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Related Experiment Video

Updated: Jan 8, 2026

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Basic Science and Pathogenesis.

Metin Yesiltepe1, Luciano D'Adamio1

  • 1Rutgers Biomedical and Health Sciences, Newark, NJ, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
PubMed
Summary

Familial Danish Dementia (FDD) model rats show increased synaptic excitability and impaired long-term potentiation (LTP) with age. The App δ58 allele did not improve these synaptic deficits in FDD rats.

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Neurodegenerative Diseases

Background:

  • Familial Danish Dementia (FDD) is linked to a heterozygous Itm2b mutation.
  • Previous research identified increased basal synaptic transmission (BST) in young FDD knock-in (KI) rats.
  • Limited data exists on age-related long-term potentiation (LTP) changes and the influence of the App δ58 allele.

Purpose of the Study:

  • To investigate age-related synaptic alterations in FDD-KI rats.
  • To evaluate the impact of the App δ58 allele on synaptic function in FDD models.
  • To characterize changes in basal synaptic transmission (BST) and long-term potentiation (LTP) over time.

Main Methods:

  • Electrophysiological recordings (BST and LTP) were performed on hippocampal slices from 7-month-old FDD-KI/Apph/h rats.

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  • FDD-KI rats were crossed with Appδ58/h rats to assess the App δ58 allele's effects.
  • Recordings included basal synaptic transmission (BST), fiber volley (FV) amplitude, and short-term potentiation (STP).

    • Main Results:

    • 7-month-old FDD-KI/Apph/h rats exhibited increased BST and elevated fiber volley (FV) amplitude compared to controls.
    • Long-term potentiation (LTP), including early (E-LTP) and late phases (L-LTP), was significantly impaired in aged FDD-KI/Apph/h rats.
    • The App δ58 allele did not rescue the observed LTP deficits in FDD-KI/Appδ58/h rats, despite similar increases in BST and FV.

    Conclusions:

    • Synaptic excitability increases with age in the FDD rat model.
    • Progressive impairments in LTP are evident with aging in FDD-KI rats.
    • The Itm2b mutation's impact on hippocampal function persists, and the App δ58 allele does not ameliorate LTP deficits.