▪ Esteves T et al. (2014) Loss of association of REEP2 with membranes leads to hereditary spastic paraplegia. Am J Hum Genet 92(2):268-77. doi: 10.1016/j.ajhg.2013.12.005. ▪ Di Gregorio E et al. (2014) ELOV5 mutations cause spinocerebellar ataxia 38. Am J HUM Genet 92(2):209-17. doi: 10.1016/j.ajhg.2014.07.001 ▪ Coutelier M et al. (2015) GRID2 mutations span from congenital to mild adult-onset cerebellar ataxia. Neurology 84(17):1751-9. doi: 10.1212/WNL.0000000000001524. ▪ Coutelier M et al. (2015) Alteration of ornithine metabolism leads to dominant and recessive hereditary spastic. Brain 138(Pt 8):2191-205. doi: 10.1093/brain/awv143. ▪ Hirst J et al. 2015) Loss of AP-5 results in accumulation of aberrant endolysosomes: defining a new type of lysosomal storage disease. Hum Mol Genet 24(17):4984-96. doi: 10.1093/hmg/ddv220. ▪ Coutelier M et al. (2015) A recurrent mutation in CACNA1G alters Cav3.1. T-type calcium-channel conduction and causes autosomal-dominant cerebellar ataxia. Am J Hum Genet 97(5):726-37. doi: 10.1016/j.ajhg.2015.09.007 ▪ Elsayed LE et al. (2015) A novel nonsense mutation in DNAJC6 expands the phenotype of autosomal recessive juvenile-onset Parkinson disease. Ann Neurol [Epub ahead of print] doi: 10.1002/ana.24591.


Prof. Paul Saftig, Biochemisches Institut, Christian-Albrechts-Universität zu Kiel, together with
Prof. Stefan Lichtenthaler, Lehrstuhl für Neuroproteomik, Technische Universität München
Therapeutic potential of the Alzheimer alpha-secretase ADAM10
Finished: It has been shown which of the already identified ADAM10 substrate hits are true substrates, which of them undergo increased proteolytic cleavage upon activation of ADAM10, and which of the substrates contribute to the phenotypic changes observed in brains with altered ADAM10 activity. The mouse model was especially helpful and successful. The experimental procedure sets a standard and can now be applied to other substrates in order to determine their potential contribution to the pathogenesis of Alzheimer's disease. The study was funded with 20 000 €.

Papers: Saftig P, Lichtenthaler SF (2015) The alpha secretase ADAM10: A metalloprotease with multiple functions in the brain. Prog. Neurobiol 135:1-20. doi: 10.1016/j.pneurobio.2015.10.003 ▪ Damme M et al. (2014) Autophagy in neuronal cells: general principles and pathological functions. Acta Neuropathol 129(3):337-62. doi: 10.1007/s00401-014-1361-4.


Prof. Paul Saftig, Biochemisches Institut, Christian-Albrechts-Universität zu Kiel together with
Prof. Gerd Multhaup, Pharmacology & Therapeutics Faculty, McGill University, Montreal
Tetraspanins in Alzheimer‘s disease
Finished: It has been shown that tetraspanin encoding genes, especially TSPAN15 and TSPAN3, are susceptible to transcriptional regulation mediated by nuclear Abeta, how far the expression levels of tetraspanins affect APP (Amyloid Precursor Protein) processing and Abeta generation, how tetraspanins affect intracellular APP transport and interaction with other proteins and secretases, and how tetraspanin-expression does affect APP metabolism in vivo. For the experiments transgenic TSPAN mice havebeen generated. The results show a conceptual progress, among others, for the identification of novel biomarkers. The study was funded with 15 000 €.

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