Behavioral and neural network abnormalities in human APP transgenic mice resemble those of App knock-in mice and are modulated by familial Alzheimer's disease mutations but not by inhibition of BACE1

Johnson, Erik C. B.; Ho, Kaitlyn; Yu, Gui-Qiu; Das, Melanie; Sanchez, Pascal E.; Djukic, Biljana; Lopez, Isabel; Yu, Xinxing; Gill, Michael; Zhang, Weiping; Paz, Jeanne T.; Palop, Jorge J.; Mucke, Lennart

doi:10.1186/s13024-020-00393-5

Cited by 75Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Behavioral and neural network abnormalities in human APP transgenic mice resemble those of App knock-in mice and are modulated by familial Alzheimer's disease mutations but not by inhibition of BACE1

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Johnson, Erik C. B., Ho, Kaitlyn, Yu, Gui-Qiu, Das, Melanie, Sanchez, Pascal E., Djukic, Biljana, Lopez, Isabel, Yu, Xinxing +5 more·2020·Molecular Neurodegeneration

DOI 10.1186/s13024-020-00393-5PMC PMC7489007

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Abstract

Background: Alzheimer’s disease (AD) is the most frequent and costly neurodegenerative disorder. Although diverse lines of evidence suggest that the amyloid precursor protein (APP) is involved in its causation, the precise mechanisms remain unknown and no treatments are available to prevent or halt the disease. A favorite hypothesis has been that APP contributes to AD pathogenesis through the cerebral accumulation of the amyloid-β peptide (Aβ), which is derived from APP through sequential proteolytic cleavage by BACE1 and γ-secretase. However, inhibitors of these enzymes have failed in clinical trials despite clear evidence for target engagement. Methods: To further elucidate the roles of APP and its metabolites in AD pathogenesis, we analyzed transgenic mice overexpressing wildtype human APP (hAPP) or hAPP carrying mutations that cause autosomal dominant familial AD (FAD), as well as App knock-in mice that do not overexpress hAPP but have two mouse App alleles with FAD mutations and a humanized Aβ sequence. Results: Although these lines of mice had marked differences in cortical and hippocampal levels of APP, APP C-terminal fragments, soluble Aβ, Aβ oligomers and age-dependent amyloid deposition, they all developed cognitive deficits as well as non-convulsive epileptiform activity, a type of network dysfunction that also occurs in a substantive proportion of humans with AD. Pharmacological inhibition of BACE1 effectively reduced levels of amyloidogenic APP C-terminal fragments (C99), soluble Aβ, Aβ oligomers, and amyloid deposits in transgenic mice expressing FAD-mutant hAPP, but did not improve their network dysfunction and behavioral abnormalities, even when initiated at early stages before amyloid deposits were detectable. Conclusions: hAPP transgenic and App knock-in mice develop similar pathophysiological alterations. APP and its metabolites contribute to AD-related functional alterations through complex combinatorial mechanisms that may be difficult to block with BACE inhibitors and, possibly, also with other anti-Aβ treatments.

