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News and literature on Leukodystrophy! For more information on Leukodystophy visit <a href="http://www.ELAEV.de" rel="nofollow">www.ELAEV.de</a>
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Seltene Krankheiten: Niemann-Pick: Wenn Kinder Symptome zeigen wie Greise - Seltene Krankheiten

Seltene Krankheiten: Niemann-Pick: Wenn Kinder Symptome zeigen wie Greise - Seltene Krankheiten | Leukodystrophy | Scoop.it
Betroffene verlernen zu gehen und können irgendwann nicht mehr sprechen: Niemann-Pick ist eine seltene Krankheit, die Menschen wie im Alter frühzeitig verlernen und vergessen lässt. Eine Mutter berichtet über den langen Weg bis zur Diagnose ihrer Tochter.
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Metachromatic Leukodystrophy | Real Heroes Don't Wear Capes

Metachromatic Leukodystrophy | Real Heroes Don't Wear Capes | Leukodystrophy | Scoop.it
Posts about Metachromatic Leukodystrophy written by Erin Ramsay
leukodystrophy blog's insight:

Diese dieser Videoserie erzählt die australische Familie Windeyer vom Leiden ihre beiden Jungs, v.a. von ihrem sechsjähriger Sohn Mason bei dem Metachromatic Leukodystrophie diagnostiziert wurde

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The leukodystrophies

Leukodystrophies are a group of genetically determined disorders that affect development or maintenance of central nervous system myelin. Leukodystrophies have a reported incidence of 1 in 7500 live births, but fewer than half of patients receive a specific diagnosis. In this review, the authors discuss types of leukodystrophies: their prevalence, clinical presentation, symptoms, and diagnosis, as well as current and future treatments. Diagnosis is based on a combination of history, exam, radiological, and laboratory findings, including genetic testing. Leukodystrophies can present at any age from infancy to adulthood, with variability in disease progression and clinical presentation, ranging from developmental delay to seizures to spasticity. Although there are few cures, there are significant opportunities for care and improvements in patient well-being. Their high prevalence, combined with rapid advances in imaging, genetics, and potential treatments, makes an understanding of the leukodystrophies necessary for care providers in genetics and neurology.

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The Children's Hospital of Philadelphia to Launch Leukodystrophy Center of Excellence for Children with Degenerative Inherited White Matter Diseases

...CHOP's Leukodystrophy Center of Excellence is a diagnostic, clinical care, and research initiative launched in response to legislation in Pennsylvania and New Jersey that has added Krabbe and 5 other related diseases in Pennsylvania, and four others in New Jersey, to the newborn screening panel. This will result in an increase of patients requiring specialized and integrated clinical care.  CHOP's new leukodystrophy initiative was established to support the needs of these families. ...

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The difficulty in diagnosing X linked adrenoleucodystrophy and the importance of identifying cerebral involvement

Two patients are described, a mother and son, who were initially clinically diagnosed with hereditary spastic paraparesis. This was rectified after very long chain fatty acid testing confirmed adrenomyeloneuropathy (AMN). The son's initial symptoms were characteristic of AMN (the commonest phenotype) but progressed to show symptoms of cerebral involvement. This evolution from non-cerebral to cerebral AMN is recognised in the medical literature and is increasingly important to consider in light of the availability of potential treatments such as haematopoietic stem cell transplantation.

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Krabbe Leukodystrophy (Before & After): Judson

Visit http://JudsonsLegacy.org to learn more about Judson and Krabbe disease and consider partnering with Judson's Legacy, a 501(c)3 nonprofit charity, to he...
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„Lili löst sich auf“

„Lili löst sich auf“ | Leukodystrophy | Scoop.it
„Lili löst sich auf“ - Stellen Sie sich einmal vor, Sie wünschen sich sehnlichst ein Kind und werden schwanger. Mit Freude und Dankbarkeit  über die Geburt und jeden einzelnen Tag beobachten Sie, wie es wächst, lernt und Stück für Stück mehr am Leben teilnimmt. Doch plötzlich entwickelt sich Ihr Kind nicht weiter. Die Geschichte von Lili.
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Drug-based modulation of endogenous stem cells promotes functional remyelination in vivo

