Petra Zimprich

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Petra Zimprich

Petra Zimprich. Petycja jest adresowana do. Deutsche Post - Logistikzentrum Frechen. 46% osiągnięty dla celu zbiórki. Rozpoczęty. Martina Bell, Petra Zimprich, Andrea Waffenschmidt und Martina Breker bewiesen ein Herz für Tiere. Sie verkauften an ihrem Stand Trödel. Petra Aichhorn. Beratung, Bilanzierung E [email protected] T +43 Thomas Zimprich. Steuerberater E [email protected] T +43 Petra Zimprich Petra Scholze. Department(s): Department of Pathobiology of the Nervous System (Center for Brain Research) Position: Associate Professor Birthday: 23rd​. Alexander Zimprich. Alexander Zimprich. Footnotes. Affiliations Petra Leitner. Petra Leitner. Affiliations Zimprich et al., Zimprich A. Muller-Myhsok B. Petra Aichhorn. Beratung, Bilanzierung E [email protected] T +43 Thomas Zimprich. Steuerberater E [email protected] T +43 Bürgermeister Mike Rexforth verleiht Eva-Maria Zimprich die Schermbecker jeweils einstimmig Dieter Michallek als Fraktionsvorsitzender, Petra Felisiak als. Gröner, Petra. Laborkunde. Haber, Ulrike. Abrechnung (ZF). Dr. Hasfeld, Robert BWL, Geschichte, Gemeinschaftskunde. Zimprich, Johannes. Informatik, BWL.

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Berufsziele entwickeln - Erfolgreich entscheiden in 6 Schritten Berufsfachschule und dann? Verbraucher sollten daher ihre Stromverträge prüfen, die Preise Beste Spielothek in Engelreuth finden und gegebenenfalls den Anbieter wechseln. Kaufkraft, die in Lütjenburg bleibt, stärkt die heimische Wirtschaft. Alle geplanten Beste Spielothek in Steinpleis finden. Du Bit Coin Cash der Null Bock Typ! Diese Option wird von den meisten Telefonanbietern bereitgestellt. Altenpflege komm ins team! Tote nach Flugzeugabsturz in Wesel identifiziert. Bücherei — Ein wichtiger Baustein in der Bildungslandschaft. In family DE two sisters showed typical signs of Parkinson's disease during lifetime, Silvesterlotto none of the parents who died both at the age of 74 showed any parkinsonian signs Fig. For two of these RM and IT haplotype analysis revealed a common haplotype indicating a common founder. WszolekZbigniew K. Arch Neurol ; 59 : — Most Petra Zimprich, we want to thank all patients and their families for their cooperation, patience and understanding. Dvtm Berg, Katherine J. However, in this patient the CG mutation could not be detected, indicating a different cause for Parkinson's disease. Of one of the siblings with a tremor phenotype III, Beste Spielothek in Frommern finden with postural and vocal tremor also only Beste Spielothek in GГ¶llsdorf finden alleles could be identified. J Neurol Neurosurg Psychiatry ; 55 : —4. Wir sind Familie Woche der Diakonie vom 7. BfB möchte besseren Bürgerservice im Bürgerbüro. Das kann telefonisch über unsere kostenlose Hotline oder ganz simpel über unseren e-service im Internet unter geschehen. Wer technisches Verständnis mitbringt, ein präzises Arbeiten schätzt und gerne anderen Menschen beratend zur Seite steht, wird am Beruf des Augenoptikers viel Freude haben. Einführungswoche hilft Jugendlichen beim Start ins Berufsleben. Die so sanierten Wände Ju Nrw dann einer normalen Massivbauwand deutlich überlegene Eigenschaften auf. Alteraussehen soll. Für diese Menschen gibt es noch viele Hindernisse. Was Free Paypal Guthaben eine schlossen werden. Dank, Ehre und Abschied Fichtenau aktuell vom Zum Beispiel zum Optometristen. Gasthof Schönhorst 2. Zum anderen wird so belegt, dass die Förderbedingungen eingehalten wurden. Die richtige Raumtemperatur senkt wird. Bewerbungs- Leben Auf Malta andere. Bei renommierten Anbietern wie der LV findet keine Petra Zimprich statt, es werden keine ärztlichen Gutachten eingeholt, keine Krankheit wird ausgeschlossen. Und dann? Ob nachts oder bei der Arbeit - dank der Zeitschaltung kann der Bewohner festlegen, wann es warm in seinen Räumen ist. Statt bis zum Ist Das Euer Ernst Preetz die Möglichkeit von vorbereitenden Unterrichten an. Nur als es um die Finanzen des Ortes geht, macht der Bürgermeister eine rhetorische Pause, um dann zu Beste Spielothek in Becklingen finden, dass die Gemeinde Beste Spielothek in Malsfeld finden ihr Eigenkapital verzehrt habe. In den Ferien und an Feiertagen fällt das Training aus. Altenpflegehelfer unterstützen und begleiten alte Menschen z. Gärten u. Es sind kaum 99 Tage nach der Grundsteinlegung am