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Humanized App knockin (KI) and APP transgenic mouse models mimic certain aspects of AD pathogenesis, including progressive amyloidosis, gliosis, and neuroinflammation, as well as network hyperexcitability and cognitive impairment, albeit to different degrees of severity across models and paradigms.
“Humanized App knockin (KI) and APP transgenic mouse models mimic certain aspects of AD pathogenesis, including progressive amyloidosis, gliosis, and neuroinflammation, as well as network hyperexcitability and cognitive impairment, albeit to different degrees of severity across models and paradigms.15-27”
From Machine learning reveals prominent spontaneous behavioral changes and treatment efficacy in humanized and transgenic Alzheimer's disease models (2024) · cites this paper as [19]
The Discussion reports abnormal Aβ accumulation, epileptiform activity, and learning and memory deficits in KI and J20 mice; the Results describe different degrees of Aβ deposition across models. The Results also report plaque-associated microgliosis in J20 mice, but do not establish gliosis or neuroinflammation in both model types, or progressive amyloidosis across them; notably, I5 mice had no detectable Aβ deposition at 9–10 months. (LLM, conf=0.86)
Experimental — accuracy not yet measured
AD-related spontaneous behavioral alterations do not require APP overexpression and are likely linked to the pathologically elevated levels of amyloid in AppNL-G-F mice.
“These results also indicate that AD-related spontaneous behavioral alterations do not require APP overexpression and are likely linked to the pathologically elevated levels of amyloid in AppNL-G-F mice.16,19”
From Machine learning reveals prominent spontaneous behavioral changes and treatment efficacy in humanized and transgenic Alzheimer's disease models (2024) · cites this paper as [19]
The Results section (‘Behavioral abnormalities observed in all three lines’) reports altered elevated-plus-maze behavior in knock-in mice, supporting the point that APP overexpression is not required. It raises Aβ or C99 as possible explanations, while the Discussion says their contributions cannot be distinguished; it does not specifically link the behavior to elevated amyloid. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Spontaneous behavioral abnormalities were age dependent and therefore tracked the progression of AD-related pathological and cognitive alterations.
“Second, spontaneous behavioral abnormalities were age dependent and therefore tracked the progression of AD-related pathological and cognitive alterations.16,19,23”
From Machine learning reveals prominent spontaneous behavioral changes and treatment efficacy in humanized and transgenic Alzheimer's disease models (2024) · cites this paper as [19]
The Results section, “Behavioral abnormalities observed in all three lines” (page not provided), reports behavioral and cognitive deficits in the mouse models, and the Discussion notes differences in when functional deficits began across lines. The paper does not show that spontaneous behavioral abnormalities changed with age in step with AD-related pathology and cognitive alterations; that tracking claim goes beyond its findings. (LLM, conf=0.82)
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“It is also worth considering Aη-α fragments in this context, which are derived from APP by η- and αsecretase cleavage and have been shown to impair synaptic and neuronal functions in acute hippocampal slices [148, 149].”
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Thalamic synchrony and dynamic regulation of global forebrain oscillations
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Alzheimer disease γ-secretase: a complex story of GxGD-type presenilin proteases
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Human Brain-Derived Aβ Oligomers Bind to Synapses and Disrupt Synaptic Activity in a Manner That Requires APP
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Astroglial Expression of Human α1-Antichymotrypsin Enhances Alzheimer-like Pathology in Amyloid Protein Precursor Transgenic Mice
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Vulnerability of Dentate Granule Cells to Disruption of Arc Expression in Human Amyloid Precursor Protein Transgenic Mice
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Decreased amyloid-β and increased neuronal hyperactivity by immunotherapy in Alzheimer's models
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Electrical Stimulation Modulates High γ Activity and Human Memory Performance
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Expression of A152T human tau causes age‐dependent neuronal dysfunction and loss in transgenic mice
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Bapineuzumab captures the N-terminus of the Alzheimer's disease amyloid-beta peptide in a helical conformation
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Overexpression of wild-type human APP in mice causes cognitive deficits and pathological features unrelated to Aβ levels
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Istradefylline reduces memory deficits in aging mice with amyloid pathology
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Reduced Sodium Channel Nav1.1 Levels in BACE1-null Mice*
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The Arctic Alzheimer mutation favors intracellular amyloid‐β production by making amyloid precursor protein less available to α‐secretase
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Anti-Aβ antibodies incapable of reducing cerebral Aβ oligomers fail to attenuate spatial reference memory deficits in J20 mice
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The Arctic mutation interferes with processing of the amyloid precursor protein
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The integration site of the APP transgene in the J20 mouse model of Alzheimer’s disease
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The β‐secretase (BACE) inhibitor NB‐360 in preclinical models: From amyloid‐β reduction to downstream disease‐relevant effects
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Navβ2 knockdown improves cognition in APP/PS1 mice by partially inhibiting seizures and APP amyloid processing
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Discrete Pools of Oligomeric Amyloid-β Track with Spatial Learning Deficits in a Mouse Model of Alzheimer Amyloidosis
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Seizures exacerbate excitatory: inhibitory imbalance in Alzheimer’s disease and 5XFAD mice
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“16,19 We also tested the role of neuroinflammation in AD-related spontaneous behavioral alterations by blocking fibrinogen-microglia interactions in 5xFAD-Fgg γ 390–396A mice.”
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Microglial extracellular vesicles induce Alzheimer’s disease-related cortico-hippocampal network dysfunction
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Mouse midbrain dopaminergic neurons survive loss of the PD-associated mitochondrial protein CHCHD2
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Excitation-inhibition imbalance disrupts visual familiarity in amyloid and non-pathology conditions
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Phenotypic Differences between the Alzheimer’s Disease-Related hAPP-J20 Model and HeterozygousZbtb20Knock-Out Mice
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CHCHD2 mutant mice link mitochondrial deficits to PD pathophysiology
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Recommendations for Preclinical Testing of Treatments Against Alzheimer’s Disease-Related Epileptiform Spikes in Transgenic Rodent Models
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Additional file 17 of Novel App knock-in mouse model shows key features of amyloid pathology and reveals profound metabolic dysregulation of microglia
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Self-citation
Additional file 1 of SNCA genetic lowering reveals differential cognitive function of alpha-synuclein dependent on sex
Brown, J. L., Hart, D. W., Boyle, G. E., Brown, T. G., LaCroix, M., Baraibar, A. M., Pelzel, R. J., Kim, M., Sherman, M. A., Boes, S., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26554280
Additional file 10 of Novel App knock-in mouse model shows key features of amyloid pathology and reveals profound metabolic dysregulation of microglia
Xia, D., Lianoglou, S., Sandmann, T., Calvert, M., Suh, J. H., Thomsen, E. R., Dugas, J. C., Pizzo, M. E., DeVos, S. L., Earr, T., et al. (2022) · Figshare · doi:10.6084/m9.figshare.20056359
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Additional file 9 of Novel App knock-in mouse model shows key features of amyloid pathology and reveals profound metabolic dysregulation of microglia
Xia, D., Lianoglou, S., Sandmann, T., Calvert, M., Suh, J. H., Thomsen, E. R., Dugas, J. C., Pizzo, M. E., DeVos, S. L., Earr, T., et al. (2022) · Figshare · doi:10.6084/m9.figshare.20056422
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Additional file 2 of SNCA genetic lowering reveals differential cognitive function of alpha-synuclein dependent on sex
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Additional file of Behavioral and neural network abnormalities in human APP transgenic mice resemble those of App knock-in mice and are modulated by familial Alzheimer’s disease mutations but not by inhibition of BACE1
Johnson, E. C. B., Ho, K., Yu, G.-Q., Das, M. M., Sanchez, P. E., Djukic, B., Lopez, I., Yu, X., Gill, M., Zhang, W., et al. (2021) · Figshare · doi:10.6084/m9.figshare.14433572
Self-citation
Behavioral and neural network abnormalities of human APP transgenic mice resemble those of App knockin mice but are not prevented by early inhibition of BACE1
Johnson, E. C. B., Ho, K., Das, M. M., Sanchez, P. E., Djukic, B., Yu, X., Álvarez, I., Gill, M., Paz, J. T., Palop, J. J., et al. (2020)
Self-citation
P1‐092: Impacts of partial reduction of BACE1 on synaptic and memory dysfunction in Alzheimer's transgenic mice
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BACE/APPV717F Double-Transgenic Mice Develop Cerebral Amyloidosis and Inflammation
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Knock-In of Human BACE1 Cleaves Murine APP and Reiterates Alzheimer-like Phenotypes
ska, K. P., Crouch, B., Koss, D. J., Robinson, L., Siebrecht, M., Riedel, G., & Platt, B. (2014) · Journal of Neuroscience · doi:10.1523/jneurosci.0433-14.2014 · Cited by 62 · see citing works

