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Semantic Variant of Primary Progressive Aphasia (svPPA) has often been considered as a loss of knowledge stored in semantic memory, but might also be due to a general disruption of mechanisms allowing the acquisition, storage, and retrieval of semantic memories. In order to assess any parallelism in svPPA patients between loss of semantic knowledge and inability to acquire new semantic information, we administered a battery of semantic learning tasks to healthy individuals and svPPA patients, where they were requested to learn new conceptual representations and new word forms, and to associate the former with the latter. A strong relation was found between loss of semantic knowledge and disruption of semantic learning: (a) patients with severe svPPA had the lowest scores in the semantic learning tasks; (b) significant correlations were found between scores obtained in semantic learning tasks and scores obtained in semantic memory disorders in svPPA patients.

We performed an actigraphic assessment of sleep characteristics in healthy subjects and patients with cognitive impairment. Thirty subjects were included and classified into controls (10 subjects), mild cognitive impairment (10 patients) and mild-to-moderate Alzheimer’s disease (10 patients). Sleep quality was assessed using the Pittsburgh Sleep Quality Index. Participants had a 7-day actigraphic record. Sleep parameters collected were time in bed, total sleep time, sleep efficiency, sleep latency, wakefulness after sleep onset, number of awakenings, and mean motor activity. Significant differences between mild cognitive impairment and controls patients were found for sleep latency (p = 0.05); Alzheimer’s disease patients had significantly worse scores for Pittsburgh Sleep Quality Index (p = 0.01), time in bed (p = 0.001), total sleep time (p = 0.04), sleep latency, sleep efficiency, motor activity (p = 0.0001) and wakefulness after sleep onset (p = 0.001) compared to controls. When comparing Alzheimer’s disease and mild cognitive impairment, differences were significant for sleep latency (p = 0.01), wakefulness after sleep onset (p = 0.004), sleep efficiency, number of awakenings and motor activity (p = 0.0001). In addition to showing a high prevalence of sleep alterations in subjects with cognitive impairment, our data suggest that they are evident from the earliest stages of cognitive decline. Further studies are needed to assess whether early correction of sleep alterations can positively influence the evolution of cognitive impairment. The opportunity to provide clinically meaningful information with a simple assessment of sleep characteristics based on actigraphy suggests that wider use of the approach in patients with cognitive decline should be considered.

Alzheimer’s disease (AD) and Multiple Sclerosis (MS) represent an emerging health problem on a global scale, as they are responsible for a significant contribution to the burden of disability in Western countries. Limited numbers of cerebrospinal fluid (CSF) diagnostic markers are available for each disease (amyloid and tau deposition markers for AD and oligoclonal bands for MS) representing mostly state markers that provide few, if any, clues about the severity of the clinical phenotype. α-CGRP is a neuropeptide implied in nociception, vasodilation, synaptic plasticity and immune functions. This neuropeptide is expressed in encephalic regions connected to memory, attention, autonomic and behavioral functions and is also expressed by spinal motor neurons. The present work confronted α-CGRP levels between 19 AD, 27 MS and 17 control subjects using an ELISA/EIA assay. We measured higher CSF α-CGRP contents in control subjects with respect to AD, as shown in previous studies, as well as in MS patients in comparison to AD. The control subjects and MS patients did not significantly differ between each other. We did not observe a relationship between CSF protein content, albumin quotient and α-CGRP. We also describe, retrospectively, an association between higher CSF CGRP content and higher MRI overall lesion count in MS and between lower α-CGRP and worse attention and visuo-perceptual skills in AD. We speculate that α-CGRP could be differentially involved in both disabling diseases.