Loading…
Histone deacetylase inhibition mitigates cognitive deficits and astrocyte dysfunction induced by amyloid‐β (Aβ) oligomers
Background and Purpose Inhibitors of histone deacetylases (iHDACs) are promising drugs for neurodegenerative diseases. We have evaluated the therapeutic potential of the new iHDAC LASSBio‐1911 in Aβ oligomer (AβO) toxicity models and astrocytes, key players in neuroinflammation and Alzheimer's...
Saved in:
Published in: | British journal of pharmacology 2024-10, Vol.181 (20), p.4028-4049 |
---|---|
Main Authors: | , , , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | |
---|---|
cites | cdi_FETCH-LOGICAL-c2439-375977734ad8b9b6c6d754ec9bcfab48e9cd2adfb2dc110a7f992e3f55a40d353 |
container_end_page | 4049 |
container_issue | 20 |
container_start_page | 4028 |
container_title | British journal of pharmacology |
container_volume | 181 |
creator | Diniz, Luan Pereira Morgado, Juliana Bergamo Araujo, Ana Paula Silva Antônio, Leticia Maria Mota‐Araujo, Hannah Paola Sena Murteira Pinheiro, Pedro Sagrillo, Fernanda Savacini Cesar, Gabriele Vargas Ferreira, Sérgio T. Figueiredo, Cláudia Pinto Manssour Fraga, Carlos Alberto Gomes, Flávia Carvalho Alcantara |
description | Background and Purpose
Inhibitors of histone deacetylases (iHDACs) are promising drugs for neurodegenerative diseases. We have evaluated the therapeutic potential of the new iHDAC LASSBio‐1911 in Aβ oligomer (AβO) toxicity models and astrocytes, key players in neuroinflammation and Alzheimer's disease (AD).
Experimental Approach
Astrocyte phenotype and synapse density were evaluated by flow cytometry, Western blotting, immunofluorescence and qPCR, in vitro and in mice. Cognitive function was evaluated by behavioural assays using a mouse model of intracerebroventricular infusion of AβO.
Key Results
LASSBio‐1911 modulates reactivity and synaptogenic potential of cultured astrocytes and improves synaptic markers in cultured neurons and in mice. It prevents AβO‐triggered astrocytic reactivity in mice and enhances the neuroprotective potential of astrocytes. LASSBio‐1911 improves behavioural performance and rescues synaptic and memory function in AβO‐infused mice.
Conclusion and Implications
These results contribute to unveiling the mechanisms underlying astrocyte role in AD and provide the rationale for using astrocytes as targets to new drugs for AD.
▪ |
doi_str_mv | 10.1111/bph.16439 |
format | article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_3073231314</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3073231314</sourcerecordid><originalsourceid>FETCH-LOGICAL-c2439-375977734ad8b9b6c6d754ec9bcfab48e9cd2adfb2dc110a7f992e3f55a40d353</originalsourceid><addsrcrecordid>eNp1kU9O3TAQxi1EBa_AoheoLLGBRcCOnTheAmr7KiG1C1hb_jN5GCX2I05AWVTqEXoWDsIhepIaHu0CqbMZzcxvPs3oQ-gDJSc0x6lZ35zQmjO5hRaUi7qoWEO30YIQIgpKm2YXvU_plpA8FNUO2mWNZDUnYoF-LH0aYwDsQFsY504nwD7ceONHHwPuc1rpERK2cRVycf-Mtt76MWEdHNZpHKKdx9yeUzsF-7Lmg5ssOGxmrPu5i979_vnr6REfnT09HuPY-VXsYUj76F2ruwQHr3kPXX_-dHWxLC6_ffl6cXZZ2DJ_VTBRSSEE49o1Rpra1k5UHKw0ttWGNyCtK7VrTekspUSLVsoSWFtVmhPHKraHjja66yHeTZBG1ftkoet0gDglxYhgJaOM8owevkFv4zSEfJ1ilHIuSiZlpo43lB1iSgO0aj34Xg-zokQ9e6KyJ-rFk8x-fFWcTA_uH_nXhAycboAH38H8fyV1_n25kfwDKPKaWA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3114472399</pqid></control><display><type>article</type><title>Histone deacetylase inhibition mitigates cognitive deficits and astrocyte dysfunction induced by amyloid‐β (Aβ) oligomers</title><source>Wiley-Blackwell Read & Publish Collection</source><creator>Diniz, Luan Pereira ; Morgado, Juliana ; Bergamo Araujo, Ana Paula ; Silva Antônio, Leticia Maria ; Mota‐Araujo, Hannah Paola ; Sena Murteira Pinheiro, Pedro ; Sagrillo, Fernanda Savacini ; Cesar, Gabriele Vargas ; Ferreira, Sérgio T. ; Figueiredo, Cláudia Pinto ; Manssour Fraga, Carlos Alberto ; Gomes, Flávia Carvalho Alcantara</creator><creatorcontrib>Diniz, Luan Pereira ; Morgado, Juliana ; Bergamo Araujo, Ana Paula ; Silva Antônio, Leticia Maria ; Mota‐Araujo, Hannah Paola ; Sena Murteira Pinheiro, Pedro ; Sagrillo, Fernanda Savacini ; Cesar, Gabriele Vargas ; Ferreira, Sérgio T. ; Figueiredo, Cláudia Pinto ; Manssour Fraga, Carlos Alberto ; Gomes, Flávia Carvalho Alcantara</creatorcontrib><description>Background and Purpose
