Objective. To verify whether systemic biometals dysfunctions affect neurotransmission in living Alzheimer’s disease (AD) patients. Methods. We performed a case-control study using magnetoencephalography to detect sensorimotor fields of AD patients, at rest and during median nerve stimulation. We analyzed position and amount of neurons synchronously activated by the stimulation in both hemispheres to investigate the capability of the primary somatosensory cortex to reorganize its circuitry disrupted by the disease. We also assessed systemic levels of copper, ceruloplasmin, non-Cp copper (i.e., copper not bound to ceruloplasmin), peroxides, transferrin, and total antioxidant capacity. Results. Patients’ sensorimotor generators appeared spatially shifted, despite no change of latency and strength, while spontaneous activity sources appeared unchanged. Neuronal reorganization was greater in moderately ill patients, while delta activity increased in severe patients. Non-Cp copper was the only biological variable appearing to be associated with patient sensorimotor transmission. Conclusions. Our data strengthen the notion that non-Cp copper, not copper in general, affects neuronal activity in AD. Significance. High plasticity in the disease early stages in regions controlling more commonly used body parts strengthens the notion that physical and cognitive activities are protective factors against progression of dementia. 1. Introduction In the last decade, increasing evidence has revealed the role of biometals dysfunctions in Alzheimer’s disease (AD) (see [1] for a review). AD is characterized by a progressive degradation of cognitive abilities, inexorably leading to dementia, due to a gradual loss of neurons and synapses. Also sensori-motor deficits are characteristic of the disease but they usually appear in the late severe stages of the disease. Topographic and frequency changes of the sensorimotor cortex’s electro- and magneto-encephalographic activities have been observed to follow the progression of the disease [2, 3]. These changes are not attributable to lesion densities, since the density of plaques and tangles in the sensorimotor cortex of AD brains has been shown to be equivalent to that of other brain areas more specific to AD [4]. Evidently, other phenomena play a role and one of them is likely to be the sensorimotor cortex’s formidable capability to reorganize its circuitry damaged by AD degeneration into new and still healthy locations [3, 5, 6]. The aim of the present paper was to investigate reorganization within the primary sensorimotor
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