Evidence map›Paper›PMID 28011307›Full record

ArticleNeurobiology of disease2018

The olfactory bulb as the entry site for prion-like propagation in neurodegenerative diseases.

Nolwen L Rey, Daniel W Wesson, Patrik Brundin

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
171citing papers in PubMed, 10 pooled it
9.9field-weighted citation impact, top 1% 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

171 citing papers in PubMed, 10 syntheses or guidelines pooled it, 255 citations in OpenAlex.

  1. Pooled it
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  7. Radon Exposure and Neurodegenerative Disease.International journal of environmental research and public health · 2020
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  17. Glial pathology networks reveal early olfactory vulnerability in post mortem human Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  18. Olfactory decline tracks central-to-peripheral spread of tau pathology in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  19. Association between α-synuclein in plasma neuron-derived exosomes and clinical symptoms in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  20. Article

111 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

3 authors at 2 institutions in 1 country.

Nolwen L ReyCenter for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI 49503, USA. Electronic address: Nolwen.Rey@vai.org.
Daniel W WessonDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
Patrik BrundinCenter for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI 49503, USA.
Van Andel Institute · USUniversity School · US

Funding

Linking Synucleinopathy and Dysfunction of Olfactory PathwaysR01DC016519 · NIDCD · VAN ANDEL RESEARCH INSTITUTE · PI MOORE, DARREN JOHN, WESSON, DANIEL W · 2017 to 2021
$2.8M
INTER-REGIONAL CODING OF ODOR VALENCE BY NEURAL ENSEMBLESR01DC014443 · NIDCD · UNIVERSITY OF FLORIDA · PI WESSON, DANIEL W · 2015 to 2019
$2.3M
NIDCD NIH HHS R01 DC014443NIDCD NIH HHS R01 DC016519
6 · The paper itself

Abstract

Olfactory deficits are present in numerous neurodegenerative disorders and are accompanied by pathology in related brain regions. In several of these disorders, olfactory disturbances appear early and are considered as prodromal symptoms of the disease. In addition, pathological protein aggregates affect olfactory regions prior to other regions, suggesting that the olfactory system might be particularly vulnerable to neurodegenerative diseases. Exposed to the external environment, the olfactory epithelium and olfactory bulb allow pathogen and toxin penetration into the brain, a process that has been proposed to play a role in neurodegenerative diseases. Determining whether the olfactory bulb could be a starting point of pathology and of pathology spread is crucial to understanding how neurodegenerative diseases evolve. We argue that pathological changes following environmental insults contribute to the initiation of protein aggregation in the olfactory bulb, which then triggers the spread of the pathology within the brain by a templating mechanism in a prion-like manner. We review the evidence for the early involvement of olfactory structures in neurodegenerative diseases and the relationship between neuropathology and olfactory function. We discuss the vulnerability and putative underlying mechanisms by which pathology could be initiated in the olfactory bulb, from the entry of pathogens (promoted by increased permeability of the olfactory epithelium with aging or inflammation) to the sensitivity of the olfactory system to oxidative stress and inflammation. Finally, we review changes in protein expression and neural excitability triggered by pathogenic proteins that can promote pathogenesis in the olfactory bulb and beyond.

Indexed as

AnimalsHumansNeurodegenerative DiseasesOlfaction DisordersOlfactory BulbOlfactory MucosaAlpha-synucleinAlzheimer's diseaseBeta-amyloidNeuroinflammationOlfactory systemParkinson's diseaseSynucleinopathiesTauTauopathiesTDP-43

Identifiers

PMID28011307
PMCPMC5972535
OpenAlexW2563994157

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.