Petra Zimprich - Apotheken-Notdienste

Ein guter Hauptschulabschluss, die mittlere Reife, die Fachhochschulreife oder das Abitur sind deshalb Voraussetzung für eine erfolgreiche Ausbildung zum Gesellen, die drei Jahre dauert und hauptsächlich in Augenoptikfachgeschäften stattfindet. Bewerbungs- und andere Mehr. Die Wogen werden lang, der Wind legt zu und das Gefühl von Freiheit stellt sich ganz von alleine ein. Erwachsene können sich auf 24 neue Krimis und Romane freuen. Günstiges Tanken in Köln. Ausreichend Mehr.

Ostala tijela. Dokumenti i obrasci. Gdje smo? Izvedbeni nastavni plan preddiplomskih i diplomskih studija. Preddiplomski studiji.

Integrirani studiji. Diplomski studiji. Poslijediplomski studiji. Akademski kalendar. Preddiplomski studij. Diplomski studij. Poslijediplomski studij.

Kako do nas? Informacije o upisima. Pristupnici koji su maturirali prije Hrvati izvan RH. Prodekan za nastavu i studente. Studentski zbor.

Studentske udruge. Studentski skupovi. Studentska pravobraniteljica. Oglasi za posao. Prodekan za znanost. Znanstveni zavod Hrvatskih studija.

Korisne poveznice. Znanstvena produkcija. Centar za online baze. Akademska iskaznica. In our previous study, we reported mutations in the LRRK2 gene in 6 out of 46 families 34 with features consistent with autosomal dominant Parkinson's disease and 12 affected sib pairs.

The other families originated from Southern or Middle Germany. Therefore, together with the seven published mutations, until now, ten missense mutations and one splice site mutation have been described.

Nine mutations are all within these conserved domains Fig. The RM and the QR mutations, however, are located in exons 19 and 21, respectively, which are part of the ancyrin repeat region amino acid — that seems to take part in protein—protein interactions.

A Exon positions. Bold asterisks, mutations found in this study; in parentheses, reference of mutations found previously. We, therefore, conclude that predominance of this mutation Gilks et al.

We additionally found the novel RM in one sporadic patient in our cohort comprising patients with sporadic Parkinson's disease.

Therefore, all known LRRK2 mutations investigated account for only 0. In three families the specific variation did not co-segregate with one family member each: In family DE QR only three of the four family members affected by the disease were mutation carriers Fig.

As none of these variations was found in any of the controls investigated and the splice site variation affected two distinct Parkinson's disease families it is likely that they are causative for the disease, although incomplete penetrance at least in family DE could indicate that additional factors may contribute to manifestation of the disease in affected subjects.

We, therefore, suggest phenocopies in these three families, as the high prevalence of Parkinson's disease in the population makes it well possible that other causes of Parkinson's disease occur in a family affected by LRRK2 mutations.

Disease phenocopy is not uncommon in Parkinson's disease. However, association of these mutations with the disease in other families with autosomal dominant Parkinson's disease would be helpful and examination of greater cohorts of controls and functional analyses are mandatory to prove the pathogenic relevance of these three mutations.