Drug-based modulation of endogenous stem cells promotes functional remyelination in vivo | Leukodystrophy | Scoop.it

.... To discover therapeutic compounds for enhancing myelination from endogenous oligodendrocyte progenitor cells, we screened a library of bioactive small molecules on mouse pluripotent epiblast stem-cell-derived oligodendrocyte progenitor cells. Here we show seven drugs function at nanomolar doses selectively to enhance the generation of mature oligodendrocytes from progenitor cells in vitro. Two drugs, miconazole and clobetasol, are effective in promoting precocious myelination in organotypic cerebellar slice cultures, and in vivo in early postnatal mouse pups. Systemic delivery of each of the two drugs significantly increases the number of new oligodendrocytes and enhances remyelination in a lysolecithin-induced mouse model of focal demyelination.....

leukodystrophy blog's insight:

Ideas to initiate remyelination is an important need not only for treatment of multiple sclerosis, but also for any kind of Leukodystrophy. One way may be to induce the differentiation of progenitor cells into oligodendrocytes, a cell type which is getting lost in most of the Leukodystrophy diseases.

In this article two medicament candidates have been identified which induce the differentiation of precursor cells into oligodentrocytes. This could be show in mice models as well as in human cell cultures. Also these compounds increase myelination speed during early myelination. The next steps would be either the identification of optimized compounds or the examination of these compounds within a first study.

 

Wege um Remyelinisierung anzuregen sind nicht nur dringend für die Behandlung von MS erforderlich, sondern auch zwingend für die Behandlung von Leukodystrophien. Ein Weg ist sicherlich die Differenzierung von Vorläuferzellen in Oligodendrozyten anzuregen, ein Zelltyp der bei den meisten Leukodystrophien betroffen ist.

In diesem Artikel in der Zeitschrift Nature wurden zwei Wirkstoffe identifiziert die genau das können sollen. Beides zugelassene Medikamente mit einer „safe use“ Geschichte für die Behandlung anderer Erkrankungen. Beide können die Blut-Hirnschranke überschreiten. Gezeigt wurde eine schnellere Myelinisierung in der frühen Entwicklung, oder verbesserte Myelinisierung bei induzierten Schädigungen.  Allerdings basieren diese Ergebnisse auf Mausmodellen und auf menschlichen Zellkulturen. Das Potential in einer echten Studie zu testen steht noch aus. Dennoch ist das aktuelle Ergebnis möglicherweise ein Durchbruch für eine Reihe von Erkrankungen.

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Hematopoietic SCT: a useful treatment for late metachromatic leukodystrophy

Hematopoietic SCT: a useful treatment for late metachromatic leukodystrophy | Leukodystrophy | Scoop.it

In metachromatic leukodystrophy (MLD), the deficiency of the lysosomal enzyme arylsulfatase A (ARSA) leads to demyelination in the central and peripheral nervous system and ultimately to death. Allogeneic hematopoietic SCT (HSCT) is currently the only treatment for adult and late-onset juvenile MLD, although it is still in question because of insufficient follow-up. We wanted to determine whether HSCT could halt the progression of adult and late-onset juvenile MLD. Four treated unrelated patients and three untreated siblings were included in the study, and followed regularly for up to 18 years after transplantation. The patients were assessed from clinical examination, ARSA enzyme levels, magnetic resonance imaging of the brain and neuropsychological and neurophysiological tests. In the treated patients, ARSA levels were normal up to 18 years after transplantation. The parameters evaluated stabilized and remained stable after a latency period of 12–24 months. Two patients live normal lives, partially in a protected environment. The other two patients stabilized at a low cognitive and functional level. One of the controls is demented, one is in a vegetative state and one died. We conclude that, in comparison with their untreated siblings, HSCT halted the progression of the disease in our treated patients.

leukodystrophy blog's insight:

Nach einer Transplantation von Blutstammzellen können diese im Körper wandern und die Bluthirnschranke überwinden. Im Gehirn angelangt differenzieren sie sich zu Microglia und können so die Körpereigenen Micro-Glia ersetzen und Arylsulfatase A produzieren.

