The Italian–German meeting ‘Neurodegeneration and energy metabolism: from chemistry to clinics’ was hosted last Spring in the wonderful Villa Vigoni, close to the Como lake. Within the tradition of these meetings, about 30 scientists, biochemists and neurologists, deeply dissected the biochemical mechanisms of neurodegeneration and their pathophysiological role, actively exchanging ideas between basic and clinical science. Some particularly hot topics emerged during discussion and are reported here.

Parkinson's disease (PD) is the second most frequent neurodegenerative disorder. The clinical picture of the disease consists of a typical triad of motor symptoms – tremor, bradikinesia and rigidity – which impair the ability of parkinsonian patients to execute voluntary movements in an appropriate manner. The pathological substrate of the disease is the progressive loss of dopaminergic neurons of the substantia nigra pars compacta (SNc) projecting to the corpus striatum. SNc and striatum are part of the basal ganglia nuclei whose primary task is to allow the proper execution of voluntary movements. SNc cell loss and resulting dopaminergic denervation of the striatum trigger a cascade of functional changes in the basal ganglia circuitry, ultimately leading to hyperactivity of the subthalamic nucleus (STN) – the only excitatory (glutamatergic) nucleus of the circuit – which keeps the basal ganglia output nuclei under direct control.1 This alteration is now recognized as the neural substrate for PD motor symptoms, but there is also increasing evidence that subthalamic hyperactivity or, more in general, increased glutamatergic tone within the circuit, may contribute to the neurodegenerative process underlying the disease.

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