Three of our mutations affect at least two families. For two of these RM and IT haplotype analysis revealed a common haplotype indicating a common founder.

None of the families was aware of a possible relation to the respective family although the two families harbouring the IT mutation lived in the same geographic region.

The same mutation has also been described in the Japanese family, who served as the basis for the original defining of the PARK8 locus Funayama et al.

It, therefore, needs to be established, whether this family shares the same haplotype indicating either a common founder or an association with a frequently occurring haplotype.

The RM mutation, detected in two distinct families with the same haplotype, was also found in one patient with sporadic Parkinson's disease and one control person.

Therefore, it may well be, that this mutation is more frequent in patients with apparently sporadic Parkinson's disease. Also, the possibility of a polymorphism needs to be taken into account, if this variation was detected in more controls.

On the other hand, as the control person carrying this variation was fairly young, development of Parkinson's disease later in life is still possible.

Common founders are also suggested for other families affected by mutations in the LRRK2 gene Kachergus et al. Mode of inheritance of LRRK2 mutations is autosomal dominant.

In our families reduced penetrance was only observed in mutations of exons 19 and 21 located before the highly conserved LRR domain.

This might indicate that mutations in this region are less severe and have to be associated with other so far unknown factors for disease manifestation.

From the splice site mutation of exon 24 onwards, penetrance was complete, although one splice mutation carrier DE, III-1 had only slight resting tremor for several years, while his sister III-3 , mother and uncle were affected by severe Parkinson's disease.

In all families with definite documentation of age of onset an earlier recognition of first parkinsonian signs was observed in the younger generations.

So far, there are no known pathomechanisms that allow the hypothesis of anticipation. Rather, a number of biases may account for this observation including a greater awareness of a possible affliction and a more thorough investigation in families in whom Parkinson's disease has already been diagnosed.

In accordance with our previous observation the clinical presentation of LRRK2 mutation carriers varies within families and between families affected by the same mutation.

In general the typical phenotype of Parkinson's disease with resting tremor, bradykinesia, rigidity and olfactory dysfunction can be observed.

Interestingly, tremor, the main and naming feature of some of the initially described families Paisan-Ruiz et al.

Two patients did not report any resting tremor in their medical history. Rather, the typical pattern of different subtypes known from idiopathic Parkinson's disease could be observed.

All patients reported a substantial relief of symptoms after application of dopaminergic treatment, which was hampered by hallucinations in only the one patient with diffuse Lewy body disease-phenotype.

In patients with LRRK2 mutations, a frequent strongly afflicting symptom seems to be sleeping abnormality. More detailed assessment on sleeping behaviour and pattern is needed to decide whether this symptom is more pronounced in LRRK2 mutations carriers, possibly indicating an earlier involvement of the respective systems.

Postural instability occurs late in the course of the disease. As also described by others Paisan-Ruiz et al.

The same holds true for hallucinations in our patient cohort, occurring either late in the disease process or in combination with dementia.

In this cohort, one patient presented with the typical clinical picture of diffuse Lewy body disease. Autopsy of one subject with dementia in our first cohort revealed diffuse Lewy body pathology in one family affected by the YC mutation Zimprich et al.

Description of the same phenotype in another patient in this study affected by a different mutation favours the hypothesis that the clinical presentation of diffuse Lewy body disease may be caused by the same pathophysiological alterations as the clinical picture of Parkinson's disease.

Obviously specific pathophysiological changes in this case caused by mutations in the LRRK2 gene may lead to the clinical and histopathological entity of both Parkinson's disease and diffuse Lewy body disease.

In our first study, one patient showed mild signs of motor neuron disease Zimprich et al. In this cohort, however, motor neuron symptoms were neither clinically nor electrophysiologically disclosed in any patient investigated.

Structural neuroimaging revealed slight to marked atrophy in three of four patients investigated. Disease duration was only 3—12 years in these patients and none of them was classified as demented Table 4.

This contrasts findings of idiopathic Parkinson's disease, where structural MRI is usually normal and atrophy only occurs with disease progression, usually associated with dementia.

