Evidence map›Paper›PMID 34092653›Full record

ArticleJournal of Parkinson's disease2021

The Human Hippocampus in Parkinson's Disease: An Integrative Stereological and Proteomic Study.

Sandra Villar-Conde, Veronica Astillero-Lopez, Melania Gonzalez-Rodriguez, Patricia Villanueva-Anguita, Daniel Saiz-Sanchez, Alino Martinez-Marcos, Alicia Flores-Cuadrado, Isabel Ubeda-Bañon

Open access · hybridAbstract read
In one paragraph

Article in Journal of Parkinson's disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 73 citations in OpenAlex.

  1. Increased Binding of [Synapse (New York, N.Y.) · 2026
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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

8 authors at 1 institution in 1 country.

Sandra Villar-CondeNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, Ciudad Real, Spain.
Veronica Astillero-LopezNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, Ciudad Real, Spain.
Melania Gonzalez-RodriguezNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, Ciudad Real, Spain.
Patricia Villanueva-AnguitaNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, Ciudad Real, Spain.
Daniel Saiz-SanchezNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, Ciudad Real, Spain.
Alino Martinez-MarcosNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, Ciudad Real, Spain.
Alicia Flores-CuadradoNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, Ciudad Real, Spain.
Isabel Ubeda-BañonNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, Ciudad Real, Spain.
University of Castilla-La Mancha · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundParkinson's disease (PD) is a prevalent neurodegenerative disease that is pathologically described as a six-stage α-synucleinopathy. In stage 4, α-synuclein reaches the hippocampus, inducing cognitive deficits, from which it progresses to the isocortex, leading to dementia. Among hippocampal fields, cornu ammonis 2 is particularly affected by this α-synucleinopathy and critical for cognitive decline. Volumetric studies using magnetic resonance imaging have produced controversial results, with only some reporting volume loss, whereas stereological data obtained using nonspecific markers do not reveal volume changes, neural or glial loss. Proteomic analysis has not been carried out in the hippocampus of patients with PD.

objectiveThis study aims to explain hippocampal changes in patients with PD at the cellular and proteomic levels.

methodsα-Synuclein inclusions, volume and neural (NeuN), microglial (Iba-1) and astroglial (GFAP) populations were stereologically analyzed. SWATH-MS quantitative proteomic analysis was also conducted.

resultsArea fraction fractionator probe revealed a higher area fraction α-synucleinopathy in cornu ammonis 2. No volume change, neurodegeneration, microgliosis or astrogliosis was detected. Proteomic analysis identified 1,634 proteins, of which 83 were particularly useful for defining differences among PD and non-PD groups. Among them, upregulated (PHYIP, CTND2, AHSA1 and SNTA1) and downregulated (TM163, REEP2 and CSKI1) proteins were related to synaptic structures in the diseased hippocampus.

conclusionThe distribution of α-synuclein in the hippocampus is not associated with volumetric, neural or glial changes. Proteomic analysis, however, reveals a series of changes in proteins associated with synaptic structures, suggesting that hippocampal changes occur at the synapse level during PD.

Indexed as

HippocampusParkinson Diseasealpha-SynucleinHumansProteomicsSynucleinopathiesalpha-Synucleinalpha synucleinastrocyteshippocampushumanmicroglianeuronsParkinson disease

Identifiers

PMID34092653
PMCPMC8461741
OpenAlexW3169623058

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.