Reversal of LTP-Like Cortical Plasticity in Alzheimer's Disease Patients with Tau-Related Faster Clinical Progression.
| Autor: | Koch, Giacomo, Di Lorenzo, Francesco, Fernandez del Olmo, Miguel, Bonní, Sonia, Ponzo, Viviana, Caltagirone, Carlo, Bozzali, Marco, Martorana, Alessandro, Del Olmo, Miguel Fernandez |
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| Předmět: |
ALZHEIMER'S disease
AMYLOID beta-protein LONG-term synaptic depression TRANSCRANIAL magnetic stimulation CEREBROSPINAL fluid COGNITION EVOKED potentials (Electrophysiology) FRONTAL lobe NEUROPSYCHOLOGICAL tests NERVE tissue proteins NEUROPLASTICITY PEPTIDES PHOSPHORYLATION PSYCHOLOGICAL tests DISEASE progression |
| Zdroj: | Journal of Alzheimer's Disease; 2016, Vol. 50 Issue 2, p605-616, 12p |
| Abstrakt: | 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. [ABSTRACT FROM AUTHOR] |
| Databáze: | Complementary Index |
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