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J Alzheimers Dis. 2016;50(2):605-16. doi: 10.3233/JAD-150813.

Reversal of LTP-Like Cortical Plasticity in Alzheimer's Disease Patients with Tau-Related Faster Clinical Progression.

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Non Invasive Brain Stimulation Unit/Department of Behavioural and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy.
Stroke Unit, Department of Neuroscience, Tor Vergata Policlinic, Rome, Italy.
Faculty of Sciences of Sport and Physical Education, Department of Physical Education, University of A Coruña, Pazos-Liáns, Oleiros, A Coruña, Spain.
Neuroimaging Laboratory, Santa Lucia Foundation, IRCCS, Rome, Italy.


Cerebrospinal fluid (CSF) concentrations of amyloid-β (Aβ), total tau (t-tau), and phosphorylated tau proteins are associated with different clinical progression in Alzheimer's disease (AD). We enrolled forty newly diagnosed AD patients, who underwent lumbar puncture, and carried out a K-means cluster analysis based on CSF biomarkers levels, resulting in two AD patient groups: Cluster 1 showed relatively high levels of Aβ and low levels of tau; Cluster 2 showed relatively low levels of Aβ and high levels of tau. Cortical plasticity was tested using the intermittent and continuous theta burst stimulation (iTBS and cTBS) protocols evoking respectively long-term potentiation (LTP) and depression (LTD). Cholinergic transmission was tested by the short-latency afferent inhibition protocol. Neurophysiological evaluation showed that the two AD groups differed in terms of cortical plasticity: after iTBS, Cluster 2 patients showed a remarkable reversal of LTP toward LTD that was not observed in Cluster 1. LTD and central cholinergic transmission did not differ between groups. Patients were assessed longitudinally with Mini-Mental State Examination at 6, 12, and 18 month follow-ups. Cluster 2 AD had a faster cognitive decline already evident at the 12 month follow-up. High tau CSF levels were associated with LTD-like cortical plasticity and faster clinical progression. These results suggest that more aggressive tau pathology is associated with prominent LTD-like mechanisms of cortical plasticity and faster cognitive decline.


Alzheimer’s disease; amyloid-beta; cortical plasticity; long-term depression; long-term potentiation; tau; transcranial magnetic stimulation

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