What We Do
2000, I have pursued work as a physician-scientist focusing on Parkinson
disease (PD), Lewy body dementia (DLB) and multiple system atrophy (MSA). Since opening my new laboratory at the OHRI in
2007, my team has focused on: (i) better modeling the pathogenesis of PD and DLB in mice; (ii) understanding the functions of 4 disease-linked genes (SNCA; GBA; LRRK2; Parkin); (iii) creating new tools, including animal models, platforms and antibodies; and (iv) exploring biological markers of PD, DLB and MSA.
Tomlinson JJ et al. Protocol for Mouse Whole Head Mounting
Facilitates the Visualization of alpha-Synuclein Throughout the
Olfactory System and the Detection of its Protective, Antimicrobial Effect. 2017; under review.
Schlossmacher MG et al. Modelling idiopathic Parkinson disease as a
complex illness can inform incidence rate in healthy adults : the PREDIGT
score. Eur J Neuroci. 2017;
Cullen V* et al. Acid beta-glucosidase mutations linked to Gaucher disease, Parkinson's and Lewy body dementia dysregulate alpha-synuclein in vivo. Ann Neurol 2011;69:940-53
*This paper was awarded the editor's ‘Annals of Neurology Prize' in 2012
Hakimi M et al. Parkinson's-linked
LRRK2 is expressed in immune cells and upregulated after the recognition of
microbial structures. J Neural
Mollenhauer B* et al. Cerebrospinal fluid values of alpha-synuclein and tau in patients
presenting with parkinsonism. Lancet Neurol
2011;10:230-40 and Lancet Neurol 2011;10:681-3;
*See also the opinion piece published
in: Lancet Neurol 2011;10(3):203-5
Meet the Schlossmacher Lab
The Schlossmacher team unites a group of trainees, research staff and collaborators from diverse scientific interests and backgrounds - including neuroscience, biochemistry, immunology, virology, animal studies and pathology. This reflects our different approaches to studying and modelling Parkinson disease variants and related dementias.
Potential trainees, please send inquiries to:
email@example.com or firstname.lastname@example.org