Evidence map›Paper›PMID 30883351›Full record

ArticleJournal of Alzheimer's disease : JAD2019

Modulation of SPARC/Hevin Proteins in Alzheimer's Disease Brain Injury.

Maximilian Strunz, Juliet T Jarrell, David S Cohen, Eric R Rosin, Charles R Vanderburg, Xudong Huang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 42 citations in OpenAlex.

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  8. Alpha-neurexins in health and disease.Frontiers in molecular neuroscience · 2025
    Review
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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

6 authors at 1 institution in 1 country.

Maximilian StrunzDepartment of Neurology, Harvard NeuroDiscovery Center, Advanced Tissue Resource Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Juliet T JarrellDepartment of Psychiatry, Neurochemistry Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
David S CohenDepartment of Psychiatry, Neurochemistry Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Eric R RosinDepartment of Psychiatry, Neurochemistry Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Charles R VanderburgDepartment of Neurology, Harvard NeuroDiscovery Center, Advanced Tissue Resource Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Xudong HuangDepartment of Psychiatry, Neurochemistry Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Harvard University · US

Funding

Nanoneurotoxicity of Metal Oxide Nanomaterials and NeurodegenerationR01AG056614 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HUANG, XUDONG · 2017 to 2020
$1.5M
NIA NIH HHS R01 AG056614
6 · The paper itself

Abstract

Alzheimer's disease (AD) is an age-related progressive form of dementia that features neuronal loss, intracellular tau, and extracellular amyloid-β (Aβ) protein deposition. Neurodegeneration is accompanied by neuroinflammation mainly involving microglia, the resident innate immune cell population of the brain. During AD progression, microglia shift their phenotype, and it has been suggested that they express matricellular proteins such as secreted protein acidic and rich in cysteine (SPARC) and Hevin protein, which facilitate the migration of other immune cells, such as blood-derived dendritic cells. We have detected both SPARC and Hevin in postmortem AD brain tissues and confirmed significant alterations in transcript expression using real-time qPCR. We suggest that an infiltration of myeloid-derived immune cells occurs in the areas of diseased tissue. SPARC is highly expressed in AD brain and collocates to Aβ protein deposits, thus contributing actively to cerebral inflammation and subsequent tissue repair, and Hevin may be downregulated in the diseased state. However, further research is needed to reveal the exact roles of SPARC and Hevin proteins and associated signaling pathways in AD-related neuroinflammation. Nevertheless, normalizing SPARC/Hevin protein expression such as interdicting heightened SPARC protein expression may confer a novel therapeutic opportunity for modulating AD progression.

Indexed as

AdultAgedAged, 80 and overAlzheimer DiseaseBrain InjuriesCalcium-Binding ProteinsExtracellular Matrix ProteinsFemaleHumansLaser Capture MicrodissectionMaleMiddle AgedOsteonectinCalcium-Binding ProteinsExtracellular Matrix ProteinsOsteonectinSPARCL1 protein, humanSPARC protein, humanAlzheimer’s diseaseamyloid-βdendritic cellsHevin/SPARCL1 proteinmacrophagesmicrogliaSPARC protein

Identifiers

PMID30883351
PMCPMC6481539
OpenAlexW2922419793

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.