Francesco Di Lorenzo1, Caterina Motta1, Sonia Bonnì2, Nicola Biagio Mercuri3, Carlo Caltagirone1, Alessandro Martorana1, Giacomo Koch4. 1. Non Invasive Brain Stimulation Unit/Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy; Department of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy. 2. Non Invasive Brain Stimulation Unit/Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy. 3. Department of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy. 4. Non Invasive Brain Stimulation Unit/Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy; Stroke Unit, Tor Vergata Policlinic, Rome, Italy. Electronic address: g.koch@hsantalucia.it.
Abstract
BACKGROUND: Alzheimer's disease (AD) is characterized by a primary impairment of long-term declarative memory caused by deposition of misfolded protein aggregates. Experimental studies showed that AD neuropathological alterations impair synaptic plasticity and memory performance. Transcranial Magnetic Stimulation protocols have been recently introduced to investigate altered mechanisms of cortical plasticity in AD patients. AIM: To investigate relationship between Long-Term Potentiation (LTP)-like cortical plasticity and patients' neuropsychological performance. METHODS: We applied intermittent theta burst stimulation and extensive neuropshycological battery in 75 newly diagnosed AD patients. RESULTS: We found that LTP-like cortical plasticity impairment is selectively associated to a less efficient verbal memory (r = 0.45; p = 0.002), but not to other cognitive functions, independently from biomarkers and other demographic and clinical factors. CONCLUSION: These findings suggest that LTP-like cortical plasticity may represent a neurophysiological surrogate of memory in AD patients by evaluating the weight of pathological changes responsible for cognitive dysfunction.
BACKGROUND:Alzheimer's disease (AD) is characterized by a primary impairment of long-term declarative memory caused by deposition of misfolded protein aggregates. Experimental studies showed that AD neuropathological alterations impair synaptic plasticity and memory performance. Transcranial Magnetic Stimulation protocols have been recently introduced to investigate altered mechanisms of cortical plasticity in ADpatients. AIM: To investigate relationship between Long-Term Potentiation (LTP)-like cortical plasticity and patients' neuropsychological performance. METHODS: We applied intermittent theta burst stimulation and extensive neuropshycological battery in 75 newly diagnosed ADpatients. RESULTS: We found that LTP-like cortical plasticity impairment is selectively associated to a less efficient verbal memory (r = 0.45; p = 0.002), but not to other cognitive functions, independently from biomarkers and other demographic and clinical factors. CONCLUSION: These findings suggest that LTP-like cortical plasticity may represent a neurophysiological surrogate of memory in ADpatients by evaluating the weight of pathological changes responsible for cognitive dysfunction.
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