Evidence map›Paper›PMID 32597805›Full record

ArticleJournal of Alzheimer's disease : JAD2020

Upregulation of Alzheimer's Disease Amyloid-β Protein Precursor in Astrocytes Both in vitro and in vivo.

Yingxia Liang, Frank Raven, Joseph F Ward, Sherri Zhen, Siyi Zhang, Haoqi Sun, Sean J Miller, Se Hoon Choi, Rudolph E Tanzi, Can Zhang

Open access · greenAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Intracellular protein GBF1 displays significant associations with amyloid pathology in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  8. Amyloid precursor protein induces reactive astrogliosis.bioRxiv : the preprint server for biology · 2023
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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

10 authors at 2 institutions in 2 countries.

Yingxia LiangGenetics and Aging Research Unit, McCance Center for Brain Health, MassGeneral Institute for Neurodegenerative Diseases (MIND), Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Frank RavenGenetics and Aging Research Unit, McCance Center for Brain Health, MassGeneral Institute for Neurodegenerative Diseases (MIND), Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Joseph F WardGenetics and Aging Research Unit, McCance Center for Brain Health, MassGeneral Institute for Neurodegenerative Diseases (MIND), Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Sherri ZhenGenetics and Aging Research Unit, McCance Center for Brain Health, MassGeneral Institute for Neurodegenerative Diseases (MIND), Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Siyi ZhangGenetics and Aging Research Unit, McCance Center for Brain Health, MassGeneral Institute for Neurodegenerative Diseases (MIND), Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Haoqi SunDepartment of Neurology, Massachusetts General Hospital, Boston, MA, USA.
Sean J MillerGenetics and Aging Research Unit, McCance Center for Brain Health, MassGeneral Institute for Neurodegenerative Diseases (MIND), Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Se Hoon ChoiGenetics and Aging Research Unit, McCance Center for Brain Health, MassGeneral Institute for Neurodegenerative Diseases (MIND), Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Rudolph E TanziGenetics and Aging Research Unit, McCance Center for Brain Health, MassGeneral Institute for Neurodegenerative Diseases (MIND), Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Can ZhangGenetics and Aging Research Unit, McCance Center for Brain Health, MassGeneral Institute for Neurodegenerative Diseases (MIND), Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
MaineGeneral Medical Center · USMassachusetts General Hospital · US

Funding

Characterizing the roles of novel soluble GSMs in AD pathology.R01AG055784 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI ZHANG, CAN MARTIN · 2018 to 2022
$2.1M
Characterization of ATXN1 in APP processing and AD pathogenesisR00AG039482 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI ZHANG, CAN MARTIN · 2014 to 2016
$740k
NIA NIH HHS R00 AG039482NIA NIH HHS R01 AG055784
6 · The paper itself

Abstract

backgroundThe amyloid cascade hypothesis of Alzheimer's disease (AD) posits that amyloid-β (Aβ) protein accumulation underlies the pathogenesis of the disease by leading to the formation of amyloid plaques, a pathologic hallmark of AD. Aβ is a proteolytic product of amyloid-β protein precursor (AβPP; APP), which is expressed in both neurons and astrocytes. Although considerable evidence shows that astrocytes may play critical roles in the pathogenesis of AD, the longitudinal changes of amyloid plaques in relationship to AβPP expression in astrocytes and cellular consequences are largely unknown.

objectiveHere, we aimed to investigate astrocyte-related pathological changes of Aβ and AβPP using immunohistochemistry and biochemical studies in both animal and cell models. METHODS/

resultsWe utilized 5XFAD transgenic mice and found age-dependent upregulation of AβPP in astrocytes demonstrated with astrocytic reactive properties, which followed appearance of amyloid plaques in the brain. We also observed that AβPP proteins presented well-defined punctate immuno reactivity in young animals, whereas AβPP staining showed disrupted structures surrounding amyloid plaques in older mice. Moreover, we utilized astrocyte cell models and showed that pretreatment of Aβ42 resulted in downstream astrocyte autonomous changes, including up regulation in AβPP and BACE1 levels, as well as prolonged amyloidogenesis that could be reduced by pharmacological inhibition of BACE1.

conclusionCollectively, our results show that age-dependent AβPP up regulation in astrocytes is a key feature in AD, which will not only provide novel insights for understanding AD progression, but also may offer new therapeutic strategies for treating AD.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAstrocytesBrainDisease Models, AnimalMiceNeuronsPlaque, AmyloidUp-RegulationAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAlzheimer’s diseaseamyloidogenesisamyloid pathologyamyloid-βamyloid-β protein precursorastrocyteautonomous

Identifiers

PMID32597805
PMCPMC7571426
OpenAlexW3037831457

What OpenQuestion holds

Textmetadata
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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.