Evidence map›Paper›PMID 26235241›Full record

ArticleHippocampus2016

Glial alterations from early to late stages in a model of Alzheimer's disease: Evidence of autophagy involvement in Aβ internalization.

Carlos Pomilio, Patricio Pavia, Roxana Mayra Gorojod, Angeles Vinuesa, Agustina Alaimo, Veronica Galvan, Monica Lidia Kotler, Juan Beauquis, Flavia Saravia

Open access · bronzeAbstract read
In one paragraph

Article in Hippocampus, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

43 citing papers in PubMed, 79 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

9 authors at 2 institutions in 2 countries.

Carlos PomilioDepartamento De Quimica Biologica, Facultad De Ciencias Exactas Y Naturales, Universidad De Buenos Aires, Instituto De Biologia Y Medicina Experimental Conicet, Buenos Aires, Argentina.
Patricio PaviaDepartamento De Quimica Biologica, Facultad De Ciencias Exactas Y Naturales, Universidad De Buenos Aires, Instituto De Biologia Y Medicina Experimental Conicet, Buenos Aires, Argentina.
Roxana Mayra GorojodDepartamento De Quimica Biologica, Facultad De Ciencias Exactas Y Naturales, Universidad De Buenos Aires, IQUIBICEN-Conicet, Buenos Aires, Argentina.
Angeles VinuesaDepartamento De Quimica Biologica, Facultad De Ciencias Exactas Y Naturales, Universidad De Buenos Aires, Instituto De Biologia Y Medicina Experimental Conicet, Buenos Aires, Argentina.
Agustina AlaimoDepartamento De Quimica Biologica, Facultad De Ciencias Exactas Y Naturales, Universidad De Buenos Aires, IQUIBICEN-Conicet, Buenos Aires, Argentina.
Veronica GalvanDepartment of Physiology, Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, Texas.
Monica Lidia KotlerDepartamento De Quimica Biologica, Facultad De Ciencias Exactas Y Naturales, Universidad De Buenos Aires, IQUIBICEN-Conicet, Buenos Aires, Argentina.
Juan BeauquisDepartamento De Quimica Biologica, Facultad De Ciencias Exactas Y Naturales, Universidad De Buenos Aires, Instituto De Biologia Y Medicina Experimental Conicet, Buenos Aires, Argentina.
Flavia SaraviaDepartamento De Quimica Biologica, Facultad De Ciencias Exactas Y Naturales, Universidad De Buenos Aires, Instituto De Biologia Y Medicina Experimental Conicet, Buenos Aires, Argentina.
Fundación Ciencias Exactas y Naturales · ARLongevity Biotech (United States) · US

Funding

TRANSGENIC COREP30AG013319 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Xianlin Han · 1995 to 2026
$30.6M
Brain cellular senescence as a driver of Alzheimers DiseaseRF1AG057964 · NIA · OREGON STATE UNIVERSITY · PI GALVAN, VERONICA, MAGNUSSON, KATHY R · 2017 to 2019
$2.3M
Tau-induced astrocyte senescence in Alzheimer's diseaseRF1AG068283 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GALVAN, VERONICA, VAN REMMEN, HOLLY · 2020 to 2020
$1.6M
Pathogenic Tau Promotes Brain Vascular Dysfunction in Alzheimer's DiseaseI01BX002211 · VA · SOUTH TEXAS VETERANS HEALTH CARE SYSTEM · PI GALVAN, VERONICA · 2015 to 2025
–
BLRD VA I01 BX002211NIA NIH HHS P30 AG013319NIA NIH HHS RF1 AG057964NIA NIH HHS RF1 AG068283
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease without effective therapy. Brain amyloid deposits are classical histopathological hallmarks that generate an inflammatory reaction affecting neuronal and glial function. The identification of early cell responses and of brain areas involved could help to design new successful treatments. Hence, we studied early alterations of hippocampal glia and their progression during the neuropathology in PDAPP-J20 transgenic mice, AD model, at 3, 9, and 15 months (m) of age. At 3 m, before deposits formation, microglial Iba1+ cells from transgenic mice already exhibited signs of activation and larger soma size in the hilus, alterations appearing later on stratum radiatum. Iba1 immunohistochemistry revealed increased cell density and immunoreactive area in PDAPP mice from 9 m onward selectively in the hilus, in coincidence with prominent amyloid Congo red + deposition. At pre-plaque stages, GFAP+ astroglia showed density alterations while, at an advanced age, the presence of deposits was associated with important glial volume changes and apparently being intimately involved in amyloid degradation. Astrocytes around plaques were strongly labeled for LC3 until 15 m in Tg mice, suggestive of increased autophagic flux. Moreover, β-Amyloid fibrils internalization by astrocytes in in vitro conditions was dependent on autophagy. Co-localization of Iba1 with ubiquitin or p62 was exclusively found in microglia contacting deposits from 9 m onward, suggesting torpid autophagy. Our work characterizes glial changes at early stages of the disease in PDAPP-J20 mice, focusing on the hilus as an especially susceptible hippocampal subfield, and provides evidence that glial autophagy could play a role in amyloid processing at advanced stages.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAutophagyCell Line, TumorCells, CulturedDentate GyrusDisease Models, AnimalMiceMice, Inbred C57BLMice, TransgenicNeurogliaRatsAmyloid beta-PeptidesADastrocyteshilusLC3microglianeuroinflammationstratum radiatumubiquitin

Identifiers

PMID26235241
PMCPMC5467976
OpenAlexW1839303532

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.