Publications en collaboration avec des chercheurs de University of Bonn (17)

2023

  1. Erratum: Author Correction: Common variants in Alzheimer's disease and risk stratification by polygenic risk scores (Nature communications (2021) 12 1 (3417))

    Nature communications

2022

  1. New insights into the genetic etiology of Alzheimer's disease and related dementias

    Nature genetics, Vol. 54, Núm. 4, pp. 412-436

2021

  1. Common variants in Alzheimer's disease and risk stratification by polygenic risk scores

    Nature communications, Vol. 12, Núm. 1, pp. 3417

  2. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1

    Autophagy, Vol. 17, Núm. 1, pp. 1-382

2020

  1. Correction to: A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer’s disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity (Acta Neuropathologica, (2019), 138, 2, (237-250), 10.1007/s00401-019-02026-8)

    Acta Neuropathologica

2019

  1. A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer’s disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity

    Acta Neuropathologica, Vol. 138, Núm. 2, pp. 237-250

2016

  1. Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

    Autophagy

2015

  1. MAPT H1 haplotype is associated with late-onset Alzheimer's disease risk in APOE ε 4 noncarriers: Results from the dementia genetics Spanish consortium

    Journal of Alzheimer's Disease, Vol. 49, Núm. 2, pp. 343-352

2014

  1. Investigation of the role of rare TREM2 variants in frontotemporal dementia subtypes

    Neurobiology of Aging, Vol. 35, Núm. 11, pp. 2657.e13-2657.e19

2013

  1. Janus-faced microglia: Beneficial and detrimental consequences of microglial phagocytosis

    Frontiers in Cellular Neuroscience

2012

  1. Dispersible amyloid β-protein oligomers, protofibrils, and fibrils represent diffusible but not soluble aggregates: Their role in neurodegeneration in amyloid precursor protein (APP) transgenic mice

    Neurobiology of Aging, Vol. 33, Núm. 11, pp. 2641-2660

2009

  1. Capillary cerebral amyloid angiopathy is associated with vessel occlusion and cerebral blood flow disturbances

    Neurobiology of Aging, Vol. 30, Núm. 12, pp. 1936-1948

2008

  1. Inter-laboratory comparison of neuropathological assessments of β-amyloid protein: A study of the BrainNet Europe consortium

    Acta Neuropathologica, Vol. 115, Núm. 5, pp. 533-546

  2. Tracing of temporo-entorhinal connections in the human brain: Cognitively impaired argyrophilic grain disease cases show dendritic alterations but no axonal disconnection of temporo-entorhinal association neurons

    Acta Neuropathologica, Vol. 115, Núm. 2, pp. 175-183

2006

  1. Selective vulnerability of different types of commissural neurons for amyloid β-protein-induced neurodegeneration in APP23 mice correlates with dendritic tree morphology

    Brain, Vol. 129, Núm. 11, pp. 2992-3005

  2. The development of amyloid beta protein deposits in the aged brain.

    Science of aging knowledge environment : SAGE KE, Vol. 2006, Núm. 6

2005

  1. Apolipoprotein E co-localizes with newly formed amyloid β-protein (Aβ) deposits lacking immunoreactivity against N-terminal epitopes of Aβ in a genotype-dependent manner

    Acta Neuropathologica, Vol. 110, Núm. 5, pp. 459-471