Evidence map›Paper›PMID 29239314›Full record

ReviewNeural regeneration research2017

Taking out the garbage: cathepsin D and calcineurin in neurodegeneration.

Andreas Aufschnaiter, Verena Kohler, Sabrina Büttner

Open access · goldAbstract readReview
In one paragraph

Review in Neural regeneration research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 38 citations in OpenAlex.

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  8. The Role of VPS35 in the Pathobiology of Parkinson's Disease.Cellular and molecular neurobiology · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 2 countries.

Andreas AufschnaiterInstitute of Molecular Biosciences, University of Graz, Humboldtstraße 50, 8010 Graz, Austria.
Verena KohlerInstitute of Molecular Biosciences, University of Graz, Humboldtstraße 50, 8010 Graz, Austria.
Sabrina BüttnerInstitute of Molecular Biosciences, University of Graz, Humboldtstraße 50, 8010 Graz, Austria; Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Svante Arrheniusväg 20C, 106 91 Stockholm, Sweden.
University of Graz · AT

Funding

Austrian Science Fund FWF P 27183
6 · The paper itself

Abstract

Cellular homeostasis requires a tightly controlled balance between protein synthesis, folding and degradation. Especially long-lived, post-mitotic cells such as neurons depend on an efficient proteostasis system to maintain cellular health over decades. Thus, a functional decline of processes contributing to protein degradation such as autophagy and general lysosomal proteolytic capacity is connected to several age-associated neurodegenerative disorders, including Parkinson's, Alzheimer's and Huntington's diseases. These so called proteinopathies are characterized by the accumulation and misfolding of distinct proteins, subsequently driving cellular demise. We recently linked efficient lysosomal protein breakdown via the protease cathepsin D to the Ca2

Indexed as

cathepsin D, calcineurinendosomal sortinglysosomeneurodegenerationParkinson's diseaseretromeryeastα-synuclein

Identifiers

PMID29239314
PMCPMC5745822
OpenAlexW2769842768

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.