J. Kros

发表

The DNA repair-ubiquitin-associated HR23 proteins are constituents of neuronal inclusions in specific neurodegenerative disorders without hampering DNA repair

B. Oostra, J. Hoeijmakers, W. Vermeulen, 2006, Neurobiology of Disease.

Mechanisms underlying cerebellar motor deficits due to mGluR1‐autoantibodies

D. Linden, R. Shigemoto, C. D. De Zeeuw, 2003, Annals of neurology.

Filamin A mutation, a common cause for periventricular heterotopia, aneurysms and cardiac defects

R. Verdijk, J. Kros, M. D. de Wit, 2008, Journal of Neurology, Neurosurgery, and Psychiatry.

Molecular misreading: the occurrence of frameshift proteins in different diseases.

W. Kamphorst, J. Kros, R. D. de Vos, 2006, Biochemical Society transactions.

Alzheimer dementia characterized by amyloid angiopathy and large amyloid core type senile plaques in the APP 692 Ala → Gly mutation

A. Hofman, C. Broeckhoven, L. Hendriks, 1998 .

Mutation in the AP4M1 gene provides a model for neuroaxonal injury in cerebral palsy.

C. Catsman-Berrevoets, J. Dudink, M. Lequin, 2009, American journal of human genetics.

A rare missense variant in RCL1 segregates with depression in extended families

A. Hofman, S. Kushner, H. Tiemeier, 2017, Molecular Psychiatry.

Hereditary frontotemporal dementia is linked to chromosome 17q21—q22: A genetic and clinicopathological study of three dutch families

P. Heutink, B. Oostra, C. V. van Duijn, 1997, Annals of neurology.

Dense-core senile plaques in the Flemish variant of Alzheimer's disease are vasocentric.

Cornelia M van Duijn, Jean-Pierre Timmermans, Rong Wang, 2002, The American journal of pathology.

Presenile Alzheimer dementia characterized by amyloid angiopathy and large amyloid core type senile plaques in the APP 692Ala→Gly mutation

A. Hofman, C. Broeckhoven, C. van Broeckhoven, 1998, Acta Neuropathologica.

Loss of nuclear UBE3A causes electrophysiological and behavioral deficits in mice and is associated with Angelman syndrome

S. Kushner, D. Rotaru, Y. Elgersma, 2019, Nature Neuroscience.

Variable phenotypic expression and extensive tau pathology in two families with the novel tau mutation L315R

W. Kamphorst, R. Ravid, P. Heutink, 2003, Annals of neurology.

Frameshift proteins in autosomal dominant forms of Alzheimer disease and other tauopathies

G. Leuba, E. Hol, D. Mann, 2006, Neurology.

Loss of nuclear UBE3A causes electrophysiological and behavioral deficits in mice and is associated with Angelman syndrome

S. Kushner, D. Rotaru, Y. Elgersma, 2019, Nature Neuroscience.

The development of the rat prefrontal cortex. Its size and development of connections with thalamus, spinal cord and other cortical areas.

H. Uylings, C. V. van Eden, J. Kros, 1990, Progress in brain research.