Alzheimer's disease (AD) has a devastating impact on aged people worldwide. Although sophisticated and advanced molecular methods have been developed for its diagnosis since early phases, pharmacological treatment still represents an unresolved topic. The more the disease progresses, the more the uneffectiveness of antidementia drugs emerges. New and encouraging results from experimental works indicate that glutamate pathway may play a substantial role in the pathogenesis since early stages of the disease. Several experimental data together with the clinical use of the uncompetitive N-methyl-d-aspartate (NMDA) antagonist memantine strengthen this idea. Unfortunately, definitive data on the glutamatergic transmission involvement in AD are still incomplete. Moreover, clinical results indicate only temporarily limited effects of memantine. Currently, memantine is indicated for moderate-to-severe cases of AD, an indication that may limit its efficacy and impact on Alzheimer's dementia. The association of memantine with the acetylcholinesterase inhibitor drugs used to treat dementia symptoms appears to be beneficial, in both experimental and clinical studies. Because cholinergic and glutamatergic dysfunction occurs early in AD, the coadministration of appropriate treatment in early stages of the disease might represent a valid option from the beginning of cognitive decline. Moreover, to better evaluate drug efficacy, the association of the recently introduced biomarkers with a clinical AD profile should be considered an aim to pursue.

Ultrasonography can have a role not only in the diagnosis, but also in the severity stratification of patients with UNE.

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The results of 7 open-label clinical studies on oxcarbazepine (OXC) in different neuropathic pain conditions, sharing the same protocols, were pooled together in order to evaluate whether the results obtained in the individual trials were confirmed in the pooled analysis of this larger sample, providing more evidence for efficacy and tolerability of OXC in these conditions. Eligible patients (>18 years old) with a diagnosis of neuropathic pain were enrolled in seven open-label trials, consisting of a one-week prospective Screening Phase followed by an eight-week Treatment Phase. Treatment with OXC was initiated at 150 mg/day, and the daily dose was increased by 150 mg/day on a 2-3 day basis to the maximum tolerated dose over four weeks, up to 1800 mg/day. The primary outcome measure was the change in the actual pain rating assessed on the visual analogue scale (VAS) between the end of the Screening Phase and the end of the Treatment Phase. One hundred and thirty-six patients were enrolled in the trials. The mean VAS score dropped from 77.13 at the end of the Screening Phase to 38.41 at the end of the trial for a mean reduction of 50.2%. The percentage of responders (mean VAS score reduction > or = 50%) was 49.2%. OXC was well tolerated, with the most common adverse events consisting of vertigo, tremor, somnolence, hypotension and nausea. The results of this analysis suggest that OXC administered as monotherapy is an efficacious and safe option for the symptomatic treatment of pain associated with neuropathies.