Diese Studie bewertet den Erfolg der Transplantation von Hämatopoetischen Stammzellen (Blutstammzellen) anhand von 4 Patienten mit adult onset MLD sowie 3 Geschwisterkinden die keine Stammzelltransplantation erhalten haben. Die Patienten wurden bis bis zu 18 Jahren nach der Transplantation anhand von Klinischen Untersuchungen, MRT, ARSA Enzymspiegel und neurophysiologischen Tests bewertet. Leider fehlen manche quantitative Analysen bei den Kontrollpatienten, dennoch ist das Ergebnis für diese Patientengruppe eindeutig. Bei Patienten bei denen Stammzellen transplantiert wurden stabilisierte sich der Zustand und alle vier leben ein selbstbestimmtes Leben, auch wenn alle auf intensive Hilfe angewiesen sind. Bei den Geschwisterkindern ohne Stammzelltransplantation erfolgte eine dramatische Verschlechterung des Zustandes.

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What the Doctor Didn’t Say Out Loud Meant So Much to Me

What the Doctor Didn’t Say Out Loud Meant So Much to Me | Leukodystrophy | Scoop.it

We spent most of Good Friday in the ER, the first time we have needed a trip there since October. Eden had some scary symptoms during the week, and we needed to see if they were a part of the “normal” disease progression or an infection that would require antibiotics.

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Anyway.....Life Goes On

Anyway.....Life Goes On | Leukodystrophy | Scoop.it

I live across the street from a really great family. From looking out the window and into their world, they have it seems, everything I hoped our family life would be. In the sense that they have what is considered in our era a "large" family, (something I have wanted & tried to achieve) all the children are living and growing up together. They are always busy doing much of the stuff in life I thought that our family would be doing...

leukodystrophy blog's insight:

Dieser Bericht auf “MLD has a face” beschreibt welche Herausforderungen das Leben mit Leukodystrophien mit sich bringen kann. Und dennoch meistert diese Familie mit mehreren gesunden und mehreren kranken Kindern ihren Weg. So traurig sich dieser Bericht liest, es zeigt am Ende doch dass man nicht allein mit diesem Schicksal ist.

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Progesterone antagonist therapy in a Pelizaeus-Merzbacher Mouse Model

Progesterone antagonist therapy in a Pelizaeus-Merzbacher Mouse Model | Leukodystrophy | Scoop.it

Pelizaeus-Merzbacher disease (PMD) is a severe hypomyelinating disease, characterized by ataxia, intellectual disability, epilepsy, and

premature death. In the majority of cases, PMD is caused by duplication of PLP1 that is expressed in myelinating oligodendrocytes. Despite detailed knowledge of PLP1, there is presently no curative therapy for PMD. We used a Plp1 transgenic PMD mouse model to test the therapeutic effect of Lonaprisan, an antagonist of the nuclear progesterone receptor, in lowering Plp1 mRNA overexpression.

We applied placebo-controlled Lonaprisan therapy to PMD mice for 10 weeks and performed the grid slip analysis to assess the clinical

phenotype. Additionally, mRNA expression and protein accumulation as well as histological analysis of the central nervous system were

performed. Although Plp1 mRNA levels are increased 1.8-fold in PMD mice compared to wild-type controls, daily Lonaprisan treatment

reduced overexpression at the RNA level to about 1.5-fold, which was sufficient to significantly improve the poor motor phenotype. Electron

microscopy confirmed a 25% increase in the number of myelinated axons in the corticospinal tract when compared to untreated

PMD mice. Microarray analysis revealed the upregulation of proapoptotic genes in PMD mice that could be partially rescued by Lonaprisan

treatment, which also reduced microgliosis, astrogliosis, and lymphocyte infiltration.