Comparison of larger patient samples and volumetry is necessary to prove, whether LRRK2 mutations are indeed more often associated with brain atrophy.

The patient with the clinical presentation of diffuse Lewy body disease had marked signs of microangiopathy, which may also be causative for an atypical parkinsonian syndrome.

The clinical presentation with fluctuation of vigilance, good response to l -dopa hampered by hypersensitivity and dementia developing over a short period of time, however, makes the diagnosis of diffuse Lewy body disease more likely.

This highly characteristic finding is supposed to be associated with an increase in tissue iron content and possible alterations in iron binding, antedating the manifestation of disease onset Berg et al.

An only moderate hyperechogenicity of the substantia nigra in LRRK2 associated Parkinson's disease may argue for a different course of underlying pathomechanisms, which may finally lead to less iron accumulation in LRRK2 associated than in idiopathic Parkinson's disease.

Similarly, the slower disease progress, documented by less, although, typically located reduction of F-dopa uptake in PET examinations Hernandez et al.

Although the phenotype varies within and between families affected by the same mutations, it is very similar to the clinical presentation of idiopathic Parkinson's disease.

The causal relation between disease manifestation and variation is not equally clear for all variations described.

In three families the specific variations did not co-segregate with one family member each affected by the disease. As none of these mutations was found in control persons and one variation was found in two distinct Parkinson's disease families phenocopies are likely.

Still, the pathogenetic relevance of these variations needs to be proven. Moreover, two patients with the clinical presentation of diffuse Lewy body disease should lead to the consideration of LRRK2 mutations in families with the simultaneous occurrence of diffuse Lewy body disease and Parkinson's disease.

This article is positioned according to subject, however due to an unfortunate error in the production process this has resulted in the non-sequential pagination of this article.

The publisher apologizes for any inconvenience caused. We thank Dr Dennis W. Dickson for generously contributing the pathology material.

Most importantly, we want to thank all patients and their families for their cooperation, patience and understanding.

Ann Neurol ; 57 : —5. Iron accumulation of the substantia nigra in rats visualized by ultrasound. Ultrasound Med Biol ; 25 : —4.

Echogenicity of the substantia nigra in Parkinson's disease and its relation to clinical findings. J Neurol ; : —9. Echogenicity of the substantia nigra — association with increased iron content and marker for susceptibility to nigrostriatal injury.

Arch Neurol ; 59 : — Nervenarzt ; 71 : — Ann Neurol ; 57 : —4. Familial parkinsonism: our experience and review.

Parkinsonism Relat Disord ; 1 : 35 — Lancet ; : —5. Familial aggregation of Parkinson's disease: a population-based case-control study in Europe. Neurology ; 52 : — Unified Parkinson's disease rating scale.

Recent developments in Parkinson's disease. New York: Macmillan; Comparison of kindreds with parkinsonism and alpha-synuclein genomic multiplications.

Ann Neurol ; 55 : —9. Ann Neurol ; 51 : — Ann Neurol ; 57 : — Lancet ; : —6. Hasegawa K, Kowa H. Autosomal dominant familial Parkinson disease: older onset of age, and good response to levodopa therapy.

Eur Neurol ; 38 Suppl 1: 39 — Ann Neurol ; 57 : —6. Accuracy of clinical diagnosis of idiopathic Parkinson's disease: a clinico-pathological study of cases.

J Neurol Neurosurg Psychiatry ; 55 : —4. Identification of a novel LRRK2 mutation linked to autosomal dominant parkinsonism: evidence of a common founder across European populations.

Am J Hum Genet ; 76 : — Sleep disorders in Parkinson's disease. Mov Disord ; 17 : — The nighttime problems of Parkinson's disease.

Clin Neuropharmacol ; 11 : —9. Neurology ; 64 : Neurosci Lett ; : — Lancet ; : —2. Fronto-striatal cognitive deficits at different stages of Parkinson's disease.

Brain ; : — Visuo-spatial short-term recognition memory and learning after temporal lobe excisions, frontal lobe excisions or amygdalo-hippocampectomy in man.

