BACE1 inhibition by microdose lithium formulation NP03 rescues memory loss and early stage amyloid neuropathology

Wilson, E N; Do Carmo, S; Iulita, M F; Hall, H; Ducatenzeiler, A; Marks, A R; Allard, S; Jia, D T; Windheim, J; Cuello, A C

doi:10.1038/tp.2017.169

Cited by 56Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchCholinesterase and Neurodegenerative Diseases

BACE1 inhibition by microdose lithium formulation NP03 rescues memory loss and early stage amyloid neuropathology

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Wilson, E N, Do Carmo, S, Iulita, M F, Hall, H, Ducatenzeiler, A, Marks, A R, Allard, S, Jia, D T +2 more·2017·Translational Psychiatry

DOI 10.1038/tp.2017.169PMC PMC5611736

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Abstract

Lithium is first-line therapy for bipolar affective disorder and has recently been shown to have protective effects in populations at risk for Alzheimer's disease (AD). However, the mechanism underlying this protection is poorly understood and consequently limits its possible therapeutic application in AD. Moreover, conventional lithium formulations have a narrow therapeutic window and are associated with a severe side effect profile. Here we evaluated a novel microdose formulation of lithium, coded NP03, in a well-characterized rat model of progressive AD-like amyloid pathology. This formulation allows microdose lithium delivery to the brain in the absence of negative side effects. We found that NP03 rescued key initiating components of AD pathology, including inactivating GSK-3β, reducing BACE1 expression and activity, and reducing amyloid levels. Notably, NP03 rescued memory loss, impaired CRTC1 promoter binding of synaptic plasticity genes and hippocampal neurogenesis. These results raise the possibility that NP03 be of therapeutic value in the early or preclinical stages of AD.

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Chronic exposure to lithium chloride slows cognitive decline and histopathological alterations associated with reduced BACE1 activity in animal trials.
“Two recent animal trials used chronic exposure to lithium chloride–a therapeutic agent approved for major psychiatric disorders–and showed slowdown of cognitive decline and histopathological alterations associated with reduced BACE1 activity (109,110).”
From The β-Secretase BACE1 in Alzheimer’s Disease (2021) · cites this paper as [110]

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Heinrich, A., von der Heyde, A. S., Böer, U., et al. (2012) · Cellular Signalling · doi:10.1016/j.cellsig.2012.09.016 · Cited by 20 · see citing works
Stimulation by lithium of the interaction between the transcription factor CREB and its co-activator TORC
Heinrich, A., Böer, U., Tzvetkov, M. V., et al. (2008) · Bioscience Reports · doi:10.1042/bsr20080116 · Cited by 20 · see citing works

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The β-Secretase BACE1 in Alzheimer’s Disease
Hampel, H., Vassar, R., De Strooper, B., Hardy, J., Willem, M., Singh, N., Zhou, J., Yan, R., Vanmechelen, E., De Vos, A., et al. (2021) · Biological Psychiatry · doi:10.1016/j.biopsych.2020.02.001 · Cited by 694 · see citing works
Early intraneuronal amyloid triggers neuron-derived inflammatory signaling in APP transgenic rats and human brain
Welikovitch, L. A., Do Carmo, S., Maglóczky, Z., Malcolm, J. C., Lőke, J., Klein, W. L., Freund, T., & Cuello, A. C. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1914593117 · Cited by 116 · see citing works
Self-citation

Authors: Wilson, E. N., Do Carmo, S., Iulita, M. F., Hall, H., Ducatenzeiler, A., Marks, A. R., Allard, S., Jia, D. T., Windheim, J., & Cuello, A. C.
Affiliations: McGill University (CA)
Corresponding author: Cuello, A C
ORCID: Wilson, E N
Iulita, M F
Marks, A R
Cuello, A C
Venue: Translational Psychiatry
Publisher: Springer Science and Business Media LLC
Published: 2017-08-01
Volume: 7
Issue: 8
Pages: e1190-e1190
ISSN: 2158-3188 (ISSN-L)
DOI: 10.1038/tp.2017.169
PMC: PMC5611736
OpenAlex: W2739769016
Cited by: 56
References: 77
Citations by year: 2026: 6 · 2025: 8 · 2024: 9 · 2023: 5 · 2022: 3 · 2021: 5 · 2020: 7 · 2019: 8 · 2018: 4 · 2017: 1
FWCI: 4.01
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by-nc-nd
creativecommons.org/licenses/by-nc-nd/4.0 (tdm)
creativecommons.org/licenses/by-nc-nd/4.0 (vor)
Locations: Translational Psychiatry (publishedVersion, cc-by-nc-nd)
Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
PubMed Central (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
Funders: Consortium canadien en neurodégénérescence associée au vieillissement
Alzheimer Society
Merck Canada
Canadian Institutes of Health Research (102752)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Health Sciences › Medicine › Pharmacology › Cholinesterase and Neurodegenerative Diseases
Keywords: lithium, BACE1 inhibition, Alzheimer's disease, amyloid pathology, memory loss, CRTC1, hippocampal neurogenesis, preclinical Alzheimer's disease, rat model
MeSH terms: Alzheimer Disease, Animals, Female, Hippocampus, Lithium, Male, Memory, Memory Disorders, Amyloid beta-Peptides, Aspartic Acid Endopeptidases, Neuroprotective Agents, Rats, Amyloid Precursor Protein Secretases, Neurogenesis, Rats, Transgenic

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BACE1 inhibition by microdose lithium formulation NP03 rescues memory loss and early stage amyloid neuropathology

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