leukodystrophy blog's insight:

Der genaue Mechanismus durch den PMD in Patienten mit PLP1 Duplikation ausgelöst wird ist nicht völlig geklärt. Ursächlich ist aber offenbar die verstärkte Produktion des PLP1 Proteins verantwortlich. In dieser Publikation wird versucht am Mausmodel die Produktion vom PLP1 durch ein Krebsmedikament (Lonaprisan) zu drosseln. Dies gelingt t.w. was in einer verbesserten Myeliniesierung resultiert. Darüber hinaus findet man Hinweise, dass das Absterben von Zellen im Verlaufe der Krankheit zurückgeht.

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Combined gene/cell therapies provide long-term and pervasive rescue of multiple pathological symptoms in a murine model of globoid cell leukodystrophy

Combined gene/cell therapies provide long-term and pervasive rescue of multiple pathological symptoms in a murine model of globoid cell leukodystrophy | Leukodystrophy | Scoop.it

Globoid cell leukodystrophy (GLD) is a lysosomal storage disease caused by deficient activity of β-galactocerebrosidase (GALC). The infantile forms manifest with rapid and progressive central and peripheral demyelination, which represent a major hurdle for any treatment approach. We demonstrate here that neonatal lentiviral (LV)-mediated intracerebral gene therapy (IC GT) or transplantation (T) of GALC-overexpressing neural stem cells (NSC) synergize with bone marrow transplant (BMT) providing dramatic extension of lifespan and global clinical-pathological rescue in a relevant GLD murine model. We show that timely and long-lasting delivery of functional GALC in affected tissues ensured by the exclusive complementary mode of action of the treatments underlies the outstanding benefit. In particular, the ontribution of NSCT and IC GT during the early asymptomatic stage of the disease is instrumental to enhance long-term advantage upon BMT. We clarify the input of CNS, PNS and periphery to the disease, and the relative contribution of treatments to the final therapeutic outcome, with important implications for treatment strategies to be tried in human patients. This study gives proof-of-concept of efficacy, tolerability, and clinical relevance of the combined gene/cell therapies proposed here, which may constitute a feasible and effective therapeutic opportunity for children affected by GLD.

leukodystrophy blog's insight:

Maybe nothing completely new and “only” in the mouse model, but still this publication demonstrates that only the combination of several state of the art treatment approaches may lead to significant symptom reduction for GLD.

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Seltene Krankheiten: "Papa, hast du schon eine Medizin gefunden?"

Seltene Krankheiten: "Papa, hast du schon eine Medizin gefunden?" | Leukodystrophy | Scoop.it
Die Krankheit seines Sohnes ist selten, Therapien sind nicht in Sicht. Um sein Kind dennoch zu retten, nimmt ein Vater die medizinische Forschung selbst in die Hand.
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Patient/family views on data sharing in rare diseases: study in the European LeukoTreat project

The purpose of this study was to explore patient and family views on the sharing of their medical data in the context of compiling a European leukodystrophies database. A survey questionnaire was delivered with help from referral centers and the European Leukodystrophies Association, and the questionnaires returned were both quantitatively and qualitatively analyzed. This study found that patients/families were strongly in favor of participating. Patients/families hold great hope and trust in the development of this type of research. They have a strong need for information and transparency on database governance, the conditions framing access to data, all research conducted, partnerships with the pharmaceutical industry, and they also need access to results. Our findings bring ethics-driven arguments for a process combining initial broad consent with ongoing information. On both, we propose key item-deliverables to database participants

leukodystrophy blog's insight:

Diese Studie die im Rahmen die in Zusammenarbeit mit ELA erstellt wurde zeigt, dass Patienten / Familien sehr große Hoffnung und Vertrauen in die Entwicklung von medizinischen Datenbanken setzen. Sie haben ein starkes Bedürfnis nach Information und Transparenz über Datenbankführung.