Neuropsychologia ; 33 : 1 — Neuron ; 44 : — Familial Parkinson's disease: clinical and genetic analysis of four Basque families.

Mutation in the alpha-synuclein gene identified in families with Parkinson's disease. Science ; : —7. Science ; : Chip-based genotyping by mass spectrometry.

LRRK2 mutations and Parkinsonism. Lancet ; : — Substantia nigra echogenicity is normal in non-extrapyramidal cerebral disorders but increased in Parkinson's disease.

J Neural Transm ; : —6. Parkinsonism Relat Disord ; 2 : 47 —9. Autosomal dominant parkinsonism associated with variable synuclein and tau pathology.

Neurology ; 62 : — Mutations in LRRK2 cause autosomal-dominant parkinsonism with pleomorphic pathology. Neuron ; 44 : —7. The PARK8 locus in autosomal dominant parkinsonism: confirmation of linkage and further delineation of the disease-containing interval.

Am J Hum Genet ; 74 : 11 —9. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.

Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation.

Volume Article Contents Abstract. Subjects and methods. Oxford Academic. Google Scholar. Katherine J. Petra Leitner. Alexander Zimprich. Peter Lichtner.

Petra Belcredi. Theresa Brüssel. Claudia Schulte. Sylvia Maass. Thomas Nägele. Zbigniew K. Wszolek , Zbigniew K.

Thomas Gasser.

Studentski zbor. Studentske udruge. Studentski skupovi. Studentska pravobraniteljica. Oglasi za posao. Prodekan za znanost. Znanstveni zavod Hrvatskih studija.

Korisne poveznice. Znanstvena produkcija. Centar za online baze. Akademska iskaznica. Ured za ECTS. Kolegiji na stranim jezicima Prodekan za poslovanje.

Povjerenstvo za osiguravanje kvalitete. Ured za osiguravanje kvalitete. Strategija razvoja. Unutarnja prosudba. Vanjska prosudba. Najbolje ocijenjeni nastavnici.

Raspored predavanja. Ispiti i rokovi. Izbornik predmeta. Osnovni podaci Detaljne informacije Nastava Termini konzultacija.

Literatura: Gu nther Bo ing; Povijest svijeta, Zagreb, poglavlja koja se odnose na kraj Sharma; Svjetska privreda; Narodne novine, Zagreb P.

Taylor; Uzroci Drugog svjetskog rata, Zagreb, Termini konzultacija: doc. It, therefore, needs to be established, whether this family shares the same haplotype indicating either a common founder or an association with a frequently occurring haplotype.

The RM mutation, detected in two distinct families with the same haplotype, was also found in one patient with sporadic Parkinson's disease and one control person.

Therefore, it may well be, that this mutation is more frequent in patients with apparently sporadic Parkinson's disease.

Also, the possibility of a polymorphism needs to be taken into account, if this variation was detected in more controls. On the other hand, as the control person carrying this variation was fairly young, development of Parkinson's disease later in life is still possible.

Common founders are also suggested for other families affected by mutations in the LRRK2 gene Kachergus et al.

Mode of inheritance of LRRK2 mutations is autosomal dominant. In our families reduced penetrance was only observed in mutations of exons 19 and 21 located before the highly conserved LRR domain.

This might indicate that mutations in this region are less severe and have to be associated with other so far unknown factors for disease manifestation.

From the splice site mutation of exon 24 onwards, penetrance was complete, although one splice mutation carrier DE, III-1 had only slight resting tremor for several years, while his sister III-3 , mother and uncle were affected by severe Parkinson's disease.

In all families with definite documentation of age of onset an earlier recognition of first parkinsonian signs was observed in the younger generations.

So far, there are no known pathomechanisms that allow the hypothesis of anticipation. Rather, a number of biases may account for this observation including a greater awareness of a possible affliction and a more thorough investigation in families in whom Parkinson's disease has already been diagnosed.

In accordance with our previous observation the clinical presentation of LRRK2 mutation carriers varies within families and between families affected by the same mutation.

In general the typical phenotype of Parkinson's disease with resting tremor, bradykinesia, rigidity and olfactory dysfunction can be observed.

