Evidence map›Paper›PMID 40108701›Full record

ArticleAlzheimer's research & therapy2025

Tau-PET pathology in the subregions of the amygdala and its associations with cognitive performance and neuropsychiatric symptoms in autosomal dominant Alzheimer's disease.

Catarina Tristão-Pereira, Stephanie Langella, Justin S Sanchez, Vincent Malotaux, Bing He, Jorge Alcina, Jairo E Martinez, Zoe Rubinstein, Ana Baena, Clara Vila-Castelar and 10 more

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
  2. Article
  3. The Amygdala and Politics.Brain sciences · 2026
    Review
  4. Neurotransmitter Systems in Alzheimer's Disease.Current issues in molecular biology · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Defining the contributions of tau pathology in the amygdala to increasing depressive symptoms in aging.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  9. 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

20 authors.

Catarina Tristão-Pereira *Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Stephanie Langella *Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Justin S SanchezMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Vincent MalotauxMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Bing HeMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Jorge AlcinaMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Jairo E MartinezMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Zoe RubinsteinMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Ana BaenaGrupo de Neurociencias de Antioquia, Universidad de Antioquia, Medellin, Colombia.
Clara Vila-CastelarMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Averi GiudicessiMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Liliana Ramirez GomezMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Claudia RamosGrupo de Neurociencias de Antioquia, Universidad de Antioquia, Medellin, Colombia.
Daniel VasquezGrupo de Neurociencias de Antioquia, Universidad de Antioquia, Medellin, Colombia.
David AguillonGrupo de Neurociencias de Antioquia, Universidad de Antioquia, Medellin, Colombia.
Heidi I L JacobsMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Reisa A SperlingMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Keith JohnsonMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Jennifer R GatchelMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Yakeel T QuirozMassachusetts General Hospital, Harvard Medical School, Boston, MA, USA. yquiroz@mgh.harvard.edu.

Funding

Tracking the origin of tau pathology: dovetailing (pre-)preclinical biomarker trajectoriesR01AG062559 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Heidi Irma Jacobs · 2019 to 2026
$4.8M
The wandering nerve: gateway to boost Alzheimer's disease related cognitive performanceR01AG068062 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI JACOBS, HEIDI IRMA · 2021 to 2025
$4.6M
Locus coeruleus network architecture of Alzheimer's disease vulnerabilityR01AG082006 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Heidi Irma Jacobs, Jorge Sepulcre · 2023 to 2026
$2.7M
Elevated locus coeruleus metabolism as mechanism driving Alzheimer's disease pathologyR21AG074220 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI JACOBS, HEIDI IRMA · 2021 to 2022
$477k
NIA NIH HHS R01 AG062559NIA NIH HHS R01 AG068062NIA NIH HHS R01 AG082006NIA NIH HHS R21 AG074220
6 · The paper itself

Abstract

backgroundThe amygdala plays a role in behavior and emotional response and is vulnerable to Alzheimer's disease (AD) pathology, yet little is known about amygdala tau accumulation before clinical symptom onset. To investigate whether certain amygdala nuclei are particularly vulnerable to degeneration and might underlie early neuropsychiatric symptoms in AD, we aimed to characterize subregional amygdala tau pathology and its correlates associations with established biomarkers of early AD and cognitive-behavioral measures in Presenilin-1 E280A mutation carriers of autosomal dominant AD.

methodsParticipants included 25 cognitively unimpaired mutation carriers and 37 non-carrier family members from the Colombia-Boston (COLBOS) Biomarker Study. Measures included 18F-flortaucipir, 11C-Pittsburgh compound B, Consortium to Establish a Registry for Alzheimer's Disease Word List Learning, Trail Making Test, Geriatric Depression Scale, and Geriatric Anxiety Inventory. We examined group differences in amygdala tau levels (whole amygdala, lateral nucleus and basal nucleus) and analyzed tau associations with disease markers and clinical measures.

resultsAmygdala tau levels were higher in unimpaired carriers compared to non-carriers. Among carriers, the basal nucleus showed a greater tau burden than the lateral nucleus, and tau accumulation correlated with closer estimated age to clinical onset and increased cortical amyloid. Additionally, tau in both the basal and lateral amygdala was associated with poorer working memory, lower executive function and greater depressive symptoms. However, amygdala tau did not correlate with symptoms of anxiety. Notably, tau levels in the basal amygdala differentiated carriers from non-carriers, with higher predictive accuracy when neuropsychiatric measures were included.

conclusionsThese findings suggest that in autosomal dominant AD, tau accumulation in the amygdala begins early in the basal nucleus, while both the basal and the lateral nuclei are associated with early cognitive deficits and depressive symptoms. The nuclei's differential vulnerability to pathology underscores the importance of investigating tau spread within amygdala-associated networks, relative to the early clinical manifestations of AD. This study reinforces the potential of amygdala tau burden as a valuable biomarker for preclinical AD.

Indexed as

Alzheimer DiseaseAmygdalatau ProteinsAdultAgedAniline CompoundsCognitionFemaleHumansMaleMiddle AgedMutationNeuropsychological TestsPositron-Emission TomographyPresenilin-1Aniline CompoundsMAPT protein, humanPresenilin-1PSEN1 protein, humantau ProteinsAmygdalaAutosomal-dominant Alzheimer’s diseaseNeuropsychiatric symptomsPET imagingTau pathology

Identifiers

PMID40108701
PMCPMC11924723

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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.