ArticlePsychopharmacology2026
Photostimulation of locus coeruleus CA1 catecholaminergic terminals reversed Spatial memory impairment in an alzheimer's disease mouse model.
Article in Psychopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- The monoaminergic systems as drivers of Alzheimer's disease pathophysiology and symptomatology.Current opinion in neurology · 2026Review
- A locus coeruleus-centric framework for novelty, salience, and gamma oscillations: implications for neurostimulation, aging, and disease.Frontiers in aging neuroscience · 2026Article
- Research progress on the role of the locus coeruleus in cognitive function.Frontiers in human neuroscience · 2026Review
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Authors and funding
4 authors.
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Abstract
rationaleOne of the earliest changes associated with Alzheimer's disease (AD) is the loss of catecholaminergic terminals in the cortex and hippocampus originating from the Locus Coeruleus (LC). This decline leads to reduced catecholaminergic neurotransmitters in the hippocampus, affecting synaptic plasticity and spatial memory. However, it is unclear whether restoring catecholaminergic transmission in the terminals from the LC may alleviate the spatial memory deficits associated with AD.
objectivesThis study aims to investigate the effects of optogenetic stimulation of LC catecholaminergic projections on alleviating spatial memory and synaptic plasticity deficits associated with AD.
methodsWe conducted experiments using a 12-month-old 3xTgAD mouse model (AD-TH) that expresses Cre recombinase under the control of the tyrosine hydroxylase (TH) gene. This model enabled us to photostimulate the terminals from the LC in the hippocampal CA1 region before performing two different spatial memory tasks and inducing long-term plasticity.
resultsOptogenetic stimulation successfully reversed the impairment of spatial memory retrieval in aging AD-TH mice. Furthermore, this stimulation restored levels of catecholaminergic neurotransmitters in the hippocampus and enhanced synaptic plasticity, as demonstrated by a long-term potentiation (LTP) protocol.
conclusionsThese findings suggest a critical role for the LC-hippocampal CA1 catecholaminergic circuitry in disrupting synaptic plasticity and the spatial memory deficits characteristic of the early stages of AD. The study highlights the potential for targeting LC catecholaminergic pathways as a therapeutic strategy to improve cognitive deficits experienced by AD patients.
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