Hannu Kalimo, MD, PhD
Affiliations: | Pathology | University of Helsinki, Helsingfors, Finland |
Area:
http://www.biomedexperts.com/Profile.bme/662986/Hannu_KalimoWebsite:
http://www.hi.helsinki.fi/english/research/groups/pathology/cadasil.htmlGoogle:
"Hannu Kalimo"Bio:
http://www.linkedin.com/pub/hannu-kalimo/3b/579/288
Mean distance: 106866
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Publications
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Koskelainen S, Zhao F, Kalimo H, et al. (2019) Severe elastolysis in hereditary gelsolin (AGel) amyloidosis. Amyloid : the International Journal of Experimental and Clinical Investigation : the Official Journal of the International Society of Amyloidosis. 1-8 |
Rajani RM, Ratelade J, Domenga-Denier V, et al. (2019) Blood brain barrier leakage is not a consistent feature of white matter lesions in CADASIL. Acta Neuropathologica Communications. 7: 187 |
Munteanu I, Kalimo H, Saraste A, et al. (2017) Cardiac autophagic vacuolation in severe X-linked myopathy with excessive autophagy. Neuromuscular Disorders. 27: 185-187 |
Koskelainen S, Pihlamaa T, Suominen S, et al. (2016) Gelsolin amyloid angiopathy causes severe disruption of the arterial wall. Apmis : Acta Pathologica, Microbiologica, Et Immunologica Scandinavica |
Craggs L, Taylor J, Slade JY, et al. (2015) Clusterin/Apolipoprotein J immunoreactivity is associated with white matter damage in cerebral small vessel diseases. Neuropathology and Applied Neurobiology |
Saraste A, Koskenvuo JW, Airaksinen J, et al. (2015) No cardiomyopathy in X-linked myopathy with excessive autophagy. Neuromuscular Disorders : Nmd. 25: 485-7 |
Dowling JJ, Moore SA, Kalimo H, et al. (2015) X-linked myopathy with excessive autophagy: a failure of self-eating. Acta Neuropathologica. 129: 383-90 |
Tikka S, Baumann M, Siitonen M, et al. (2014) CADASIL and CARASIL. Brain Pathology (Zurich, Switzerland). 24: 525-44 |
Järvinen TA, Järvinen M, Kalimo H. (2013) Regeneration of injured skeletal muscle after the injury. Muscles, Ligaments and Tendons Journal. 3: 337-45 |
Kalimo H, Lalowski M, Bogdanovic N, et al. (2013) The Arctic AβPP mutation leads to Alzheimer's disease pathology with highly variable topographic deposition of differentially truncated Aβ. Acta Neuropathologica Communications. 1: 60 |