Evidence map›Paper›PMID 34272583›Full record

ArticleActa neuropathologica2021

Neuronal spreading and plaque induction of intracellular Aβ and its disruption of Aβ homeostasis.

Tomas T Roos, Megg G Garcia, Isak Martinsson, Rana Mabrouk, Bodil Israelsson, Tomas Deierborg, Asgeir Kobro-Flatmoen, Heikki Tanila, Gunnar K Gouras

Open access · hybridAbstract read
In one paragraph

Article in Acta neuropathologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 53 citations in OpenAlex.

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  5. Multiscale Organization of Neural Networks in a 3D Bioprinted Matrix.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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 3 institutions in 3 countries.

Tomas T RoosExperimental Dementia Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden. tomas.roos@med.lu.se.
Megg G GarciaExperimental Dementia Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Isak MartinssonExperimental Dementia Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Rana MabroukA. I. Virtanen Institute, University of Eastern Finland, Kuopio, Finland.
Bodil IsraelssonExperimental Dementia Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Tomas DeierborgExperimental Neuroinflammation Laboratory, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Asgeir Kobro-FlatmoenKavli Institute for Systems Neuroscience, Trondheim, Norway.
Heikki TanilaA. I. Virtanen Institute, University of Eastern Finland, Kuopio, Finland.
Gunnar K GourasExperimental Dementia Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden. gunnar.gouras@med.lu.se.ORCID 0000-0002-5500-6325
Lund University · SEUniversity of Eastern Finland · FINorwegian Environment Agency · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The amyloid-beta peptide (Aβ) is thought to have prion-like properties promoting its spread throughout the brain in Alzheimer's disease (AD). However, the cellular mechanism(s) of this spread remains unclear. Here, we show an important role of intracellular Aβ in its prion-like spread. We demonstrate that an intracellular source of Aβ can induce amyloid plaques in vivo via hippocampal injection. We show that hippocampal injection of mouse AD brain homogenate not only induces plaques, but also damages interneurons and affects intracellular Aβ levels in synaptically connected brain areas, paralleling cellular changes seen in AD. Furthermore, in a primary neuron AD model, exposure of picomolar amounts of brain-derived Aβ leads to an apparent redistribution of Aβ from soma to processes and dystrophic neurites. We also observe that such neuritic dystrophies associate with plaque formation in AD-transgenic mice. Finally, using cellular models, we propose a mechanism for how intracellular accumulation of Aβ disturbs homeostatic control of Aβ levels and can contribute to the up to 10,000-fold increase of Aβ in the AD brain. Our data indicate an essential role for intracellular prion-like Aβ and its synaptic spread in the pathogenesis of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsDisease Models, AnimalHomeostasisMiceMice, Inbred C57BLMice, TransgenicPlaque, AmyloidAmyloid beta-PeptidesAlzheimer’s diseaseAmyloidEntorhinal cortexHippocampusInterneuronsPrion-like

Identifiers

PMID34272583
PMCPMC8423700
OpenAlexW3181865734

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.