Evidence map›Paper›PMID 26861289›Full record

ReviewInternational journal of molecular sciences2016

Genetic and Transcriptomic Profiles of Inflammation in Neurodegenerative Diseases: Alzheimer, Parkinson, Creutzfeldt-Jakob and Tauopathies.

Irene López González, Paula Garcia-Esparcia, Franc Llorens, Isidre Ferrer

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
–field-weighted citation impact
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

50 citing papers in PubMed.

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  16. Repurposing Pomalidomide as a Neuroprotective Drug: Efficacy in an Alpha-Synuclein-Based Model of Parkinson's Disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
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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

4 authors.

Irene López GonzálezInstitute of Neuropathology, Bellvitge University Hospital, IDIBELL, Barcelona 08034, Spain. ilopez@idibell.cat.
Paula Garcia-EsparciaInstitute of Neuropathology, Bellvitge University Hospital, IDIBELL, Barcelona 08034, Spain. pgarcia@idibell.cat.
Franc LlorensInstitute of Neuropathology, Bellvitge University Hospital, IDIBELL, Barcelona 08034, Spain. franc.llorens@gmail.com.
Isidre FerrerInstitute of Neuropathology, Bellvitge University Hospital, IDIBELL, Barcelona 08034, Spain. 8082ifa@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polymorphisms in certain inflammatory-related genes have been identified as putative differential risk factors of neurodegenerative diseases with abnormal protein aggregates, such as sporadic Alzheimer's disease (AD) and sporadic Parkinson's disease (sPD). Gene expression studies of cytokines and mediators of the immune response have been made in post-mortem human brain samples in AD, sPD, sporadic Creutzfeldt-Jakob disease (sCJD) subtypes MM1 and VV2, Pick's disease (PiD), progressive supranuclear palsy (PSP) and frontotemporal lobar degeneration linked to mutation P301L in MAPT Frontotemporal lobar degeneration-tau (FTLD-tau). The studies have disclosed variable gene regulation which is: (1) disease-dependent in the frontal cortex area 8 in AD, sPD, sCJD MM1 and VV2, PiD, PSP and FTLD-tau; (2) region-dependent as seen when comparing the entorhinal cortex, orbitofrontal cortex, and frontal cortex area 8 (FC) in AD; the substantia nigra, putamen, FC, and angular gyrus in PD, as well as the FC and cerebellum in sCJD; (3) genotype-dependent as seen considering sCJD MM1 and VV2; and (4) stage-dependent as seen in AD at different stages of disease progression. These observations show that regulation of inflammation is much more complicated and diverse than currently understood, and that new therapeutic approaches must be designed in order to selectively act on specific targets in particular diseases and at different time points of disease progression.

Indexed as

Genetic Predisposition to DiseaseTranscriptomeAlzheimer DiseaseBiomarkersBrainCreutzfeldt-Jakob SyndromeDiagnosis, DifferentialDisease ProgressionGene Expression RegulationGenetic Association StudiesHumansInflammationNeurodegenerative DiseasesParkinson DiseaseProtein Aggregation, PathologicalRisk FactorsBiomarkersRNA, MessengerAlzheimer’s diseasechemokinescomplementCreutzfeldt-Jakob’s diseasecytokinesinflammationmicrogliaParkinson’s diseasetauopathiestoll-like receptors

Identifiers

PMID26861289
PMCPMC4783939

What OpenQuestion holds

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Registered trials

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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.