Evidence map›Paper›PMID 32493457›Full record

ReviewTranslational neurodegeneration2020

The human olfactory system in two proteinopathies: Alzheimer's and Parkinson's diseases.

Isabel Ubeda-Bañon, Daniel Saiz-Sanchez, Alicia Flores-Cuadrado, Ernesto Rioja-Corroto, Melania Gonzalez-Rodriguez, Sandra Villar-Conde, Veronica Astillero-Lopez, Juan Pablo Cabello-de la Rosa, Maria Jose Gallardo-Alcañiz, Julia Vaamonde-Gamo and 5 more

Open access · goldAbstract readReview
In one paragraph

Review in Translational neurodegeneration, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 6 pooled it
4.5field-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

66 citing papers in PubMed, 6 syntheses or guidelines pooled it, 128 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Greater Motor and Nonmotor Burden at Diagnosis Is Associated With Amyloid Copathology in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026
    Article
  8. Article
  9. Article
  10. Article
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  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Olfactory receptors and human diseases.Cell and tissue research · 2025
    Review
  18. Article
  19. Opposite causal effects of type 2 diabetes and metformin on Alzheimer's disease.The journal of prevention of Alzheimer's disease · 2025
    Article
  20. Review

6 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

15 authors at 3 institutions in 1 country.

Isabel Ubeda-BañonNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, 13005, Ciudad Real, Spain.
Daniel Saiz-SanchezNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, 13005, Ciudad Real, Spain.
Alicia Flores-CuadradoNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, 13005, Ciudad Real, Spain.
Ernesto Rioja-CorrotoNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, 13005, Ciudad Real, Spain.
Melania Gonzalez-RodriguezNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, 13005, Ciudad Real, Spain.
Sandra Villar-CondeNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, 13005, Ciudad Real, Spain.
Veronica Astillero-LopezNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, 13005, Ciudad Real, Spain.
Juan Pablo Cabello-de la RosaNeurology Service, Ciudad Real General University Hospital, 13005, Ciudad Real, Spain.
Maria Jose Gallardo-AlcañizNeurology Service, Ciudad Real General University Hospital, 13005, Ciudad Real, Spain.
Julia Vaamonde-GamoNeurology Service, Ciudad Real General University Hospital, 13005, Ciudad Real, Spain.
Fernanda Relea-CalatayudPathology Service, Ciudad Real General University Hospital, 13005, Ciudad Real, Spain.
Lucia Gonzalez-LopezPathology Service, Ciudad Real General University Hospital, 13005, Ciudad Real, Spain.
Alicia Mohedano-MorianoFaculty of Health Sciences, University of Castilla-La Mancha, Talavera de la Reina, Spain.
Alberto RabanoNeuropathology Department and Tissue Bank, CIEN Foundation, Carlos III Health Institute, Madrid, Spain.
Alino Martinez-MarcosNeuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, University of Castilla-La Mancha, 13005, Ciudad Real, Spain. Alino.Martinez@uclm.es.ORCID 0000-0003-3691-3605
University of Castilla-La Mancha · ESHospital General Universitario de Ciudad Real · ESInstituto de Salud Carlos III · ES

Funding

Junta de Comunidades de Castilla-La Mancha SBPLY/17/180501/000430Secretaría de Estado de Investigación, Desarrollo e Innovación SAF2016-75768-R
6 · The paper itself

Abstract

Alzheimer's and Parkinson's diseases are the most prevalent neurodegenerative disorders. Their etiologies are idiopathic, and treatments are symptomatic and orientated towards cognitive or motor deficits. Neuropathologically, both are proteinopathies with pathological aggregates (plaques of amyloid-β peptide and neurofibrillary tangles of tau protein in Alzheimer's disease, and Lewy bodies mostly composed of α-synuclein in Parkinson's disease). These deposits appear in the nervous system in a predictable and accumulative sequence with six neuropathological stages. Both disorders present a long prodromal period, characterized by preclinical signs including hyposmia. Interestingly, the olfactory system, particularly the anterior olfactory nucleus, is initially and preferentially affected by the pathology. Cerebral atrophy revealed by magnetic resonance imaging must be complemented by histological analyses to ascertain whether neuronal and/or glial loss or neuropil remodeling are responsible for volumetric changes. It has been proposed that these proteinopathies could act in a prion-like manner in which a misfolded protein would be able to force native proteins into pathogenic folding (seeding), which then propagates through neurons and glia (spreading). Existing data have been examined to establish why some neuronal populations are vulnerable while others are resistant to pathology and to what extent glia prevent and/or facilitate proteinopathy spreading. Connectomic approaches reveal a number of hubs in the olfactory system (anterior olfactory nucleus, olfactory entorhinal cortex and cortical amygdala) that are key interconnectors with the main hubs (the entorhinal-hippocampal-cortical and amygdala-dorsal motor vagal nucleus) of network dysfunction in Alzheimer's and Parkinson's diseases.

Indexed as

Alzheimer DiseaseHumansOlfaction DisordersOlfactory BulbOlfactory PathwaysParkinson DiseaseSmellAmyloid-βAnterior olfactory nucleus, hyposmiaTau proteinα-Synuclein

Identifiers

PMID32493457
PMCPMC7271529
OpenAlexW3032289835

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.