Inhibitors of histone deacetylases (iHDACs) are promising drugs for neurodegenerative diseases. We have evaluated the therapeutic potential of the new iHDAC LASSBio‐1911 in Aβ oligomer (AβO) toxicity models and astrocytes, key players in neuroinflammation and Alzheimer's disease (AD).
Experimental Approach
Astrocyte phenotype and synapse density were evaluated by flow cytometry, Western blotting, immunofluorescence and qPCR, in vitro and in mice. Cognitive function was evaluated by behavioural assays using a mouse model of intracerebroventricular infusion of AβO.
Key Results
LASSBio‐1911 modulates reactivity and synaptogenic potential of cultured astrocytes and improves synaptic markers in cultured neurons and in mice. It prevents AβO‐triggered astrocytic reactivity in mice and enhances the neuroprotective potential of astrocytes. LASSBio‐1911 improves behavioural performance and rescues synaptic and memory function in AβO‐infused mice.
Conclusion and Implications
These results contribute to unveiling the mechanisms underlying astrocyte role in AD and provide the rationale for using astrocytes as targets to new drugs for AD.
▪</description><identifier>ISSN: 0007-1188</identifier><identifier>ISSN: 1476-5381</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/bph.16439</identifier><identifier>PMID: 38936407</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Alzheimer's disease ; Amyloid beta-Peptides - metabolism ; Amyloid beta-Peptides - toxicity ; Animal models ; Animals ; astrocyte ; Astrocytes ; Astrocytes - drug effects ; Astrocytes - metabolism ; Cells, Cultured ; Cognitive ability ; Cognitive Dysfunction - chemically induced ; Cognitive Dysfunction - drug therapy ; Cognitive Dysfunction - metabolism ; Drug development ; Flow cytometry ; Histone deacetylase ; histone deacetylase inhibitor ; Histone Deacetylase Inhibitors - pharmacology ; Immunofluorescence ; Male ; Mice ; Mice, Inbred C57BL ; multitarget drugs ; Neurodegenerative diseases ; neuroinflammation ; Neuroprotection ; Neuroprotective Agents - administration & dosage ; Neuroprotective Agents - pharmacology ; Oligomers ; Phenotypes ; reactivity ; Synapses ; Synapses - drug effects ; Synapses - metabolism ; Synaptic density ; Toxicity ; Western blotting ; β-Amyloid</subject><ispartof>British journal of pharmacology, 2024-10, Vol.181 (20), p.4028-4049</ispartof><rights>2024 British Pharmacological Society.</rights><rights>2024 The British Pharmacological Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c2439-375977734ad8b9b6c6d754ec9bcfab48e9cd2adfb2dc110a7f992e3f55a40d353</cites><orcidid>0000-0003-2966-0638 ; 0000-0003-4148-4243</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38936407$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Diniz, Luan Pereira</creatorcontrib><creatorcontrib>Morgado, Juliana</creatorcontrib><creatorcontrib>Bergamo Araujo, Ana Paula</creatorcontrib><creatorcontrib>Silva Antônio, Leticia Maria</creatorcontrib><creatorcontrib>Mota‐Araujo, Hannah Paola</creatorcontrib><creatorcontrib>Sena Murteira Pinheiro, Pedro</creatorcontrib><creatorcontrib>Sagrillo, Fernanda Savacini</creatorcontrib><creatorcontrib>Cesar, Gabriele Vargas</creatorcontrib><creatorcontrib>Ferreira, Sérgio T.</creatorcontrib><creatorcontrib>Figueiredo, Cláudia Pinto</creatorcontrib><creatorcontrib>Manssour Fraga, Carlos Alberto</creatorcontrib><creatorcontrib>Gomes, Flávia Carvalho Alcantara</creatorcontrib><title>Histone deacetylase inhibition mitigates cognitive deficits and astrocyte dysfunction induced by amyloid‐β (Aβ) oligomers</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Background and Purpose
Inhibitors of histone deacetylases (iHDACs) are promising drugs for neurodegenerative diseases. We have evaluated the therapeutic potential of the new iHDAC LASSBio‐1911 in Aβ oligomer (AβO) toxicity models and astrocytes, key players in neuroinflammation and Alzheimer's disease (AD).
