Evidence map›Paper›PMID 38733521›Full record

ArticleNeurochemical research2024

Changes in Astroglial Water Flow in the Pre-amyloid Phase of the STZ Model of AD Dementia.

Vitor Gayger-Dias, Leonardo Menezes, Vanessa-Fernanda Da Silva, Amanda Stiborski, Ana Carolina Ribeiro Silva, Thomas Michel Sobottka, Vitória Cristine Quines-Silva, Betina Pakulski-Souto, Larissa Daniele Bobermin, André Quincozes-Santos and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

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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

12 authors.

Vitor Gayger-Dias *Biochemistry Laboratory 33, Graduate Program in Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600, Porto Alegre, 90035-003, Brazil.
Leonardo Menezes *Biochemistry Laboratory 33, Graduate Program in Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600, Porto Alegre, 90035-003, Brazil.
Vanessa-Fernanda Da SilvaBiochemistry Laboratory 33, Graduate Program in Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600, Porto Alegre, 90035-003, Brazil.
Amanda StiborskiBiochemistry Laboratory 33, Graduate Program in Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600, Porto Alegre, 90035-003, Brazil.
Ana Carolina Ribeiro SilvaBiochemistry Laboratory 33, Graduate Program in Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600, Porto Alegre, 90035-003, Brazil.
Thomas Michel SobottkaBiochemistry Laboratory 33, Graduate Program in Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600, Porto Alegre, 90035-003, Brazil.
Vitória Cristine Quines-SilvaBiochemistry Laboratory 33, Graduate Program in Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600, Porto Alegre, 90035-003, Brazil.
Betina Pakulski-SoutoBiochemistry Laboratory 33, Graduate Program in Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600, Porto Alegre, 90035-003, Brazil.
Larissa Daniele BoberminBiochemistry Laboratory 33, Graduate Program in Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600, Porto Alegre, 90035-003, Brazil.
André Quincozes-SantosBiochemistry Laboratory 33, Graduate Program in Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600, Porto Alegre, 90035-003, Brazil.
Marina Concli LeiteBiochemistry Laboratory 33, Graduate Program in Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600, Porto Alegre, 90035-003, Brazil.
Carlos-Alberto GonçalvesBiochemistry Laboratory 33, Graduate Program in Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600, Porto Alegre, 90035-003, Brazil. casg@ufrgs.br.

Funding

Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul FAPERGS, PPSUS 21/2551-0000067-8Instituto Nacional de Ciência e Tecnologia (INCT) para Saúde Cerebral CNPq/MCT 406020/2022-1
6 · The paper itself

Abstract

Alzheimer's disease (AD) is an age-dependent neurodegenerative disease that is typically sporadic and has a high social and economic cost. We utilized the intracerebroventricular administration of streptozotocin (STZ), an established preclinical model for sporadic AD, to investigate hippocampal astroglial changes during the first 4 weeks post-STZ, a period during which amyloid deposition has yet to occur. Astroglial proteins aquaporin 4 (AQP-4) and connexin-43 (Cx-43) were evaluated, as well as claudins, which are tight junction (TJ) proteins in brain barriers, to try to identify changes in the glymphatic system and brain barrier during the pre-amyloid phase. Glial commitment, glucose hypometabolism and cognitive impairment were characterized during this phase. Astroglial involvement was confirmed by an increase in glial fibrillary acidic protein (GFAP); concurrent proteolysis was also observed, possibly mediated by calpain. Levels of AQP-4 and Cx-43 were elevated in the fourth week post-STZ, possibly accelerating the clearance of extracellular proteins, since these proteins actively participate in the glymphatic system. Moreover, although we did not see a functional disruption of the blood-brain barrier (BBB) at this time, claudin 5 (present in the TJ of the BBB) and claudin 2 (present in the TJ of the blood-cerebrospinal fluid barrier) were reduced. Taken together, data support a role for astrocytes in STZ brain damage, and suggest that astroglial dysfunction accompanies or precedes neuronal damage in AD.

Indexed as

Alzheimer DiseaseAquaporin 4AstrocytesStreptozocinAnimalsBlood-Brain BarrierConnexin 43Disease Models, AnimalHippocampusMaleRatsRats, WistarWaterAqp4 protein, ratAquaporin 4Connexin 43StreptozocinWaterAlzheimer’s diseaseAquaporin 4AstrocyteGFAPGlymphatic SystemStreptozotocin

Identifiers

PMID38733521

What OpenQuestion holds

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Registered trials

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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.