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Dysfunction of Neuromuscular Synapses in the Genetic Model of Alzheimer’s Disease

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The function of synaptic transmission and presynaptic vesicular cycle in the neuromuscular synapses of the diaphragm was studied in transgenic APP/PS1 mice (Alzheimer’s disease model). The decrease in the quantal content of end-plate potential, intense depression of the amplitude of terminal plate potentials under conditions of lasting high frequency stimulation (50 Hz), a drastic prolongation of the synaptic vesicle recycling time in APP/PS1 mice in comparison with wild type mice were detected. Manifest dysfunction of the neuromuscular synapses, caused by disordered neurosecretion and recycling of the synaptic vesicles in the presynaptic nerve endings, was detected in the Alzheimer’s disease model on transgenic APP/PS1 mice. The study supplemented the notions on the pathogenesis of Alzheimer’s disease as a systemic disease, while the detected phenomena could just partially explain the development of motor disorders in this disease.

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Authors and Affiliations

  1. Kazan State Medical University, Kazan, Russia

    M. A. Mukhamedyarov, P. N. Grigor’ev, E. A. Ushanova, A. V. Leushina & A. L. Zefirov

  2. Kazan (Volga Region) Federal University, Kazan, Tatarstan Republic, Russia

    E. A. Ushanova & T. L. Zefirov

Authors
  1. M. A. Mukhamedyarov
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  2. P. N. Grigor’ev
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  3. E. A. Ushanova
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  4. T. L. Zefirov
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  5. A. V. Leushina
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  6. A. L. Zefirov
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Corresponding author

Correspondence to M. A. Mukhamedyarov.

Additional information

Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 165, No. 5, pp. 614-619, May, 2018

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Mukhamedyarov, M.A., Grigor’ev, P.N., Ushanova, E.A. et al. Dysfunction of Neuromuscular Synapses in the Genetic Model of Alzheimer’s Disease. Bull Exp Biol Med 165, 669–673 (2018). https://doi.org/10.1007/s10517-018-4238-z

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  • DOI: https://doi.org/10.1007/s10517-018-4238-z

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