Experimental Approach
Astrocyte phenotype and synapse density were evaluated by flow cytometry, Western blotting, immunofluorescence and qPCR, in vitro and in mice. Cognitive function was evaluated by behavioural assays using a mouse model of intracerebroventricular infusion of AβO.
Key Results
LASSBio‐1911 modulates reactivity and synaptogenic potential of cultured astrocytes and improves synaptic markers in cultured neurons and in mice. It prevents AβO‐triggered astrocytic reactivity in mice and enhances the neuroprotective potential of astrocytes. LASSBio‐1911 improves behavioural performance and rescues synaptic and memory function in AβO‐infused mice.
Conclusion and Implications
These results contribute to unveiling the mechanisms underlying astrocyte role in AD and provide the rationale for using astrocytes as targets to new drugs for AD.
▪</description><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Amyloid beta-Peptides - toxicity</subject><subject>Animal models</subject><subject>Animals</subject><subject>astrocyte</subject><subject>Astrocytes</subject><subject>Astrocytes - drug effects</subject><subject>Astrocytes - metabolism</subject><subject>Cells, Cultured</subject><subject>Cognitive ability</subject><subject>Cognitive Dysfunction - chemically induced</subject><subject>Cognitive Dysfunction - drug therapy</subject><subject>Cognitive Dysfunction - metabolism</subject><subject>Drug development</subject><subject>Flow cytometry</subject><subject>Histone deacetylase</subject><subject>histone deacetylase inhibitor</subject><subject>Histone Deacetylase Inhibitors - pharmacology</subject><subject>Immunofluorescence</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>multitarget drugs</subject><subject>Neurodegenerative diseases</subject><subject>neuroinflammation</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - administration & dosage</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Oligomers</subject><subject>Phenotypes</subject><subject>reactivity</subject><subject>Synapses</subject><subject>Synapses - drug effects</subject><subject>Synapses - metabolism</subject><subject>Synaptic density</subject><subject>Toxicity</subject><subject>Western blotting</subject><subject>β-Amyloid</subject><issn>0007-1188</issn><issn>1476-5381</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp1kU9O3TAQxi1EBa_AoheoLLGBRcCOnTheAmr7KiG1C1hb_jN5GCX2I05AWVTqEXoWDsIhepIaHu0CqbMZzcxvPs3oQ-gDJSc0x6lZ35zQmjO5hRaUi7qoWEO30YIQIgpKm2YXvU_plpA8FNUO2mWNZDUnYoF-LH0aYwDsQFsY504nwD7ceONHHwPuc1rpERK2cRVycf-Mtt76MWEdHNZpHKKdx9yeUzsF-7Lmg5ssOGxmrPu5i979_vnr6REfnT09HuPY-VXsYUj76F2ruwQHr3kPXX_-dHWxLC6_ffl6cXZZ2DJ_VTBRSSEE49o1Rpra1k5UHKw0ttWGNyCtK7VrTekspUSLVsoSWFtVmhPHKraHjja66yHeTZBG1ftkoet0gDglxYhgJaOM8owevkFv4zSEfJ1ilHIuSiZlpo43lB1iSgO0aj34Xg-zokQ9e6KyJ-rFk8x-fFWcTA_uH_nXhAycboAH38H8fyV1_n25kfwDKPKaWA</recordid><startdate>202410</startdate><enddate>202410</enddate><creator>Diniz, Luan Pereira</creator><creator>Morgado, Juliana</creator><creator>Bergamo Araujo, Ana Paula</creator><creator>Silva Antônio, Leticia Maria</creator><creator>Mota‐Araujo, Hannah Paola</creator><creator>Sena Murteira Pinheiro, Pedro</creator><creator>Sagrillo, Fernanda Savacini</creator><creator>Cesar, Gabriele Vargas</creator><creator>Ferreira, Sérgio T.