Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Keywords: brain ; CELLS ; DENDRITIC CELLS ; ASSOCIATION ; BONE-MARROW ; LYMPHOCYTES ; MOUSE MODEL ; CENTRAL-NERVOUS-SYSTEM ; microglia ; AMYOTROPHIC-LATERAL-SCLEROSIS ; inflammation ; FAS ; BLOOD MONOCYTES ; Parkinson's disease ; CCL2 ; FAS/FASLG
    Abstract: Despite extensive effort on studying inflammatory processes in the CNS of Parkinson's disease (PD) patients, implications of peripheral monocytes are still poorly understood. Here, we set out to obtain a comprehensive picture of circulating myeloid cells in PD patients. We applied a human primary monocyte culture system and flow cytometry-based techniques to determine the state of monocytes from PD patients during disease. We found that the classical monocytes are enriched in the blood of PD patients along with an increase in the monocyte-recruiting chemoattractant protein CCL2. Moreover, we found that monocytes from PD patients display a pathological hyperactivity in response to LPS stimulation that correlates with disease severity. Inflammatory pre-conditioning was also reflected on the transcriptome in PD monocytes using next-generation sequencing. Further, we identified the CD95/CD95L as a key regulator for the PD-associated alteration of circulating monocytes. Pharmacological neutralization of CD95L reverses the dysregulation of monocytic subpopulations in favor of non-classical monocytes. Our results suggest that PD monocytes are in an inflammatory predisposition responding with hyperactivation to a "second hit". These results provide the first direct evidence that circulating human peripheral blood monocytes are altered in terms of their function and composition in PD patients. This study provides insights into monocyte biology in PD and establishes a basis for future studies on peripheral inflammation
    Type of Publication: Journal article published
    PubMed ID: 25284487
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 1433-0407
    Keywords: Schlüsselwörter ALS ; Neurogenetik ; Exzitatorische Aminosäuren ; Cu/Zn-SOD ; Key words Amyotrophic lateral sclerosis ; Neurogenetics ; Excitatory amino acids ; Cu/Zn SOD
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary At presently, the etiology and pathogenesis of amyotrophic lateral sclerosis (ALS) are unknown. In recent years, the genetic background of hereditary motor neuron diseases has been partly defined. In particular, these advances represent an opportunity to improve our understanding of the pathogenesis of the familial and sporadic forms of ALS and thus provide a basis for rational therapeutic approaches. In this article, recent findings on the pathogenesis of the familial form of ALS and their implications for the sporadic form are discussed.
    Notes: Zusammenfassung Die Ätiologie und Pathogenese der amyotrophen Lateralsklerose (ALS) bleibt weitgehend ungeklärt. In den zurückliegenden Jahren sind bei den genetisch bedingten Varianten dieser Erkrankung wichtige Fortschritte bei der Identifizierung ihrer molekularbiologischen Grundlagen gemacht worden. Diese Fortschritte berechtigen zu der Hoffnung, daß es in Zukunft gelingt, die Pathogenese der familiären, aber auch der sporadischen Formen der Erkrankung zu erhellen und damit rationalen Therapieansätzen weiter den Weg zu bereiten. Im Rahmen dieser Übersichtsarbeit soll sowohl auf die vorliegenden Befunde bei der familiären Form der ALS (fALS) als auch auf die mögliche Bedeutung dieser Befunde für pathogenetische Vorstellungen bei der sporadischen Form der ALS (sALS) eingegangen werden.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1432-1459
    Keywords: Key words Amyotrophic lateral sclerosis ; Cu/Zn SOD ; EAAT2 ; AMPA ; Neurolathyrism ; Riluzole
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It is well accepted that excitotoxic mechanisms contribute to the pathogenesis of acute neuronal death in stroke, epilepsy, or brain trauma. It is less widely acknowledged that excitotoxic mechanisms play a role in the pathogenesis of chronic neurological disorders, in particular neurodegenerative diseases. However, evidence is accumulating that this mechanism is indeed part of the pathogenesis of late-onset neurodegenerative diseases. One of the clinical examples may be amyotrophic lateral sclerosis, a disease in which antiexcitotoxic strategies have neuroprotective effects in both, an established animal model and in man. In addition, there is accumulating neuropathological, pathobiochemical and pathophysiological evidence which indicates that excitotoxic mechanisms are part of the pathogenesis of the human disease and consequently part of the mechanisms explaining selective vulnerability (“pathoclisis”) in the human motor system.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...