Evidence map›Paper›PMID 37908010›Full record

ReviewTranslational neurodegeneration2023

Metabolic regulation of microglial phagocytosis: Implications for Alzheimer's disease therapeutics.

Izabela Lepiarz-Raba, Ismail Gbadamosi, Roberta Florea, Rosa Chiara Paolicelli, Ali Jawaid

Open access · goldAbstract readReview
In one paragraph

Review in Translational neurodegeneration, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

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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

5 authors at 3 institutions in 2 countries.

Izabela Lepiarz-RabaLaboratory for Translational Research in Neuropsychiatric Disorders (TREND), BRAINCITY: Center of Excellence for Neural Plasticity and Brain Disorders, Nencki Institute of Experimental Biology, Warsaw, Poland. i.lepiarz-raba@nencki.edu.pl.
Ismail GbadamosiLaboratory for Translational Research in Neuropsychiatric Disorders (TREND), BRAINCITY: Center of Excellence for Neural Plasticity and Brain Disorders, Nencki Institute of Experimental Biology, Warsaw, Poland.
Roberta FloreaSwiss Federal Institute of Technology (ETH), Zurich, Switzerland.
Rosa Chiara PaolicelliDepartment of Biomedical Sciences, University of Lausanne, Lausanne, Switzerland.
Ali JawaidLaboratory for Translational Research in Neuropsychiatric Disorders (TREND), BRAINCITY: Center of Excellence for Neural Plasticity and Brain Disorders, Nencki Institute of Experimental Biology, Warsaw, Poland. a.jawaid@nencki.edu.pl.
Instytut Biologii Doświadczalnej im. Marcelego Nenckiego · PLÉcole Polytechnique Fédérale de Lausanne · CHUniversity of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia, the resident immune cells of the brain, are increasingly implicated in the regulation of brain health and disease. Microglia perform multiple functions in the central nervous system, including surveillance, phagocytosis and release of a variety of soluble factors. Importantly, a majority of their functions are closely related to changes in their metabolism. This natural inter-dependency between core microglial properties and metabolism offers a unique opportunity to modulate microglial activities via nutritional or metabolic interventions. In this review, we examine the existing scientific literature to synthesize the hypothesis that microglial phagocytosis of amyloid beta (Aβ) aggregates in Alzheimer's disease (AD) can be selectively enhanced via metabolic interventions. We first review the basics of microglial metabolism and the effects of common metabolites, such as glucose, lipids, ketone bodies, glutamine, pyruvate and lactate, on microglial inflammatory and phagocytic properties. Next, we examine the evidence for dysregulation of microglial metabolism in AD. This is followed by a review of in vivo studies on metabolic manipulation of microglial functions to ascertain their therapeutic potential in AD. Finally, we discuss the effects of metabolic factors on microglial phagocytosis of healthy synapses, a pathological process that also contributes to the progression of AD. We conclude by enlisting the current challenges that need to be addressed before strategies to harness microglial phagocytosis to clear pathological protein deposits in AD and other neurodegenerative disorders can be widely adopted.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBrainHumansMicrogliaPhagocytosisAmyloid beta-PeptidesAlzheimer's diseaseInflammationMetabolismMicrogliaNeurodegenerationPhagocytosis

Identifiers

PMID37908010
PMCPMC10617244
OpenAlexW4388082182

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.