In 2007, the CIN started with 25 principal investigators as cluster applicants, as stipulated in the DFG call for bids. When the CIN cluster was approved further scientists from a range of institutions were incorporated, to make up the 48 'founding members' of the CIN. Since the beginning of 2014 the CIN has consisted of over 80 scientists in total. The membership process involves an application to the steering committee in which the candidate outlines his or her scientific profile and submits a list of publications. The committee's decision is based purely on the scientific excellence of each candidate.
Prof. Dr. Mathias Jucker
Organization: Hertie Institute of Clinical Brain Research / DZNE Tübingen
Phone number: +49 (0)7071 29 86863
Department: Dept. of Cellular Neurology
Area: CIN Members
Scientific topic: Brain Aging and Alzheimer's Disease
Field of Research
The research focus of the department is on the cellular and molecular mechanisms of brain aging and age-related neurodegenerative diseases with a special focus on the pathogenesis of Alzheimer's disease and cerebral amyloid angiopathies.
Transgenic mouse models; in vivo multiphoton imaging; neuro-stereology
brain imaging; glia; neuro-immunology; neuro-pathology; neuro-plasticity; neurodegeneration
- Meyer-Luehmann M, Coomaraswamy J, Bolmont T, Kaeser S, Schaefer C, Kilger E, Neuenschwander A, Abramowski D, Frey P, Jaton AL, Vigouret J, Paganetti P, Walsh DM, Mathews P, Ghiso J, Staufenbiel M, Walker L, Jucker M (2006) Exogenous induction of Aﬂ-amyloidogenesis is governed by intrinsic properties of agent and host. Science. 313(5794):1781-4.
- Kaeser SA, Herzig MC, Coomaraswamy J, Kilger E, Selenica MLB, Winkler D, Staufenbiel M, Levy E, Grubb A, Jucker M (2007). Cystatin C modulates cerebral ﬂ-amyloidosis. Nat Genet. 39(12):1437-9.
- Grathwohl SA, Kälin RE, Bolmont T, Prokop S, Winkelmann G, Kaeser SA, Odenthal J, Radde R, Eldh T, Gandy S, Aguzzi A, Staufenbiel M, Mathews PM, Wolburg H, Heppner FL, Jucker M (2009). Formation and maintenance of Alzheimer's disease beta-amyloid plaques in the absence of microglia. Nat Neurosci. 2012(11):1361-3.