His primary scientific interests are in Pathology, Frontotemporal lobar degeneration, Frontotemporal dementia, Alzheimer's disease and Dementia. His studies in Pathology integrate themes in fields like Cerebral cortex and Down syndrome. His Frontotemporal lobar degeneration study combines topics in areas such as Genetics, White matter, Subependymal zone, Charged multivesicular body protein 2B and Cytoplasmic inclusion.
The Frontotemporal dementia study combines topics in areas such as Progressive supranuclear palsy and Corticobasal degeneration. His Alzheimer's disease research includes elements of Molecular biology, Apolipoprotein E and Degenerative disease. His study in Dementia is interdisciplinary in nature, drawing from both Psychiatry, Cognition, Neuroscience and Amyotrophic lateral sclerosis.
David M. A. Mann mainly focuses on Pathology, Frontotemporal lobar degeneration, Alzheimer's disease, Disease and Frontotemporal dementia. Pathology is represented through his Dementia, Neuropathology, C9orf72, Senile plaques and Pathological research. His Dementia study combines topics from a wide range of disciplines, such as Tau protein, Neuroscience and Cohort study.
His research integrates issues of Cytoplasmic inclusion, Amyotrophic lateral sclerosis, Motor neurone disease and Immunostaining in his study of Frontotemporal lobar degeneration. His research in Alzheimer's disease intersects with topics in Apolipoprotein E, Amyloid, Endocrinology and Degenerative disease. His studies deal with areas such as Progressive supranuclear palsy, Genetics and Psychiatry, Aphasia as well as Frontotemporal dementia.
David M. A. Mann spends much of his time researching Pathology, Frontotemporal lobar degeneration, Disease, Frontotemporal dementia and C9orf72. He interconnects Dentate gyrus and Temporal cortex in the investigation of issues within Pathology. His research in Frontotemporal lobar degeneration tackles topics such as Cerebellum which are related to areas like Hippocampal formation.
David M. A. Mann has researched Disease in several fields, including Odds ratio, Differential diagnosis and Cohort. His Frontotemporal dementia research integrates issues from Progressive supranuclear palsy, Psychiatry, Aphasia and Amyotrophic lateral sclerosis. The concepts of his C9orf72 study are interwoven with issues in C9orf72 Protein and DNA Repeat Expansion.
David M. A. Mann focuses on Pathology, Frontotemporal lobar degeneration, Frontotemporal dementia, Disease and Alzheimer's disease. C9orf72 is the focus of his Pathology research. David M. A. Mann combines subjects such as Progressive supranuclear palsy, Psychiatry, Cognition, Amyotrophic lateral sclerosis and Tauopathy with his study of Frontotemporal dementia.
His Amyotrophic lateral sclerosis research incorporates elements of Genetics and Aphasia. His Disease research includes themes of Differential diagnosis, Genome-wide association study and Odds ratio. His Internal medicine research is multidisciplinary, relying on both Oncology and Gene mutation.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD
Alan E. Renton;Elisa Majounie;Adrian James Waite;Javier Simón-Sánchez;Javier Simón-Sánchez.
Neuron (2011)
Association of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17
M. Hutton;C. L. Lendon;P. Rizzu;M. Baker.
Nature (1998)
TDP-43 is a component of ubiquitin-positive tau-negative inclusions in frontotemporal lobar degeneration and amyotrophic lateral sclerosis
Tetsuaki Arai;Masato Hasegawa;Haruhiko Akiyama;Kenji Ikeda.
Biochemical and Biophysical Research Communications (2006)
Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease
Denise Harold;Richard Abraham;Paul Hollingworth;Rebecca Sims.
Nature Genetics (2009)
Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17
Matt Baker;Ian R. Mackenzie;Stuart M. Pickering-Brown;Jennifer Gass.
Nature (2006)
Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease.
Paul Hollingworth;Denise Harold;Rebecca Sims;Amy Gerrish.
Nature Genetics (2011)
Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature
Peter T Nelson;Irina Alafuzoff;Eileen H Bigio;Constantin Bouras.
Journal of Neuropathology and Experimental Neurology (2012)
Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration
Nigel J. Cairns;Eileen H. Bigio;Ian R A Mackenzie;Manuela Neumann.
Acta Neuropathologica (2007)
Nomenclature and nosology for neuropathologic subtypes of frontotemporal lobar degeneration: an update
Ian R. A. Mackenzie;Manuela Neumann;Eileen H. Bigio;Nigel J. Cairns.
Acta Neuropathologica (2010)
A harmonized classification system for FTLD-TDP pathology
Ian R. A. Mackenzie;Manuela Neumann;Atik Baborie;Deepak M. Sampathu.
Acta Neuropathologica (2011)
If you think any of the details on this page are incorrect, let us know.
We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below:
University of Manchester
Salford Royal NHS Foundation Trust
University of Manchester
University of Sydney
University of Tokyo
Mayo Clinic
Tokyo Metropolitan Institute of Medical Science
University College London
Inserm
University of Pennsylvania
Northeastern University
University of Cagliari
MIT
University of Kansas
CEA Grenoble
Hokkaido University
University of Groningen
Oak Ridge National Laboratory
Tohoku University
Université Paris Cité
Commonwealth Scientific and Industrial Research Organisation
University College Dublin
Brigham and Women's Hospital
United States Department of Agriculture
Spanish National Centre for Cardiovascular Research
Goldsmiths University of London