Evidence map›Paper›PMID 30618585›Full record

ReviewFrontiers in neuroscience2018

Molecular Mechanisms of Synaptotoxicity and Neuroinflammation in Alzheimer's Disease.

Mikael Marttinen, Mari Takalo, Teemu Natunen, Rebekka Wittrahm, Sami Gabbouj, Susanna Kemppainen, Ville Leinonen, Heikki Tanila, Annakaisa Haapasalo, Mikko Hiltunen

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

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  17. Roles of Non-Coding RNA in Alzheimer's Disease Pathophysiology.International journal of molecular sciences · 2023
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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

10 authors at 2 institutions in 1 country.

Mikael MarttinenInstitute of Biomedicine, University of Eastern Finland, Kuopio, Finland.
Mari TakaloInstitute of Biomedicine, University of Eastern Finland, Kuopio, Finland.
Teemu NatunenInstitute of Biomedicine, University of Eastern Finland, Kuopio, Finland.
Rebekka WittrahmInstitute of Biomedicine, University of Eastern Finland, Kuopio, Finland.
Sami GabboujInstitute of Biomedicine, University of Eastern Finland, Kuopio, Finland.
Susanna KemppainenInstitute of Biomedicine, University of Eastern Finland, Kuopio, Finland.
Ville LeinonenInstitute of Clinical Medicine - Neurosurgery, University of Eastern Finland, Kuopio, Finland.
Heikki TanilaA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
Annakaisa HaapasaloA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
Mikko HiltunenInstitute of Biomedicine, University of Eastern Finland, Kuopio, Finland.
University of Eastern Finland · FIKuopio University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disorder, which is clinically associated with a global cognitive decline and progressive loss of memory and reasoning. According to the prevailing amyloid cascade hypothesis of AD, increased soluble amyloid-β (Aβ) oligomer levels impair the synaptic functions and augment calcium dyshomeostasis, neuroinflammation, oxidative stress as well as the formation of neurofibrillary tangles at specific brain regions. Emerging new findings related to synaptic dysfunction and initial steps of neuroinflammation in AD have been able to delineate the underlying molecular mechanisms, thus reinforcing the development of new treatment strategies and biomarkers for AD beyond the conventional Aβ- and tau-targeted approaches. Particularly, the identification and further characterization of disease-associated microglia and their RNA signatures, AD-associated novel risk genes, neurotoxic astrocytes, and in the involvement of complement-dependent pathway in synaptic pruning and loss in AD have set the outstanding basis for further preclinical and clinical studies. Here, we discuss the recent development and the key findings related to the novel molecular mechanisms and targets underlying the synaptotoxicity and neuroinflammation in AD.

Indexed as

Alzheimer’s diseasemicroglianeuroinflammationsynaptotoxicitytriggering receptor expressed on myeloid cells 2

Identifiers

PMID30618585
PMCPMC6301995
OpenAlexW2904723669

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.