Evidence map›Paper›PMID 28003161›Full record

ArticleNeuroscience2017

Apolipoprotein E4 causes early olfactory network abnormalities and short-term olfactory memory impairments.

Katherine Y Peng, Paul M Mathews, Efrat Levy, Donald A Wilson

Abstract read
In one paragraph

Article in Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Association ofNeurology · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Older, non-demented apolipoprotein εNeurobiology of aging · 2020
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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 at 2 institutions in 1 country.

Katherine Y PengDepartment of Neuroscience & Physiology, New York University Langone Medical Center, 560 1st Avenue, 10016 New York, NY, USA; Department of Biochemistry & Molecular Pharmacology, New York University Langone Medical Center, 560 1st Avenue, 10016 New York, NY, USA. Electronic address: Katherine.Peng@med.nyu.edu.
Paul M MathewsDepartment of Psychiatry, New York University Langone Medical Center, 560 1st Avenue, 10016 New York, NY, USA; Center for Dementia Research, Nathan S. Kline Institute, 140 Old Orangeburg Road, Orangeburg, 10962 New York, USA. Electronic address: Paul.Mathews@nki.rfmh.org.
Efrat LevyDepartment of Biochemistry & Molecular Pharmacology, New York University Langone Medical Center, 560 1st Avenue, 10016 New York, NY, USA; Department of Psychiatry, New York University Langone Medical Center, 560 1st Avenue, 10016 New York, NY, USA; Center for Dementia Research, Nathan S. Kline Institute, 140 Old Orangeburg Road, Orangeburg, 10962 New York, USA. Electronic address: Efrat.Levy@nki.rfmh.org.
Donald A WilsonDepartment of Neuroscience & Physiology, New York University Langone Medical Center, 560 1st Avenue, 10016 New York, NY, USA; Department of Child & Adolescent Psychiatry, New York University Langone Medical Center, 560 1st Avenue, 10016 New York, NY, USA; Emotional Brain Institute, Nathan S. Kline Institute, 140 Old Orangeburg Road, Orangeburg, 10962 New York, USA. Electronic address: Donald.Wilson@nki.rfmh.org.
Nathan Kline Institute for Psychiatric Research · USNYU Langone Health · US

Funding

Uncovering Alzheimer's disease risk mechanisms through neuron-specific analysis of autophagy and endosomal-lysosomal functionP01AG017617 · NIA · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI NIXON, RALPH A. · 2000 to 2021
$40.0M
Training in Pharmacological SciencesT32GM066704 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BACH, ERIKA A · 2004 to 2018
$2.6M
Neuronal Protective Apolipoprotein E2-mediated endocytic and exocytic pathwaysRF1AG057517 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI LEVY, EFRAT, MATHEWS, PAUL M · 2017 to 2020
$2.4M
Modulation of Olfactory Sensory Function by Amyloid-betaR01AG037693 · NIA · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI LEVY, EFRAT, NIXON, RALPH A. · 2011 to 2015
$1.6M
NIA NIH HHS P01 AG017617NIA NIH HHS R01 AG037693NIA NIH HHS RF1 AG057517NIGMS NIH HHS T32 GM066704
6 · The paper itself

Abstract

While apolipoprotein (Apo) E4 is linked to increased incidence of Alzheimer's disease (AD), there is growing evidence that it plays a role in functional brain irregularities that are independent of AD pathology. However, ApoE4-driven functional differences within olfactory processing regions have yet to be examined. Utilizing knock-in mice humanized to ApoE4 versus the more common ApoE3, we examined a simple olfactory perceptual memory that relies on the transfer of information from the olfactory bulb (OB) to the piriform cortex (PCX), the primary cortical region involved in higher order olfaction. In addition, we have recorded in vivo resting and odor-evoked local field potentials (LPF) from both brain regions and measured corresponding odor response magnitudes in anesthetized young (6-month-old) and middle-aged (12-month-old) ApoE mice. Young ApoE4 compared to ApoE3 mice exhibited a behavioral olfactory deficit coinciding with hyperactive odor-evoked response magnitudes within the OB that were not observed in older ApoE4 mice. Meanwhile, middle-aged ApoE4 compared to ApoE3 mice exhibited heightened response magnitudes in the PCX without a corresponding olfactory deficit, suggesting a shift with aging in ApoE4-driven effects from OB to PCX. Interestingly, the increased ApoE4-specific response in the PCX at middle-age was primarily due to a dampening of baseline spontaneous activity rather than an increase in evoked response power. Our findings indicate that early ApoE4-driven olfactory memory impairments and OB network abnormalities may be a precursor to later network dysfunction in the PCX, a region that not only is targeted early in AD, but may be selectively vulnerable to ApoE4 genotype.

Indexed as

AgingAnimalsApolipoprotein E3Apolipoprotein E4Beta RhythmFemaleGene Knock-In TechniquesHumansMaleMemory DisordersMemory, Short-TermMice, Inbred C57BLMice, TransgenicMotor ActivityOlfactory BulbOlfactory PathwaysApolipoprotein E3Apolipoprotein E4apolipoprotein Elocal field potentialmemory deficitsolfactionolfactory bulbpiriform cortex

Identifiers

PMID28003161
PMCPMC5263091
OpenAlexW2567609502

What OpenQuestion holds

Textmetadata
LicenceTDM
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.