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An In Vitro Model for Studying Tau Aggregation Using Lentiviral-mediated Transduction of Human Neurons

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Soluble tau aggregates decrease the threshold for thalamic oscillations and increase the excitability of thalamic

Victoria Mitchell¹, Bruno G Frenguelli¹, Saskia Bakker¹

¹School of Life Sciences, University of Warwick, UK.

Neuropharmacology

|April 6, 2025

Summary

This summary is machine-generated.

Tau aggregates disrupt brain circuits crucial for sleep in Alzheimer's disease (AD) models. This research reveals how tau pathology in the thalamus may drive sleep disturbances and seizures in AD patients.

Keywords:

Electrophysiology Oscillations Tau Thalamus

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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein

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Published on: January 2, 2015

Area of Science:

Neuroscience
Neurodegenerative Diseases
Molecular Biology

Background:

Sleep disturbances are early symptoms in Alzheimer's disease (AD).
Cortico-thalamo-cortical (CTC) loop dysfunction is implicated in AD-related sleep issues.
Tau pathology in the thalamus and subsequent atrophy are observed in AD patients.

Purpose of the Study:

To investigate if human recombinant tau soluble aggregates induce dysfunction in thalamic circuits.
To explore the direct impact of tau aggregates on neuronal excitability and circuit activity.

Main Methods:

Electrophysiological recordings from rat corticothalamic slices.
Incubation of brain slices with human recombinant tau soluble aggregates.
Measurement of neuronal excitability and synaptic activity.

Main Results:

Tau aggregates lowered the threshold for spindle-like oscillations.
Thalamic neuron excitability was significantly increased by tau aggregates.
Enhanced frequency of miniature excitatory postsynaptic currents in ventrobasal thalamic neurons was observed.

Conclusions:

Tau aggregates promote pro-excitatory effects in thalamic circuits.
These effects may underlie CTC loop dysfunction in AD.
Tau-induced circuit changes could contribute to sleep disturbances and seizures in Alzheimer's disease.