</creator><creator>Figueiredo, Cláudia Pinto</creator><creator>Manssour Fraga, Carlos Alberto</creator><creator>Gomes, Flávia Carvalho Alcantara</creator><general>Blackwell Publishing Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-2966-0638</orcidid><orcidid>https://orcid.org/0000-0003-4148-4243</orcidid></search><sort><creationdate>202410</creationdate><title>Histone deacetylase inhibition mitigates cognitive deficits and astrocyte dysfunction induced by amyloid‐β (Aβ) oligomers</title><author>Diniz, Luan Pereira ; Morgado, Juliana ; Bergamo Araujo, Ana Paula ; Silva Antônio, Leticia Maria ; Mota‐Araujo, Hannah Paola ; Sena Murteira Pinheiro, Pedro ; Sagrillo, Fernanda Savacini ; Cesar, Gabriele Vargas ; Ferreira, Sérgio T. ; Figueiredo, Cláudia Pinto ; Manssour Fraga, Carlos Alberto ; Gomes, Flávia Carvalho Alcantara</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2439-375977734ad8b9b6c6d754ec9bcfab48e9cd2adfb2dc110a7f992e3f55a40d353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Amyloid beta-Peptides - toxicity</topic><topic>Animal models</topic><topic>Animals</topic><topic>astrocyte</topic><topic>Astrocytes</topic><topic>Astrocytes - drug effects</topic><topic>Astrocytes - metabolism</topic><topic>Cells, Cultured</topic><topic>Cognitive ability</topic><topic>Cognitive Dysfunction - chemically induced</topic><topic>Cognitive Dysfunction - drug therapy</topic><topic>Cognitive Dysfunction - metabolism</topic><topic>Drug development</topic><topic>Flow cytometry</topic><topic>Histone deacetylase</topic><topic>histone deacetylase inhibitor</topic><topic>Histone Deacetylase Inhibitors - pharmacology</topic><topic>Immunofluorescence</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>multitarget drugs</topic><topic>Neurodegenerative diseases</topic><topic>neuroinflammation</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - administration & dosage</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Oligomers</topic><topic>Phenotypes</topic><topic>reactivity</topic><topic>Synapses</topic><topic>Synapses - drug effects</topic><topic>Synapses - metabolism</topic><topic>Synaptic density</topic><topic>Toxicity</topic><topic>Western blotting</topic><topic>β-Amyloid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Diniz, Luan Pereira</creatorcontrib><creatorcontrib>Morgado, Juliana</creatorcontrib><creatorcontrib>Bergamo Araujo, Ana Paula</creatorcontrib><creatorcontrib>Silva Antônio, Leticia Maria</creatorcontrib><creatorcontrib>Mota‐Araujo, Hannah Paola</creatorcontrib><creatorcontrib>Sena Murteira Pinheiro, Pedro</creatorcontrib><creatorcontrib>Sagrillo, Fernanda Savacini</creatorcontrib><creatorcontrib>Cesar, Gabriele Vargas</creatorcontrib><creatorcontrib>Ferreira, Sérgio T.</creatorcontrib><creatorcontrib>Figueiredo, Cláudia Pinto</creatorcontrib><creatorcontrib>Manssour Fraga, Carlos Alberto</creatorcontrib><creatorcontrib>Gomes, Flávia Carvalho Alcantara</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Diniz, Luan Pereira</au><au>Morgado, Juliana</au><au>Bergamo Araujo, Ana Paula</au><au>Silva Antônio, Leticia Maria</au><au>Mota‐Araujo, Hannah Paola</au><au>Sena Murteira Pinheiro, Pedro</au><au>Sagrillo, Fernanda Savacini</au><au>Cesar, Gabriele Vargas</au><au>Ferreira, Sérgio T.</au><au>Figueiredo, Cláudia Pinto</au><au>Manssour Fraga, Carlos Alberto</au><au>Gomes, Flávia Carvalho Alcantara</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Histone deacetylase inhibition mitigates cognitive deficits and astrocyte dysfunction induced by amyloid‐β (Aβ) oligomers</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2024-10</date><risdate>2024</risdate><volume>181</volume><issue>20</issue><spage>4028</spage><epage>4049</epage><pages>4028-4049</pages><issn>0007-1188</issn><issn>1476-5381</issn><eissn>1476-5381</eissn><abstract>Background and Purpose
Inhibitors of histone deacetylases (iHDACs) are promising drugs for neurodegenerative diseases. We have evaluated the therapeutic potential of the new iHDAC LASSBio‐1911 in Aβ oligomer (AβO) toxicity models and astrocytes, key players in neuroinflammation and Alzheimer's disease (AD).