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Metachromatic leukodystrophy: Disease spectrum and approaches for treatment

This review discusses diagnostic process and efficacy of current and possible future therapies such as hematopoietic stem cell transplantation, enzyme replacement therapy and gene therapy. A systematic evaluation regarding the efficacy of hematopoietic stem cell transplantation and a longer follow up period for gene therapy are needed to come to a general conclusion and improve treatment options for metachromatic leukodystrophy.

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Leukodystrophy Center | The Children's Hospital of Philadelphia

The Leukodystrophy Center at CHOP is dedicated to providing clinical care, diagnostic testing and advanced treatments to infants, children and adolescents with inherited white matter diseases. 
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Emerging Treatments for Pediatric Leukodystrophies

leukodystrophy blog's insight:

The leukodystrophies are a heterogeneous group of inherited disorders with broad clinical manifestations and variable pathologic mechanisms. Improved diagnostic methods have allowed identification of the underlying cause of these diseases, facilitating identification of their pathologic mechanisms. Clinicians are now able to prioritize treatment strategies and advance research in therapies for specific disorders. Although only a few of these disorders have well-established treatments or therapies, a number are on the verge of clinical trials. As investigators are able to shift care from symptomatic management of disorders to targeted therapeutics, the unmet therapeutic needs could be reduced for these patients.

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La historia de mi vida

Cortometraje sobre Alejandro, un niño de 5 años afectado por una enfermedad rara que es un tipo de leucodistrofia llamada Pelizaeus Merzbacher. Una enfermeda...
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Breakthrough in understanding Canavan disease

Breakthrough in understanding Canavan disease | Leukodystrophy | Scoop.it
Investigators have settled a long-standing controversy surrounding the molecular basis of an inherited disorder that historically affected Ashkenazi Jews from Eastern Europe but now also arises in other populations of Semitic descent, particularly families from Saudi Arabia. Canavan disease is a type of leukodystrophy that is an incurable and progressively fatal neurological condition.
leukodystrophy blog's insight:

Zwar ist seit langem bekannt, dass Canavan disease durch eine Mutation in dem Gen für die Aspartoacylase (ASPA) verursacht wird, aber wie dies zum Entstehen der Krankheit führt warunklar. Das Enzym ASPA spaltet N-acetylaspartate (NAA) zu Acetate und  Aspartat, welche entsprechen im falle eines Gendefektes Nervensystem fehlen.In einer kürzlich erschienen Publikation wurde klar gezeigt, dass es nicht ein Fehlen des Aspertat ist, das zur Entstehung der Krankheit führt, sondern ein „zu viel“ an NAA. Diese Erkenntnis hat einen entsprechend großen Einfluss auf Behandlungsversuche von Canavans disease, denn die Acetat Behandlung muss demnach ins leer laufen. Anstatt sollte der NAA Spiegel gesenkt werden

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MLC1 protein: a likely link between leukodystrophies and brain channelopathies

MLC1 protein: a likely link between leukodystrophies and brain channelopathies | Leukodystrophy | Scoop.it

....Leukodystrophies comprise a large number of rare genetic disorders that affect mainly the CNS with different etiology and a common target. The European Leukodystrophies Association (ELA) offers a classification including the following types: peroxisomal, lysosomal, vacuolating, hypomyelinating, atypical, undetermined. Against such a heterogeneous etiopathogenesis, the common target is myelin: “either the myelin does not form, degrades, or is too abundant” (from the official ELA site: http://ela-asso.com).

Leukodystrophies have an incidence of 1 in 7,663 live births (Bonkowsky et al., 2010) and manifest themselves mostly during childhood or adolescence....

leukodystrophy blog's insight:

Mutationen in dem Gen MLC1 führen zu Megalencephalic leukoencephalopathy einer rezessive vererbten Leukodystrophie die im Kindesalter auftritt. Dieser Artikel versucht der Funktion von MLC1 auf den Grund zu gehen. Dabei werden Überschneidungen zwischen Leukodystrophien und Ionenkanalkrankheiten sichtbar. Diese Forschung wurde von ELA unterstützt.

