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Updated: Jun 21, 2025

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
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Tau-mediated synaptic dysfunction is coupled with HCN channelopathy.

Despoina Goniotaki1, Francesco Tamagnini2, Luca Biasetti3

  • 1Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology & Neuroscience, Maurice Wohl Clinical Neuroscience Institute, King's College London, London, UK.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|July 12, 2024
PubMed
Summary
This summary is machine-generated.

Pathological tau in tauopathies alters hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, leading to synaptic deficits. This study links tau dysfunction to HCN channel changes, impacting neuronal function in Alzheimer's disease and mouse models.

Keywords:
dementiahyperpolarization‐activated cyclic nucleotide‐gated channelsneurodegenerationsag voltagesynapsestauopathies

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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Tauopathies, including Alzheimer's disease (AD), involve abnormal tau processing, leading to synaptic dysfunction.
  • Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are implicated in various neurodegenerative diseases.

Purpose of the Study:

  • To investigate the functional link between tau pathology and HCN channels in the context of neurodegeneration.
  • To elucidate how tau alterations impact HCN channel expression and function.

Main Methods:

  • Histological, biochemical, ultrastructural, and functional analyses were performed on hippocampal tissues.
  • Studies included post mortem Alzheimer's disease (AD) hippocampus, age-matched controls, Tau35 mice, and Tau35 primary hippocampal neurons.

Main Results:

  • Elevated expression of specific HCN channels was observed in post mortem AD hippocampus and in Tau35 mice.
  • Tau35 mice exhibited progressive abnormalities, including increased phosphorylated tau, enhanced HCN channel expression, reduced dendritic branching, and synapse density.
  • Tau35 primary neurons showed increased HCN channel expression, altered membrane voltage "sag", and changes in synaptic activity.

Conclusions:

  • Pathological tau in tauopathies directly impacts HCN channels, contributing to structural and functional synaptic deficits.
  • These findings support a model where tau-mediated changes in HCN channels drive network-wide synaptic abnormalities.