Impaired Spike Timing Dependent Cortico-Cortical Plasticity in Alzheimer's Disease Patients

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Abstract

Background: Mechanisms of cortical plasticity have been recently investigated in Alzheimer's disease (AD) patients with transcranial magnetic stimulation protocols showing a clear impairment of long-Term potentiation (LTP) cortical-like plasticity mechanisms. Objective: We aimed to investigate mechanisms of cortico-cortical spike-Timing dependent plasticity (STDP) in AD patients investigating the connections between posterior parietal cortex (PPC) and primary motor cortex (M1). Methods: We used a cortico-cortical paired associative stimulation (cc-PAS) protocol to repeatedly activate the connection between PPC and M1 of the left-dominant hemisphere in a sample of fifteen AD patients and ten age-matched healthy subjects. PPC transcranial magnetic stimulation preceded (ccPAS +5) or followed M1 stimulation (ccPAS-5) by 5 ms. Motor-evoked potentials (MEPs) were collected to assess the time course of the after effects of cc-PAS protocol measuring MEP amplitude as index of cortico-cortical associative plasticity. Results: In healthy subjects, ccPAS-5 protocol induced the expected long-lasting increase of MEP amplitude compatible with LTP-like cortical plasticity while PAS +5 protocol induced the opposite effect. AD patients did not show any significant modification of the amplitude of MEP after both ccPAS protocols. Conclusions: Our study shows that in AD patients the time-locked activation of human cortico-cortical connections is not able to form STDP, reflecting an impairment of a multi-factor plasticity process.

Original languageEnglish
Pages (from-to)983-991
Number of pages9
JournalJournal of Alzheimer's Disease
Volume66
Issue number3
DOIs
Publication statusPublished - Jan 1 2018

Fingerprint

Motor Evoked Potentials
Alzheimer Disease
Parietal Lobe
Transcranial Magnetic Stimulation
Long-Term Potentiation
Healthy Volunteers
Motor Cortex

Keywords

  • Alzheimer's disease
  • connectivity
  • long-Term potentiation
  • motor cortex
  • parietal cortex
  • plasticity
  • spike-Timing dependent plasticity

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Psychology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health

Cite this

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title = "Impaired Spike Timing Dependent Cortico-Cortical Plasticity in Alzheimer's Disease Patients",
abstract = "Background: Mechanisms of cortical plasticity have been recently investigated in Alzheimer's disease (AD) patients with transcranial magnetic stimulation protocols showing a clear impairment of long-Term potentiation (LTP) cortical-like plasticity mechanisms. Objective: We aimed to investigate mechanisms of cortico-cortical spike-Timing dependent plasticity (STDP) in AD patients investigating the connections between posterior parietal cortex (PPC) and primary motor cortex (M1). Methods: We used a cortico-cortical paired associative stimulation (cc-PAS) protocol to repeatedly activate the connection between PPC and M1 of the left-dominant hemisphere in a sample of fifteen AD patients and ten age-matched healthy subjects. PPC transcranial magnetic stimulation preceded (ccPAS +5) or followed M1 stimulation (ccPAS-5) by 5 ms. Motor-evoked potentials (MEPs) were collected to assess the time course of the after effects of cc-PAS protocol measuring MEP amplitude as index of cortico-cortical associative plasticity. Results: In healthy subjects, ccPAS-5 protocol induced the expected long-lasting increase of MEP amplitude compatible with LTP-like cortical plasticity while PAS +5 protocol induced the opposite effect. AD patients did not show any significant modification of the amplitude of MEP after both ccPAS protocols. Conclusions: Our study shows that in AD patients the time-locked activation of human cortico-cortical connections is not able to form STDP, reflecting an impairment of a multi-factor plasticity process.",
keywords = "Alzheimer's disease, connectivity, long-Term potentiation, motor cortex, parietal cortex, plasticity, spike-Timing dependent plasticity",
author = "{Di Lorenzo}, Francesco and Viviana Ponzo and Caterina Motta and Sonia Bonn{\`i} and Silvia Picazio and Carlo Caltagirone and Marco Bozzali and Alessandro Martorana and Giacomo Koch",
year = "2018",
month = "1",
day = "1",
doi = "10.3233/JAD-180503",
language = "English",
volume = "66",
pages = "983--991",
journal = "Journal of Alzheimer's Disease",
issn = "1387-2877",
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T1 - Impaired Spike Timing Dependent Cortico-Cortical Plasticity in Alzheimer's Disease Patients

