ArticleDer Nervenarzt2023
[Parkinson's and Alzheimer's disease as system-wide neurodegenerative disorders].
Article in Der Nervenarzt, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 1 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundParkinson's and Alzheimer's disease (PD/AD) are characterized by cellular pathological changes that precede clinical manifestation and symptom onset by decades (prodromal period) as well as by a heterogeneity of clinical symptoms. Both diseases are recognized as system-wide diseases with organ-transgressing dysregulation and involvement of immunological and neuroinflammatory mechanisms facilitating pathological protein aggregation and neurodegeneration.
objectivesOverview of natural course, phenotypes and classification of PD/AD with a focus on underlying (system-wide) immunological and neuroinflammatory mechanisms.
methodsLiterature research and consideration of expert opinions.
resultsThe accumulation of misfolded proteins such as amyloid‑β and synuclein in the course of neurodegenerative processes forms the basis of the current biological classifications, understanding of course and subtypes. Protein aggregation in PD/AD induces an innate immune response by activating microglia and the release of inflammatory mediators such as cytokines and chemokines and leading to further spread of neurodegeneration and accumulation of intracellular neurofibrillary tangles (NFTs). There is also growing evidence that adaptive immune responses involving auto-antibodies or auto-antigen-specific T‑/B-cell reactions involving tau, amyloid‑β or synuclein might be involved in the disease progression or subtypes of PD/AD.
conclusionsBoth innate and adaptive immune responses seem to be substantially involved in the pathological cascade leading to neurodegeneration in PD/AD and may contribute to disease progression and clinical subtypes. Thus, future targeted interventions should not only focus on protein aggregation but also on neuroinflammatory and immunological mechanisms.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.