Evidence map›Paper›PMID 37525358›Full record

ArticleNeuropathology : official journal of the Japanese Society of Neuropathology2024

Senile plaque-associated transactive response DNA-binding protein 43 in Alzheimer's disease: A case report spanning 16 years of memory loss.

Arenn F Carlos, Shunsuke Koga, Neill R Graff-Radford, Matthew C Baker, Rosa Rademakers, Owen A Ross, Dennis W Dickson, Keith A Josephs

Open access · greenAbstract readCase Reports
In one paragraph

Article in Neuropathology : official journal of the Japanese Society of Neuropathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Review
  3. 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

8 authors at 3 institutions in 2 countries.

Arenn F CarlosDepartment of Neurology, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0002-2100-5033
Shunsuke KogaDepartment of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA.ORCID https://orcid.org/0000-0001-8868-9700
Neill R Graff-RadfordDepartment of Neurology, Mayo Clinic, Jacksonville, Florida, USA.
Matthew C BakerDepartment of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA.
Rosa RademakersVIB Center for Molecular Neurology, VIB, Antwerp, Flanders, Belgium.
Owen A RossDepartment of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA.
Dennis W DicksonDepartment of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA.
Keith A JosephsDepartment of Neurology, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0003-2930-8634
Jacksonville College · USMayo Clinic · USUniversity of Antwerp · BE

Funding

Understanding the role of TDP-43 in Alzheimers disease and FTLDR01AG037491 · NIA · MAYO CLINIC ROCHESTER · PI JOSEPHS, KEITH A · 2010 to 2024
$6.5M
NIA NIH HHS R01 AG037491
6 · The paper itself

Abstract

Transactive response DNA-binding protein 43 (TDP-43) pathological inclusions are found in frontotemporal lobar degeneration (FTLD-TDP) and Alzheimer's disease (AD-TDP). While clinically different, TDP-43 inclusions in FTLD-TDP and AD can have similar morphological characteristics. However, TDP-43 colocalizing with tau and forming "apple-bite" or "flame-shaped" neuronal cytoplasmic inclusions (NCI) are only found in AD-TDP. Here, we describe a case with AD and neuritic plaque-associated TDP-43. The patient was a 96-year-old right-handed Caucasian woman who had developed a slowly progressive amnestic syndrome compatible with typical AD at age 80. Genetic testing revealed APOE ε3/ε4, GRN r5848 CT, and MAPT H1/H2 genotype. Consistent with the old age at onset and long disease duration, limbic-predominant AD was found at autopsy, with high hippocampal yet low cortical neurofibrillary tangle (NFT) counts. Hippocampal and amygdala sclerosis were present. Immunohistochemistry for phospho-TDP-43 showed NCIs, dystrophic neurites, and rare neuronal intranuclear inclusions consistent with FTLD-TDP type A, as well as tau NFT-associated TDP-43 inclusions. These were frequent in the amygdala, entorhinal cortex, hippocampus, occipitotemporal gyrus, and inferior temporal gyrus but sparse in the mid-frontal cortex. Additionally, there were TDP-43-immunoreactive inclusions forming plaque-like structures in the molecular layer of the dentate fascia of the hippocampus. The presence of neuritic plaques in the same region was confirmed using thioflavin-S fluorescent microscopy and immunohistochemistry for phospho-tau. Double labeling immunofluorescence showed colocalization of TDP-43 and tau within neuritic plaques. Other pathologies included mild Lewy body pathology predominantly affecting the amygdala and olfactory bulb, aging-related tau astrogliopathy, and mixed small vessel disease (arteriolosclerosis and amyloid angiopathy) with several cortical microinfarcts. In conclusion, we have identified TDP-43 colocalizing with tau in neuritic plaques in AD, which expands the association of TDP-43 and tau in AD beyond NFTs. The clinical correlate of this plaque-associated TDP-43 appears to be a slowly progressive amnestic syndrome.

Indexed as

Alzheimer DiseaseFrontotemporal DementiaFrontotemporal Lobar DegenerationAged, 80 and overDNA-Binding ProteinsFemaleHumansMemory DisordersPlaque, AmyloidDNA-Binding ProteinsAD‐TDPcase reportFTLD‐TDPlimbic‐predominant ADneuritic plaque‐associated TDP‐43

Identifiers

PMID37525358
PMCPMC10828111
OpenAlexW4385441981

What OpenQuestion holds

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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.