Evidence map›Paper›PMID 29186501›Full record

ReviewJournal of neuropathology and experimental neurology2018

The Amygdala as a Locus of Pathologic Misfolding in Neurodegenerative Diseases.

Peter T Nelson, Erin L Abner, Ela Patel, Sonya Anderson, Donna M Wilcock, Richard J Kryscio, Linda J Van Eldik, Gregory A Jicha, Zsombor Gal, Ruth S Nelson and 5 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of neuropathology and experimental neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

82 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

  1. Pooled it
  2. The Amygdala and Politics.Brain sciences · 2026
    Review
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  7. Where do PDD and DLB SYNdromes fit in neuronal alpha-SYNuclein biological frameworks?Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  8. Article
  9. Article
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  11. Article
  12. The cholinergic basal forebrain and its role in neurodegeneration.Journal of neuropathology and experimental neurology · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

22 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 2 institutions in 1 country.

Peter T NelsonDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Erin L AbnerDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Ela PatelDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Sonya AndersonDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Donna M WilcockDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Richard J KryscioDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Linda J Van EldikDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Gregory A JichaDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Zsombor GalDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Ruth S NelsonDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Bela G NelsonDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Jozsef GalDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Md Tofial AzamDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
David W FardoDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Matthew D CykowskiDivision of Neuropathology; Sanders-Brown Center on Aging; Department of Pathology; Department of Epidemiology; Department of Physiology; Department of Statistics; Department of Neurology; Department of Neuroscience; Department of Molecular and Cellular Biochemistry; Department of Biostatistics, University of Kentucky, Lexington, Kentucky; and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
University of Kentucky · USMethodist Hospital · US

Funding

University of Kentucky Alzheimer's Disease Core Center - Biomarker CoreP30AG028383 · NIA · UNIVERSITY OF KENTUCKY · PI GOLD, BRIAN TIMOTHY, VAN ELDIK, LINDA J · 2006 to 2020
$23.3M
Novel pathogenetic mechanism for hippocampal sclerosis, a common Alzheimers mimicR01AG057187 · NIA · UNIVERSITY OF KENTUCKY · PI NELSON, PETER T. · 2017 to 2021
$2.2M
CELLULAR CHANGES ALTERING SYNAPTIC CONNECTIVITY IN PRECLINICAL ADR01AG042475 · NIA · UNIVERSITY OF KENTUCKY · PI NELSON, PETER T. · 2013 to 2017
$1.5M
NIA NIH HHS P30 AG028383NIA NIH HHS R01 AG042475NIA NIH HHS R01 AG057187
6 · The paper itself

Abstract

Over the course of most common neurodegenerative diseases the amygdala accumulates pathologically misfolded proteins. Misfolding of 1 protein in aged brains often is accompanied by the misfolding of other proteins, suggesting synergistic mechanisms. The multiplicity of pathogenic processes in human amygdalae has potentially important implications for the pathogenesis of Alzheimer disease, Lewy body diseases, chronic traumatic encephalopathy, primary age-related tauopathy, and hippocampal sclerosis, and for the biomarkers used to diagnose those diseases. Converging data indicate that the amygdala may represent a preferential locus for a pivotal transition from a relatively benign clinical condition to a more aggressive disease wherein multiple protein species are misfolded. Thus, understanding of amygdalar pathobiology may yield insights relevant to diagnoses and therapies; it is, however, a complex and imperfectly defined brain region. Here, we review aspects of amygdalar anatomy, connectivity, vasculature, and pathologic involvement in neurodegenerative diseases with supporting data from the University of Kentucky Alzheimer's Disease Center autopsy cohort. Immunohistochemical staining of amygdalae for Aβ, Tau, α-synuclein, and TDP-43 highlight the often-coexisting pathologies. We suggest that the amygdala may represent an "incubator" for misfolded proteins and that it is possible that misfolded amygdalar protein species are yet to be discovered.

Indexed as

alpha-SynucleinAmygdalaAmyloid beta-PeptidesDNA-Binding ProteinsHumansNeurodegenerative DiseasesProtein Foldingtau Proteinsalpha-SynucleinAmyloid beta-PeptidesDNA-Binding ProteinsTARDBP protein, humantau ProteinsAmyloidEntorhinalHippocampusNeuropathologyProteomicsSNAPSubpial

Identifiers

PMID29186501
PMCPMC5901077
OpenAlexW2769349322

What OpenQuestion holds

Textmetadata
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.