About: Matthis Synofzik

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

German neurologist

Attributes	Values
rdf:type	Item
description	forskare (sv) ikertzailea (eu) 연구원 (ko) 研究者 (ja) wetenschapper (nl) дослідник (uk) باحت (ary) изилдөөчү (ky) 研究者 (zh) German neurologist (en) neurólogo alemán (es) طبيب أعصاب ألماني (ar) deutscher Neurologe (de)
rdfs:label	Matthis Synofzik (de) Matthis Synofzik (en) Matthis Synofzik (es) Matthis Synofzik (fr) Matthis Synofzik (it) Matthis Synofzik (nl) Matthis Synofzik (pl) Matthis Synofzik (ast)
skos:prefLabel	Matthis Synofzik (de) Matthis Synofzik (en) Matthis Synofzik (es) Matthis Synofzik (fr) Matthis Synofzik (it) Matthis Synofzik (nl) Matthis Synofzik (pl) Matthis Synofzik (ast)
name	Matthis Synofzik (de) Matthis Synofzik (en) Matthis Synofzik (es) Matthis Synofzik (fr) Matthis Synofzik (it) Matthis Synofzik (nl) Matthis Synofzik (pl) Matthis Synofzik (ast)
instance of	wds:Q47504980-6A60534A-A528-42D7-B5EC-D45DBD58F7B1
instance of	Homo sapiens
skos:altLabel	Matthis Benjamin Synofzik (de) Matthis Benjamin Synofzik (en)
occupation	wds:Q47504980-9E60DC84-9EF5-418D-A22D-D3DF53D1075B
employer	wds:Q47504980-062FC35E-E09F-4C0D-970B-3CD730EF7BCF wds:Q47504980-5B3F2747-31DF-47FD-A8FB-23E53FE03B87
sex or gender	wds:Q47504980-454C24F7-8B6C-44A9-9794-DD4D27C6D4BB
ISNI	wds:Q47504980-9B5CCA7E-5CB7-40DC-8C50-A809F0D892FB
VIAF ID	wds:Q47504980-A7B483D9-0B43-4CDE-8A14-9CC48D6F9A7C
GND ID	wds:Q47504980-00B15670-21F6-41AD-AD55-A0E481614D1F
DBLP author ID	wds:Q47504980-482EA1AC-1E62-48D1-8793-E24698DE6A1C
date of birth	wds:Q47504980-22a5a1b9-452a-08c0-fda2-02e43db6e37e
educated at	wds:Q47504980-0AA332B5-18BF-4AED-9FD4-15253BAFD7A0 wds:Q47504980-14B6944C-F76D-4757-8B99-0302C8AFB55B wds:Q47504980-68DF213E-07C7-4F4F-952D-393D44F65172 wds:Q47504980-FCE1F346-5845-4237-8D15-5D51DC695FE6
WorldCat Identities ID (superseded)	wds:Q47504980-7F60AD81-1FAB-43C3-8A37-115646C7EE4E
VIAF ID	http://viaf.org/viaf/81116203
GND ID	https://d-nb.info/gnd/136837247
DBLP author ID	https://dblp.org/pid/171/9690.rdf
occupation	neurologist
employer	German Center for Neurodegenerative Diseases Hertie Institute for Clinical Brain Research
sex or gender	male
ISNI	000000005595403X
VIAF ID	81116203
GND ID	136837247
DBLP author ID	171/9690
date of birth	1979-01-01 00:00:00Z (xsd:dateTime)
educated at	Hertie Institute for Clinical Brain Research
WorldCat Identities ID (superseded)	viaf-81116203
ORCID iD	wds:Q47504980-287cc865-4c47-6565-07c5-4fb3b78b0ca8
ORCID iD	https://orcid.org/0000-0002-2280-7273
ORCID iD	0000-0002-2280-7273
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q47504980
is author of	PNPLA6 mutations cause Boucher-Neuhauser and Gordon Holmes syndromes as part of a broad neurodegenerative spectrum Ataxia meets chorioretinal dystrophy and hypogonadism: Boucher-Neuhäuser syndrome due to PNPLA6 mutations. The tumour suppressor gene WWOX is mutated in autosomal recessive cerebellar ataxia with epilepsy and mental retardation Atypical parkinsonism in C9orf72 expansions: a case report and systematic review of 45 cases from the literature Targeted high-throughput sequencing identifies a TARDBP mutation as a cause of early-onset FTD without motor neuron disease. Video game-based coordinative training improves ataxia in children with degenerative ataxia. X-linked Charcot-Marie-Tooth disease, Arts syndrome, and prelingual non-syndromic deafness form a disease continuum: evidence from a family with a novel PRPS1 mutation I move, therefore I am: a new theoretical framework to investigate agency and ownership. The cerebellum updates predictions about the visual consequences of one's behavior. The experience of agency: an interplay between prediction and postdiction Ataxia with ophthalmoplegia or sensory neuropathy is frequently caused by POLG mutations. Beyond the comparator model: a multifactorial two-step account of agency Electrodes in the brain--ethical criteria for research and treatment with deep brain stimulation for neuropsychiatric disorders A pan-European study of the C9orf72 repeat associated with FTLD: geographic prevalence, genomic instability, and intermediate repeats AP5Z1/SPG48 frequency in autosomal recessive and sporadic spastic paraplegia Autosomal recessive spastic ataxia of Charlevoix Saguenay (ARSACS): expanding the genetic, clinical and imaging spectrum Spinocerebellar ataxia type 11 (SCA11) is an uncommon cause of dominant ataxia among French and German kindreds. Mutation screen reveals novel variants and expands the phenotypes associated with DYNC1H1. Stimulating personality: ethical criteria for deep brain stimulation in psychiatric patients and for enhancement purposes Evidence for altered transport of insulin across the blood-brain barrier in insulin-resistant humans SIL1 mutations and clinical spectrum in patients with Marinesco-Sjogren syndrome NPC1 is enriched in unexplained early onset ataxia: a targeted high-throughput screening Spinocerebellar ataxia type 36 exists in diverse populations and can be caused by a short hexanucleotide GGCCTG repeat expansion. Screening in ALS and FTD patients reveals 3 novel UBQLN2 mutations outside the PXX domain and a pure FTD phenotype. The CST3 BB Genotype and Low Cystatin C Cerebrospinal Fluid Levels are Associated with Dementia in Lewy Body Disease Sensorimotor recalibration depends on attribution of sensory prediction errors to internal causes

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