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Cited by 63Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

A longitudinal multimodal in vivo molecular imaging study of the 3xTg-AD mouse model shows progressive early hippocampal and taurine loss

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Chiquita, Samuel, Ribeiro, Mário, Castelhano, João, Oliveira, Francisco, Sereno, José, Batista, Marta, Abrunhosa, Antero, Rodrigues-Neves, Ana C +6 more·2019·Human Molecular Genetics
DOI 10.1093/hmg/ddz045PMC PMC6586150
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Abstract

The understanding of the natural history of Alzheimer's disease (AD) and temporal trajectories of in vivo molecular mechanisms requires longitudinal approaches. A behavioral and multimodal imaging study was performed at 4/8/12 and 16 months of age in a triple transgenic mouse model of AD (3xTg-AD). Behavioral assessment included the open field and novel object recognition tests. Molecular characterization evaluated hippocampal levels of amyloid β (Aβ) and hyperphosphorylated tau. Magnetic resonance imaging (MRI) included assessment of hippocampal structural integrity, blood-brain barrier (BBB) permeability and neurospectroscopy to determine levels of the endogenous neuroprotector taurine. Longitudinal brain amyloid accumulation was assessed using 11C Pittsburgh compound B positron emission tomography (PET), and neuroinflammation/microglia activation was investigated using 11C-PK1195. We found altered locomotor activity at months 4/8 and 16 months and recognition memory impairment at all time points. Substantial early reduction of hippocampal volume started at month 4 and progressed over 8/12 and 16 months. Hippocampal taurine levels were significantly decreased in the hippocampus at months 4/8 and 16. No differences were found for amyloid and neuroinflammation with PET, and BBB was disrupted only at month 16. In summary, 3xTg-AD mice showed exploratory and recognition memory impairments, early hippocampal structural loss, increased Aβ and hyperphosphorylated tau and decreased levels of taurine. In sum, the 3xTg-AD animal model mimics pathological and neurobehavioral features of AD, with early-onset recognition memory loss and MRI-documented hippocampal damage. The early-onset profile suggests temporal windows and opportunities for therapeutic intervention, targeting endogenous neuroprotectors such as taurine.

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  • Previous studies have demonstrated significant functional and structural changes in the hippocampus in AD, which are likely due to impaired neurogenesis.

    “Previous studies have demonstrated significant functional and structural changes in the hippocampus in AD, which are likely due to impaired neurogenesis (Mu and Gage, 2011; Chiquita et al., 2019).”

    From Multimodal MRI combined with RNA sequencing reveals pathological signatures in the 9-month-old 3×Tg-AD mouse brain (2026) · cites this paper as Chiquita et al., 2019

    The Discussion reports hippocampal structural differences and recognition-memory impairment in 3xTg-AD mice, and notes evidence of hippocampal atrophy in AD patients. It does not attribute these changes to impaired neurogenesis; the proposed mechanism in the cited discussion is intraneuronal Aβ accumulation. The paper’s direct findings are also in a mouse model, not patients with AD. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Hippocampal neurogenesis plays a crucial role in structural plasticity and cognitive deficits observed in AD mouse models.

    “Hippocampal neurogenesis plays a crucial role in structural plasticity and cognitive deficits observed in AD mouse models, which prompted our focus on this specific region.”

    From Multimodal MRI combined with RNA sequencing reveals pathological signatures in the 9-month-old 3×Tg-AD mouse brain (2026) · cites this paper as Chiquita et al., 2019

    The Discussion (page not provided) links hippocampal structural differences in 3xTg-AD mice with object-recognition impairment. It does not examine hippocampal neurogenesis or establish that neurogenesis plays a crucial role in those changes; searches for neurogenesis, neural stem cells, and plasticity found no supporting passage. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Brain-wide volume measurements have yielded inconsistent results in the 3×Tg-AD model, with some studies reporting volumetric changes and others finding no significant differences.

    “Although most studies have reported volumetric changes throughout various brain regions over time (including both decreases and increases) (Kong et al., 2018; Chiquita et al., 2019; Rollins et al., 2019; Güell-Bosch et al., 2020), others have found no significant differences in brain volume between 3×Tg-AD mice and controls (Kastyak-Ibrahim et al., 2013; Wu et al., 2015; Montoliu-Gaya et al., 2018”

    From Multimodal MRI combined with RNA sequencing reveals pathological signatures in the 9-month-old 3×Tg-AD mouse brain (2026) · cites this paper as Chiquita et al., 2019

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Authors
Chiquita, S., Ribeiro, M., Castelhano, J., Oliveira, F., Sereno, J., Batista, M., Abrunhosa, A., Rodrigues-Neves, A. C., Carecho, R., Baptista, F., Gomes, C., Moreira, P. I., Ambrósio, A. F., & Castelo-Branco, M.
Affiliations
  • University of Coimbra (PT)
  • Coimbra Institute for Clinical and Biomedical Research, Faculty of Medicine, University of Coimbra, Coimbra, Portugal
  • Centro de Neurociências e Biologia Celular (PT)
Corresponding author
  • Ambrósio, António F
  • Castelo-Branco, Miguel
ORCID
Venue
Human Molecular Genetics
Publisher
Oxford University Press (OUP)
Published
2019-02-28
Volume
28
Issue
13
Pages
2174-2188
ISSN
  • 0964-6906 (ISSN-L)
  • 1460-2083
DOI
10.1093/hmg/ddz045
PMC
PMC6586150
OpenAlex
W2919929253
Cited by
63
References
11
Citations by year
2026: 10 · 2025: 7 · 2024: 5 · 2023: 8 · 2022: 10 · 2021: 13 · 2020: 9 · 2019: 1
FWCI
5.66
Type
journal article
Language
en
Open access
Licence
Locations
  • Human Molecular Genetics (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
  • Centro 2020 Regional Operational Programme (CENTRO-01-0145-FEDER-000016, CENTRO-01-0145-FEDER-000008)
  • COMPETE-FEDER (POCI-01-0145-FEDER-016428, POCI-01-0145-FEDER-007440)
  • Foundation for Science and Technology (SAICTPAC/0010/2015, UID/NEU/04539/2013, SFRH/BD/52045/2012)
  • Santa Casa Mantero Belard Award 2015 (MB-1049-2015)
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, 3xTg-AD mice, hippocampal atrophy, taurine, amyloid-beta, hyperphosphorylated tau, blood-brain barrier permeability, neuroinflammation, microglial activation, recognition memory impairment, locomotor activity, neuroprotective agents
MeSH terms
Alzheimer Disease, Animals, Blood-Brain Barrier, Disease Models, Animal, Hippocampus, Inflammation, Longitudinal Studies, Magnetic Resonance Imaging, Male, Memory Disorders, Mice, Inbred C57BL, Mice, Transgenic, Taurine, Biomarkers, Amyloid beta-Peptides, tau Proteins, Microglia, Maze Learning, Mice, Presenilin-1, Molecular Imaging, Multimodal Imaging

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