Cited by 36Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Human amygdala involvement in Alzheimer's disease revealed by stereological and dia‐PASEF analysis

Open access
Gonzalez‐Rodriguez, Melania, Villar‐Conde, Sandra, Astillero‐Lopez, Veronica, Villanueva‐Anguita, Patricia, Ubeda‐Banon, Isabel, Flores‐Cuadrado, Alicia, Martinez‐Marcos, Alino, Saiz‐Sanchez, Daniel·2023·Brain Pathology

Abstract

Alzheimer's disease (AD) is characterized by the accumulation of pathological amyloid‐β (Aβ) and Tau proteins. According to the prion‐like hypothesis, both proteins can seed and disseminate through brain regions through neural connections and glial cells. The amygdaloid complex (AC) is involved early in the disease, and its widespread connections with other brain regions indicate that it is a hub for propagating pathology. To characterize changes in the AC as well as the involvement of neuronal and glial cells in AD, a combined stereological and proteomic analysis was performed in non‐Alzheimer's disease and AD human samples. The synaptic alterations identified by proteomic data analysis could be related to the volume reduction observed in AD by the Cavalieri probe without neuronal loss. The pathological markers appeared in a gradient pattern with the medial region (cortical nucleus, Co) being more affected than lateral regions, suggesting the relevance of connections in the distribution of the pathology among different brain regions. Generalized astrogliosis was observed in every AC nucleus, likely related to deposits of pathological proteins. Astrocytes might mediate phagocytic microglial activation, whereas microglia might play a dual role since protective and toxic phenotypes have been described. These results highlight the potential participation of the amygdala in the disease spreading from/to olfactory areas, the temporal lobe and beyond. Proteomic data are available via ProteomeXchange with identifier PXD038322.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1111/bpa.13180

Cites

65 of 65 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Among the most upregulated DEGs, higher amounts of MMP3, IBSP, or TAGLN in the brain have been linked to increased risk of AD.

    “Among the most upregulated DEGs, higher amounts of MMP3 (52), IBSP (53), or TAGLN (54) in the brain have been linked to increased risk of AD.”

    From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [54]

    Table 2 in the Results lists TAGLN (transgelin) as an upregulated protein in AD amygdala samples, with a fold change of 1.82. The paper reports differential protein expression, not TAGLN as an upregulated DEG, and does not establish that higher TAGLN increases the risk of developing AD. Citation (54) is attached to TAGLN, so the MMP3 and IBSP claims are not assessed here. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

2 of the 67 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. [36]Mai JK, Paxinos G, Voss T. Atlas of the human brain. San Diego, CA: Academic Press; 2007.

Cited by

Sorted by citations

Authors
Gonzalez‐Rodriguez, M., Villar‐Conde, S., Astillero‐Lopez, V., Villanueva‐Anguita, P., Ubeda‐Banon, I., Flores‐Cuadrado, A., Martinez‐Marcos, A., & Saiz‐Sanchez, D.
Affiliations
  • Neuroplasticity and Neurodegeneration Laboratory, CRIB, Ciudad Real Medical School University of Castilla‐La Mancha Ciudad Real Spain
  • University of Castilla-La Mancha (ES)
Venue
Brain Pathology
Publisher
Wiley
Published
2023-06-18
Volume
33
Issue
5
Pages
e13180-e13180
ISSN
  • 1015-6305 (ISSN-L)
  • 1750-3639
OpenAlex
W4381110661
Cited by
36
References
67
Citations by year
2026: 13 · 2025: 13 · 2024: 9 · 2023: 1
FWCI
6.39
Type
journal article
Language
en
Open access
Locations
  • Brain Pathology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • RUIdeRA - Institutional University Repository (University of Castilla-La Mancha) (submittedVersion, other-oa)
Funders
  • Ministerio de Ciencia e Innovación (PID2019‐108659RB‐I00)
  • Ministerio de Economía y Competitividad (SAF2016‐75768‐R)
  • European Regional Development Fund (2021‐GRIN‐31233)
  • European Social Fund
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, amygdala, amyloid-beta, tau protein, stereology, astrocyte activation, astrocytes, microglia, synaptic changes, olfactory bulb, temporal lobe, human brain tissue
MeSH terms
Alzheimer Disease, Amygdala, Brain, Humans, Amyloid beta-Peptides, tau Proteins, Microglia, Proteomics

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review