Authors: Johnson, E. C. B., Ho, K., Yu, G.-Q., Das, M., Sanchez, P. E., Djukic, B., Lopez, I., Yu, X., Gill, M., Zhang, W., Paz, J. T., Palop, J. J., & Mucke, L.
Affiliations: Gladstone Institutes (US)
Tianjin Medical University (CN)
University of California, San Francisco (US)
Corresponding author: Mucke, Lennart
ORCID: Johnson, Erik C. B.
Sanchez, Pascal E.
Yu, Xinxing
Zhang, Weiping
Paz, Jeanne T.
Palop, Jorge J.
Mucke, Lennart
Venue: Molecular Neurodegeneration
Publisher: Springer Science and Business Media LLC
Published: 2020-09-14
Volume: 15
Issue: 1
Pages: 53-53
ISSN: 1750-1326 (ISSN-L)
DOI: 10.1186/s13024-020-00393-5
PMC: PMC7489007
OpenAlex: W3084726996
Cited by: 73
References: 166
Citations by year: 2026: 6 · 2025: 10 · 2024: 11 · 2023: 16 · 2022: 15 · 2021: 14 · 2019: 1
FWCI: 6.77
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0 (tdm)
creativecommons.org/licenses/by/4.0 (vor)
Locations: Molecular Neurodegeneration (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
eScholarship (California Digital Library) (submittedVersion)
The Novartis Repository (Novartis) (submittedVersion)
Funders: National Institutes of Health (AG011385, AG054304, AG047313, AG062234, OD021717)
Ray and Dagmar Dolby Family Fund (gift)
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, amyloid precursor protein, familial Alzheimer's disease mutations, BACE1 inhibition, amyloid-beta, APP C-terminal fragments, cognitive impairment, APP knock-in mice, APP transgenic mice, amyloid deposition, anti-amyloid therapy, neural network dysfunction
MeSH terms: Alzheimer Disease, Animals, Behavior, Animal, Brain, Disease Models, Animal, Humans, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Nerve Net, Aspartic Acid Endopeptidases, Amyloid beta-Protein Precursor, Mice, Amyloid Precursor Protein Secretases, Gene Knock-In Techniques

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Behavioral and neural network abnormalities in human APP transgenic mice resemble those of App knock-in mice and are modulated by familial Alzheimer's disease mutations but not by inhibition of BACE1

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