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1.
Corrêa-da-Silva, F.* et al.: Microglial phagolysosome dysfunction and altered neural communication amplify phenotypic severity in Prader-Willi Syndrome with larger deletion. Acta Neuropathol. 147:64 (2024)
2.
Mori, K.* et al.: Correction to: Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins. Acta Neuropathol. 148:48 (2024)
3.
Ryan, F.* et al.: Ferroptosis inhibitor improves outcome after early and delayed treatment in mild spinal cord injury. Acta Neuropathol. 147:106 (2024)
4.
Matosin, N.* et al.: Associations of psychiatric disease and ageing with FKBP5 expression converge on superficial layer neurons of the neocortex. Acta Neuropathol. 145, 439-459 (2023)
5.
LaClair, K.D.* et al.: Congenic expression of poly-GA but not poly-PR in mice triggers selective neuron loss and interferon responses found in C9orf72 ALS. Acta Neuropathol. 140, 121–142 (2020)
6.
Gomes, L.A.* et al.: A beta-induced acceleration of Alzheimer-related tau-pathology spreading and its association with prion protein. Acta Neuropathol. 138, 913-941 (2019)
7.
Hellwig, M.* et al.: TCF4 (E2-2) harbors tumor suppressive functions in SHH medulloblastoma. Acta Neuropathol. 137, 657-673 (2019)
8.
Doppler, K.* et al.: Dermal phospho-alpha-synuclein deposits confirm REM sleep behaviour disorder as prodromal Parkinson's disease. Acta Neuropathol. 133, 535-545 (2017)
9.
Schludi, M.H.* et al.: Spinal poly-GA inclusions in a C9orf72 mouse model trigger motor deficits and inflammation without neuron loss. Acta Neuropathol. 134, 241–254 (2017)
10.
Suárez-Calvet, M.* et al.: Monomethylated and unmethylated FUS exhibit increased binding to Transportin and distinguish FTLD-FUS from ALS-FUS. Acta Neuropathol. 131, 587-604 (2016)
11.
Mackenzie, I.R.* et al.: Quantitative analysis and clinico-pathological correlations of different dipeptide repeat protein pathologies in C9ORF72 mutation carriers. Acta Neuropathol. 130, 845-861 (2015)
12.
Schludi, M.H.* et al.: Distribution of dipeptide repeat proteins in cellular models and C9orf72 mutation cases suggests link to transcriptional silencing. Acta Neuropathol. 130, 537-555 (2015)
13.
Schludi, M.H.* et al.: Erratum to: Distribution of dipeptide repeat proteins in cellular models and C9orf72 mutation cases suggests link to transcriptional silencing. Acta Neuropathol. 130, 557-558 (2015)
14.
Götzl, J.K.* et al.: Common pathobiochemical hallmarks of progranulin-associated frontotemporal lobar degeneration and neuronal ceroid lipofuscinosis. Acta Neuropathol. 127, 845-860 (2014)
15.
May, S.* et al.: C9orf72 FTLD/ALS-associated Gly-Ala dipeptide repeat proteins cause neuronal toxicity and Unc119 sequestration. Acta Neuropathol. 128, 485-503 (2014)
16.
van der Zee, J.* et al.: Rare mutations in SQSTM1 modify susceptibility to frontotemporal lobar degeneration. Acta Neuropathol. 128, 397-410 (2014)
17.
Kreth, S.* et al.: In human glioblastomas transcript elongation by alternative polyadenylation and miRNA targeting is a potent mechanism of MGMT silencing. Acta Neuropathol. 125, 671-681 (2013)
18.
Lee, M.S. et al.: Transcriptome analysis of MENX-associated rat pituitary adenomas identifies novel molecular mechanisms involved in the pathogenesis of human pituitary gonadotroph adenomas. Acta Neuropathol. 126, 137-150 (2013)
19.
Mackenzie, I.R.* et al.: Dipeptide repeat protein pathology in C9ORF72 mutation cases: Clinico-pathological correlations. Acta Neuropathol. 126, 859-879 (2013)
20.
Mori, K.* et al.: Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins. Acta Neuropathol. 126, 881-893 (2013)
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