AU - Di Lorenzo, Francesco

AU - Ponzo, Viviana

AU - Motta, Caterina

AU - Bonnì, Sonia

AU - Picazio, Silvia

AU - Caltagirone, Carlo

AU - Bozzali, Marco

AU - Martorana, Alessandro

AU - Koch, Giacomo

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Background: Mechanisms of cortical plasticity have been recently investigated in Alzheimer's disease (AD) patients with transcranial magnetic stimulation protocols showing a clear impairment of long-Term potentiation (LTP) cortical-like plasticity mechanisms. Objective: We aimed to investigate mechanisms of cortico-cortical spike-Timing dependent plasticity (STDP) in AD patients investigating the connections between posterior parietal cortex (PPC) and primary motor cortex (M1). Methods: We used a cortico-cortical paired associative stimulation (cc-PAS) protocol to repeatedly activate the connection between PPC and M1 of the left-dominant hemisphere in a sample of fifteen AD patients and ten age-matched healthy subjects. PPC transcranial magnetic stimulation preceded (ccPAS +5) or followed M1 stimulation (ccPAS-5) by 5 ms. Motor-evoked potentials (MEPs) were collected to assess the time course of the after effects of cc-PAS protocol measuring MEP amplitude as index of cortico-cortical associative plasticity. Results: In healthy subjects, ccPAS-5 protocol induced the expected long-lasting increase of MEP amplitude compatible with LTP-like cortical plasticity while PAS +5 protocol induced the opposite effect. AD patients did not show any significant modification of the amplitude of MEP after both ccPAS protocols. Conclusions: Our study shows that in AD patients the time-locked activation of human cortico-cortical connections is not able to form STDP, reflecting an impairment of a multi-factor plasticity process.

AB - Background: Mechanisms of cortical plasticity have been recently investigated in Alzheimer's disease (AD) patients with transcranial magnetic stimulation protocols showing a clear impairment of long-Term potentiation (LTP) cortical-like plasticity mechanisms. Objective: We aimed to investigate mechanisms of cortico-cortical spike-Timing dependent plasticity (STDP) in AD patients investigating the connections between posterior parietal cortex (PPC) and primary motor cortex (M1). Methods: We used a cortico-cortical paired associative stimulation (cc-PAS) protocol to repeatedly activate the connection between PPC and M1 of the left-dominant hemisphere in a sample of fifteen AD patients and ten age-matched healthy subjects. PPC transcranial magnetic stimulation preceded (ccPAS +5) or followed M1 stimulation (ccPAS-5) by 5 ms. Motor-evoked potentials (MEPs) were collected to assess the time course of the after effects of cc-PAS protocol measuring MEP amplitude as index of cortico-cortical associative plasticity. Results: In healthy subjects, ccPAS-5 protocol induced the expected long-lasting increase of MEP amplitude compatible with LTP-like cortical plasticity while PAS +5 protocol induced the opposite effect. AD patients did not show any significant modification of the amplitude of MEP after both ccPAS protocols. Conclusions: Our study shows that in AD patients the time-locked activation of human cortico-cortical connections is not able to form STDP, reflecting an impairment of a multi-factor plasticity process.

KW - Alzheimer's disease

KW - connectivity

KW - long-Term potentiation

KW - motor cortex

KW - parietal cortex

KW - plasticity

KW - spike-Timing dependent plasticity

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JF - Journal of Alzheimer's Disease

SN - 1387-2877

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