Mutations within the gene MLC1 lead to Megalencephalic leukoencephalopathy an adult onset leukodystrophy. This article tries to shed light on the MLC1 function and demonstrates a interesting overlap between leukodystrophies and channelopathies. This research was funded by ELA.

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X-linked adrenoleukodystrophy: pathogenesis and treatment

X-linked adrenoleukodystrophy: pathogenesis and treatment | Leukodystrophy | Scoop.it

X-linked adrenoleukodystrophy (X-ALD) is a puzzling inborn error of metabolism with a strikingly heterogeneous clinical spectrum. All patients have mutations in the ABCD1 gene and accumulate very long chain fatty acids in all tissues. Virtually all male X-ALD patients develop adrenocortical insufficiency in childhood and progressive myelopathy and peripheral neuropathy in adulthood. A subset of male patients, however, develops a fatal cerebral demyelinating disease, cerebral adrenoleukodystrophy. Female patients also develop progressive myelopathy and peripheral neuropathy, but generally at a later age than males. They only very rarely develop adrenocortical insufficiency or cerebral adrenoleukodystrophy. This review proposes to simplify the classification of the clinical spectrum of X-ALD and reviews the largely unresolved pathophysiological mechanisms and the current treatment options.

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Mixed emotions in Paris – Fighting against leukodystrophy

As always, the annual ELA family get-together in Paris on 27, 28 and 29 March 2015, combined with the AGM and medical researchers meeting on the different leukodystrophies sent our emotions in all directions.

For some of the families that we have become friends with over the years, there’s always a few heartbreaking moments when we reunite with those who have lost a child since we last met 12 months previous. There’s so little that can be said that can make any difference. We can only embrace and cry.

Then there’s the jarring contrast of emotions when Matt and I sat in the medical researchers meeting where we both felt a re-ignition of hope, a feeling that we thought had long been extinquished.

We were given details of the first ever medical trial that may be able to treat Joseph’s illness; Aicardi Goutieres Syndrome (AGS). This trial will be held in either late summer or early autumn. We listened intently, we asked lots of questions and we came away from the weekend feeling a mix of excitement, fear, anxiety, hope, admiration for ELA for their funding (and every person who has ever donated to ELA) and awe for the incredible work of Professor Yanick Crow who has tirelessly worked on AGS over the past 18 years and who will be leading the trial at the Necker Clinic in Paris, the first paediatric hospital in the world.

This is more than we could ever have imagined or dreamed of when we started fundraising for ELA in 2008. This is such a major step forward for the future of AGS. A door of possibility has been opened, one that must stay open until we can finally close the door on this horrible illness.

We’ll be putting Joseph forward for the trial but he has to meet certain criteria before being accepted. Once we have all the details formalised we’ll give a more in-depth account of the clinical trial.

During the weekend, Professor Crow chatted and played with Sophie – another emotion thrown into the mix, one of gratitude and respect. It is thanks to the work of Professor Crow that Sophie exists.

Just as we were about to leave the hotel I turned and looked at Joseph as he rested his head on an ELA balloon, in French written on the balloon was: ‘ELA Espoir est la’ (ELA, hope is there). It certainly is.

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Research Update: News from ELA conference

Research Update: News from ELA conference | Leukodystrophy | Scoop.it
Sara and Karen travelled to Paris this weekend to attend the ELA conference and families meeting.   Important updates for our services users are as follows: Patrick Aubourg reported on the MD-1003 study in France, Germany and Spain. MD-1003 is essentially a high dose of biotin, a vitamin of the B complex which is involved in more…
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ELA Meeting recap

ELA Meeting recap | Leukodystrophy | Scoop.it

I just attended the annual ELA meeting in Paris. General Assembly The General Assembly was somewhat stormy as ELA announced...

leukodystrophy blog's insight:

Sehr guter kurzer Bericht von ELA treffen in Paris

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