Evidence map›Paper›PMID 27421577›Full record

ReviewAgeing research reviews2016

The endocytic pathway in microglia during health, aging and Alzheimer's disease.

Santiago Solé-Domènech, Dana L Cruz, Estibaliz Capetillo-Zarate, Frederick R Maxfield

Open access · greenAbstract readReview
In one paragraph

Review in Ageing research reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.

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23 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 3 countries.

Santiago Solé-DomènechExperimental Dementia Unit, Department of Medicine, Lund University, Sölvegatan 19, BMC B11, 221 84 Lund, Sweden; Department of Biochemistry, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10065, United States.
Dana L CruzDepartment of Biochemistry, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10065, United States.
Estibaliz Capetillo-ZarateDepartment of Biochemistry, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10065, United States; IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Spain; Achucarro Basque Center for Neurosciences, 48170 Zamudio, Spain; Department of Neuroscience, Faculty of Medicine and Odontology, University of the Basque Country EHU/UPV, Leioa, Spain.
Frederick R MaxfieldDepartment of Biochemistry, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10065, United States. Electronic address: frmaxfie@med.cornell.edu.
Cornell University · USIkerbasque · ESLund University · SE

Funding

Macrophage-Lipoprotein InteractionsR01HL093324 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MAXFIELD, FREDERICK R. · 2009 to 2025
$6.7M
RECEPTOR-MEDIATED ENDOCYTOSIS: MECHANISM AND FUNCTIONR37DK027083 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI MAXFIELD, FREDERICK R. · 1993 to 2014
$6.5M
Acquisition of a DeltaVision OMX SR 3D SIM system for super-resolution imagingS10RR031855 · NCRR · ROCKEFELLER UNIVERSITY · PI NORTH, ALISON JANE · 2011 to 2011
$600k
NCRR NIH HHS S10 RR031855NHLBI NIH HHS R01 HL093324NIDDK NIH HHS R37 DK027083
6 · The paper itself

Abstract

Microglia, the main phagocytes of the central nervous system (CNS), are involved in the surveillance and maintenance of nervous tissue. During normal tissue homeostasis, microglia migrates within the CNS, phagocytose dead cells and tissue debris, and modulate synapse pruning and spine formation via controlled phagocytosis. In the event of an invasion by a foreign body, microglia are able to phagocytose the invading pathogen and process it proteolytically for antigen presentation. Internalized substrates are incorporated and sorted within the endocytic pathway and thereafter transported via complex vesicular routes. When targeted for degradation, substrates are delivered to acidic late endosomes and lysosomes. In these, the enzymatic degradation relies on pH and enzyme content. Endocytosis, sorting, transport, compartment acidification and degradation are regulated by complex signaling mechanisms, and these may be altered during aging and pathology. In this review, we discuss the endocytic pathway in microglia, with insight into the mechanisms controlling lysosomal biogenesis and pH regulation. We also discuss microglial lysosome function associated with Alzheimer's disease (AD) and the mechanisms of amyloid-beta (Aβ) internalization and degradation. Finally, we explore some therapies currently being investigated to treat AD and their effects on microglial response to Aβ, with insight in those involving enhancement of lysosomal function.

Indexed as

AgingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsHumansLysosomesMicrogliaPhagocytosisSignal TransductionAmyloid beta-PeptidesAlzheimer’s diseaseAmyloid-betaEndocytosisLysosomeMicrogliaMITFTFEB

Identifiers

PMID27421577
PMCPMC5127718
OpenAlexW2465699308

What OpenQuestion holds

Textmetadata
LicenceTDM
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.