Experimental Approach
Astrocyte phenotype and synapse density were evaluated by flow cytometry, Western blotting, immunofluorescence and qPCR, in vitro and in mice. Cognitive function was evaluated by behavioural assays using a mouse model of intracerebroventricular infusion of AβO.
Key Results
LASSBio‐1911 modulates reactivity and synaptogenic potential of cultured astrocytes and improves synaptic markers in cultured neurons and in mice. It prevents AβO‐triggered astrocytic reactivity in mice and enhances the neuroprotective potential of astrocytes. LASSBio‐1911 improves behavioural performance and rescues synaptic and memory function in AβO‐infused mice.
Conclusion and Implications
These results contribute to unveiling the mechanisms underlying astrocyte role in AD and provide the rationale for using astrocytes as targets to new drugs for AD.
▪</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>38936407</pmid><doi>10.1111/bph.16439</doi><tpages>22</tpages><orcidid>https://orcid.org/0000-0003-2966-0638</orcidid><orcidid>https://orcid.org/0000-0003-4148-4243</orcidid></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0007-1188 |
ispartof | British journal of pharmacology, 2024-10, Vol.181 (20), p.4028-4049 |
issn | 0007-1188 1476-5381 1476-5381 |
language | eng |
recordid | cdi_proquest_miscellaneous_3073231314 |
source | Wiley-Blackwell Read & Publish Collection |
subjects | Alzheimer's disease Amyloid beta-Peptides - metabolism Amyloid beta-Peptides - toxicity Animal models Animals astrocyte Astrocytes Astrocytes - drug effects Astrocytes - metabolism Cells, Cultured Cognitive ability Cognitive Dysfunction - chemically induced Cognitive Dysfunction - drug therapy Cognitive Dysfunction - metabolism Drug development Flow cytometry Histone deacetylase histone deacetylase inhibitor Histone Deacetylase Inhibitors - pharmacology Immunofluorescence Male Mice Mice, Inbred C57BL multitarget drugs Neurodegenerative diseases neuroinflammation Neuroprotection Neuroprotective Agents - administration & dosage Neuroprotective Agents - pharmacology Oligomers Phenotypes reactivity Synapses Synapses - drug effects Synapses - metabolism Synaptic density Toxicity Western blotting β-Amyloid |
title | Histone deacetylase inhibition mitigates cognitive deficits and astrocyte dysfunction induced by amyloid‐β (Aβ) oligomers |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-12T06%3A23%3A56IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Histone%20deacetylase%20inhibition%20mitigates%20cognitive%20deficits%20and%20astrocyte%20dysfunction%20induced%20by%20amyloid%E2%80%90%CE%B2%20(A%CE%B2)%20oligomers&rft.jtitle=British%20journal%20of%20pharmacology&rft.au=Diniz,%20Luan%20Pereira&rft.date=2024-10&rft.volume=181&rft.issue=20&rft.spage=4028&rft.epage=4049&rft.pages=4028-4049&rft.issn=0007-1188&rft.eissn=1476-5381&rft_id=info:doi/10.1111/bph.16439&rft_dat=%3Cproquest_cross%3E3073231314%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c2439-375977734ad8b9b6c6d754ec9bcfab48e9cd2adfb2dc110a7f992e3f55a40d353%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=3114472399&rft_id=info:pmid/38936407&rfr_iscdi=true |