Evidence map›Paper›PMID 39528672›Full record

ArticleNature neuroscience2024

Astrocyte transcriptomic changes along the spatiotemporal progression of Alzheimer's disease.

Alberto Serrano-Pozo, Huan Li, Zhaozhi Li, Clara Muñoz-Castro, Methasit Jaisa-Aad, Molly A Healey, Lindsay A Welikovitch, Rojashree Jayakumar, Annie G Bryant, Ayush Noori and 17 more

Abstract read
In one paragraph

Article in Nature neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
–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

101 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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41 more citing papers are in PubMed but not listed here.

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

27 authors.

Alberto Serrano-Pozo *Massachusetts General Hospital, Department of Neurology, Boston, MA, USA.ORCID http://orcid.org/0000-0003-0899-7530
Huan Li *Massachusetts General Hospital, Department of Neurology, Boston, MA, USA.ORCID http://orcid.org/0009-0007-7401-9715
Zhaozhi Li *Massachusetts General Hospital, Department of Neurology, Boston, MA, USA.
Clara Muñoz-CastroMassachusetts General Hospital, Department of Neurology, Boston, MA, USA.ORCID http://orcid.org/0000-0002-4484-9802
Methasit Jaisa-AadMassachusetts General Hospital, Department of Neurology, Boston, MA, USA.
Molly A HealeyMassachusetts General Hospital, Department of Neurology, Boston, MA, USA.
Lindsay A WelikovitchMassachusetts General Hospital, Department of Neurology, Boston, MA, USA.
Rojashree JayakumarMassachusetts General Hospital, Department of Neurology, Boston, MA, USA.
Annie G BryantMassachusetts General Hospital, Department of Neurology, Boston, MA, USA.
Ayush NooriMassachusetts General Hospital, Department of Neurology, Boston, MA, USA.ORCID http://orcid.org/0000-0003-1420-1236
Theresa R ConnorsMassachusetts General Hospital, Department of Neurology, Boston, MA, USA.
Miwei HuMassachusetts General Hospital, Department of Neurology, Boston, MA, USA.
Karen ZhaoAbbVie, Cambridge Research Center, Cambridge, MA, USA.
Fan LiaoAbbVie, Cambridge Research Center, Cambridge, MA, USA.
Gen LinAbbVie Deutschland GmbH & Co. KG, Genomics Research Center, Ludwigshafen, Germany.
Timothy PastikaAbbVie, Cambridge Research Center, Cambridge, MA, USA.
Joseph TammAbbVie, Cambridge Research Center, Cambridge, MA, USA.
Aicha AbdourahmanAbbVie, Cambridge Research Center, Cambridge, MA, USA.
Taekyung KwonAbbVie, Cambridge Research Center, Cambridge, MA, USA.
Rachel E BennettMassachusetts General Hospital, Department of Neurology, Boston, MA, USA.ORCID http://orcid.org/0000-0001-9640-0575
Maya E WoodburyAbbVie, Cambridge Research Center, Cambridge, MA, USA.
Astrid WachterAbbVie Deutschland GmbH & Co. KG, Genomics Research Center, Ludwigshafen, Germany.ORCID http://orcid.org/0009-0001-3977-7832
Robert V TalanianAbbVie, Cambridge Research Center, Cambridge, MA, USA.
Knut BiberAbbVie Deutschland GmbH & Co. KG, Neuroscience Research, Ludwigshafen, Germany.
Eric H KarranAbbVie, Cambridge Research Center, Cambridge, MA, USA.
Bradley T HymanMassachusetts General Hospital, Department of Neurology, Boston, MA, USA.ORCID http://orcid.org/0000-0002-7959-9401
Sudeshna DasMassachusetts General Hospital, Department of Neurology, Boston, MA, USA. sdas5@mgh.harvard.edu.ORCID http://orcid.org/0000-0002-9486-6811

Funding

Research Education ComponentP30AG062421 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI STEVEN E ARNOLD · 2019 to 2026
$36.5M
Microvascular Stress as a Pathway to Neurodegeneration in Alzheimer'sR01AG071567 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Rachel Elise Bennett · 2022 to 2026
$2.1M
Astrocyte Reaction in Alzheimer's DiseaseK08AG064039 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI SERRANO-POZO, ALBERTO · 2019 to 2023
$837k
Alzheimer's Association AACF-17-524184Alzheimer's Association AACF-17-524184-RAPIDMassachusetts Life Sciences Center (MLSC) Neuroscience Consortium awardNIA NIH HHS K08 AG064039NIA NIH HHS P30 AG062421NIA NIH HHS R01 AG071567
6 · The paper itself

Abstract

Astrocytes are crucial to brain homeostasis, yet their changes along the spatiotemporal progression of Alzheimer's disease (AD) neuropathology remain unexplored. Here we performed single-nucleus RNA sequencing of 628,943 astrocytes from five brain regions representing the stereotypical progression of AD pathology across 32 donors spanning the entire normal aging to severe AD continuum. We mapped out several unique astrocyte subclusters that exhibited varying responses to neuropathology across the AD-vulnerable neural network (spatial axis) or AD pathology stage (temporal axis). The proportion of homeostatic, intermediate and reactive astrocytes changed only along the spatial axis, whereas two other subclusters changed along the temporal axis. One of these, a trophic factor-rich subcluster, declined along pathology stages, whereas the other increased in the late stage but returned to baseline levels in the end stage, suggesting an exhausted response with chronic exposure to neuropathology. Our study underscores the complex dynamics of astrocytic responses in AD.

Indexed as

Alzheimer DiseaseAstrocytesDisease ProgressionTranscriptomeAgedAged, 80 and overBrainFemaleHumansMaleMiddle Aged

Identifiers

PMID39528672
PMCPMC11614739

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.