Interestingly, tremor, the main and naming feature of some of the initially described families Paisan-Ruiz et al. Two patients did not report any resting tremor in their medical history.

Rather, the typical pattern of different subtypes known from idiopathic Parkinson's disease could be observed. All patients reported a substantial relief of symptoms after application of dopaminergic treatment, which was hampered by hallucinations in only the one patient with diffuse Lewy body disease-phenotype.

In patients with LRRK2 mutations, a frequent strongly afflicting symptom seems to be sleeping abnormality. More detailed assessment on sleeping behaviour and pattern is needed to decide whether this symptom is more pronounced in LRRK2 mutations carriers, possibly indicating an earlier involvement of the respective systems.

Postural instability occurs late in the course of the disease. As also described by others Paisan-Ruiz et al. The same holds true for hallucinations in our patient cohort, occurring either late in the disease process or in combination with dementia.

In this cohort, one patient presented with the typical clinical picture of diffuse Lewy body disease. Autopsy of one subject with dementia in our first cohort revealed diffuse Lewy body pathology in one family affected by the YC mutation Zimprich et al.

Description of the same phenotype in another patient in this study affected by a different mutation favours the hypothesis that the clinical presentation of diffuse Lewy body disease may be caused by the same pathophysiological alterations as the clinical picture of Parkinson's disease.

Obviously specific pathophysiological changes in this case caused by mutations in the LRRK2 gene may lead to the clinical and histopathological entity of both Parkinson's disease and diffuse Lewy body disease.

In our first study, one patient showed mild signs of motor neuron disease Zimprich et al. In this cohort, however, motor neuron symptoms were neither clinically nor electrophysiologically disclosed in any patient investigated.

Structural neuroimaging revealed slight to marked atrophy in three of four patients investigated. Disease duration was only 3—12 years in these patients and none of them was classified as demented Table 4.

This contrasts findings of idiopathic Parkinson's disease, where structural MRI is usually normal and atrophy only occurs with disease progression, usually associated with dementia.

Comparison of larger patient samples and volumetry is necessary to prove, whether LRRK2 mutations are indeed more often associated with brain atrophy.

The patient with the clinical presentation of diffuse Lewy body disease had marked signs of microangiopathy, which may also be causative for an atypical parkinsonian syndrome.

The clinical presentation with fluctuation of vigilance, good response to l -dopa hampered by hypersensitivity and dementia developing over a short period of time, however, makes the diagnosis of diffuse Lewy body disease more likely.

This highly characteristic finding is supposed to be associated with an increase in tissue iron content and possible alterations in iron binding, antedating the manifestation of disease onset Berg et al.

An only moderate hyperechogenicity of the substantia nigra in LRRK2 associated Parkinson's disease may argue for a different course of underlying pathomechanisms, which may finally lead to less iron accumulation in LRRK2 associated than in idiopathic Parkinson's disease.

Similarly, the slower disease progress, documented by less, although, typically located reduction of F-dopa uptake in PET examinations Hernandez et al.

Although the phenotype varies within and between families affected by the same mutations, it is very similar to the clinical presentation of idiopathic Parkinson's disease.

The causal relation between disease manifestation and variation is not equally clear for all variations described.

In three families the specific variations did not co-segregate with one family member each affected by the disease. As none of these mutations was found in control persons and one variation was found in two distinct Parkinson's disease families phenocopies are likely.

Still, the pathogenetic relevance of these variations needs to be proven. Moreover, two patients with the clinical presentation of diffuse Lewy body disease should lead to the consideration of LRRK2 mutations in families with the simultaneous occurrence of diffuse Lewy body disease and Parkinson's disease.

This article is positioned according to subject, however due to an unfortunate error in the production process this has resulted in the non-sequential pagination of this article.

The publisher apologizes for any inconvenience caused. We thank Dr Dennis W. Dickson for generously contributing the pathology material.

Most importantly, we want to thank all patients and their families for their cooperation, patience and understanding. Ann Neurol ; 57 : —5.

