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Broad consensus emerged on the protective role against dementia of leisure activities. Conflicting results were found for the association between dementia and putative risk factors (smoking) and protective factors (mild-to-moderate alcohol consumption, dietary antioxidants, Mediterranean diet, and living with others). However, studies varied largely in the quantification of lifestyle factors in terms of intensity, frequency and duration of exposure, and in the choice of confounders in statistical analyses. The need for standardized quantification criteria emerges, together with the current limitation in reliably tracking the past history of each patient, from childhood and young adulthood to midlife.

A substantial body of evidence supports the hypothesis of a vascular component in the pathogenesis of Alzheimer’s disease (AD). Cerebral hypoperfusion and blood-brain barrier dysfunction have been indicated as key elements of this pathway. Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder, frequent in AD, characterized by the accumulation of amyloid-β (Aβ) peptide in cerebral blood vessel walls. CAA is associated with loss of vascular integrity, resulting in impaired regulation of cerebral circulation, and increased susceptibility to cerebral ischemia, microhemorrhages, and white matter damage. Vasomotion— the spontaneous rhythmic modulation of arterial diameter, typically observed in arteries/arterioles in various vascular beds including the brain— is thought to participate in tissue perfusion and oxygen delivery regulation. Vasomotion is impaired in adverse conditions such as hypoperfusion and hypoxia. The perivascular and glymphatic pathways of Aβ clearance are thought to be driven by the systolic pulse. Vasomotion produces diameter changes of comparable amplitude, however at lower rates, and could contribute to these mechanisms of Aβ clearance. In spite of potential clinical interest, studies addressing cerebral vasomotion in the context of AD/CAA are limited. This study reviews the current literature on vasomotion, and hypothesizes potential paths implicating impaired cerebral vasomotion in AD/CAA. Aβ and oxidative stress cause vascular tone dysregulation through direct effects on vascular cells, and indirect effects mediated by impaired neurovascular coupling. Vascular tone dysregulation is further aggravated by cholinergic deficit and results in depressed cerebrovascular reactivity and (possibly) impaired vasomotion, aggravating regional hypoperfusion and promoting further Aβ and oxidative stress accumulation.

BackgroundSince the first well-known electrocardiogram (ECG) delineator based on Wavelet Transform (WT) presented by Li et al. in 1995, a significant research effort has been devoted to the exploitation of this promising method. Its ability to reliably delineate the major waveform components (mono- or bi-phasic P wave, QRS, and mono- or bi-phasic T wave) would make it a suitable candidate for efficient online processing of ambulatory ECG signals. Unfortunately, previous implementations of this method adopt non-linear operators such as root mean square (RMS) or floating point algebra, which are computationally demanding.MethodsThis paper presents a 32-bit integer, linear algebra advanced approach to online QRS detection and P-QRS-T waves delineation of a single lead ECG signal, based on WT.ResultsThe QRS detector performance was validated on the MIT-BIH Arrhythmia Database (sensitivity Se = 99.77%, positive predictive value P+ = 99.86%, on 109010 annotated beats) and on the European ST-T Database (Se = 99.81%, P+ = 99.56%, on 788050 annotated beats). The ECG delineator was validated on the QT Database, showing a mean error between manual and automatic annotation below 1.5 samples for all fiducial points: P-onset, P-peak, P-offset, QRS-onset, QRS-offset, T-peak, T-offset, and a mean standard deviation comparable to other established methods.ConclusionsThe proposed algorithm exhibits reliable QRS detection as well as accurate ECG delineation, in spite of a simple structure built on integer linear algebra.

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