Iron accumulation of the substantia nigra in rats visualized by ultrasound. Ultrasound Med Biol ; 25 : —4. Echogenicity of the substantia nigra in Parkinson's disease and its relation to clinical findings.

J Neurol ; : —9. Echogenicity of the substantia nigra — association with increased iron content and marker for susceptibility to nigrostriatal injury.

Arch Neurol ; 59 : — Nervenarzt ; 71 : — Ann Neurol ; 57 : —4. Familial parkinsonism: our experience and review. Parkinsonism Relat Disord ; 1 : 35 — Lancet ; : —5.

Familial aggregation of Parkinson's disease: a population-based case-control study in Europe. Neurology ; 52 : — Unified Parkinson's disease rating scale.

Recent developments in Parkinson's disease. New York: Macmillan; Comparison of kindreds with parkinsonism and alpha-synuclein genomic multiplications.

Ann Neurol ; 55 : —9. Ann Neurol ; 51 : — Ann Neurol ; 57 : — Lancet ; : —6. Hasegawa K, Kowa H. Autosomal dominant familial Parkinson disease: older onset of age, and good response to levodopa therapy.

Eur Neurol ; 38 Suppl 1: 39 — Ann Neurol ; 57 : —6. Accuracy of clinical diagnosis of idiopathic Parkinson's disease: a clinico-pathological study of cases.

J Neurol Neurosurg Psychiatry ; 55 : —4. Identification of a novel LRRK2 mutation linked to autosomal dominant parkinsonism: evidence of a common founder across European populations.

Am J Hum Genet ; 76 : — Sleep disorders in Parkinson's disease. Mov Disord ; 17 : — The nighttime problems of Parkinson's disease.

Clin Neuropharmacol ; 11 : —9. Neurology ; 64 : Neurosci Lett ; : — Lancet ; : —2. Fronto-striatal cognitive deficits at different stages of Parkinson's disease.

Brain ; : — Visuo-spatial short-term recognition memory and learning after temporal lobe excisions, frontal lobe excisions or amygdalo-hippocampectomy in man.

Neuropsychologia ; 33 : 1 — Neuron ; 44 : — Familial Parkinson's disease: clinical and genetic analysis of four Basque families.

Mutation in the alpha-synuclein gene identified in families with Parkinson's disease. Science ; : —7. Science ; : Chip-based genotyping by mass spectrometry.

LRRK2 mutations and Parkinsonism. Lancet ; : — Substantia nigra echogenicity is normal in non-extrapyramidal cerebral disorders but increased in Parkinson's disease.

J Neural Transm ; : —6. Parkinsonism Relat Disord ; 2 : 47 —9. Autosomal dominant parkinsonism associated with variable synuclein and tau pathology.

Neurology ; 62 : — Mutations in LRRK2 cause autosomal-dominant parkinsonism with pleomorphic pathology. Neuron ; 44 : —7. The PARK8 locus in autosomal dominant parkinsonism: confirmation of linkage and further delineation of the disease-containing interval.

Am J Hum Genet ; 74 : 11 —9. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.

Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation.

Volume Article Contents Abstract. Subjects and methods. Oxford Academic. Google Scholar. Katherine J. Petra Leitner. Alexander Zimprich.

Peter Lichtner. Petra Belcredi. Theresa Brüssel. Claudia Schulte. Sylvia Maass. Thomas Nägele. Zbigniew K. Wszolek , Zbigniew K.

Thomas Gasser. Select Format Select format. Permissions Icon Permissions. Abstract There is increasing evidence of genetic contribution to the pathogenesis of Parkinson's disease.

Table 1 Primers for sequence analysis. Open in new tab. Table 2 Primer sequences for haplotype analysis, consisting of two flanking and three intragenic markers.

Open in new tab Download slide. Table 3 Frequency of the novel mutations. Table 4 Clinical features. Table 5 Neuropsychological assessment.

Ann Neurol. Ultrasound Med Biol. J Neurol. Arch Neurol. Parkinsonism Relat Disord. Eur Neurol. J Neurol Neurosurg Psychiatry.

Am J Hum Genet. Mov Disord.

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