26 research outputs found
3D kinematic analysis of neck movement in control subjects: reliability of the procedure
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Progression to dementia in a population with amnestic mild cognitive impairment: clinical variables associated with conversion
No full textDriving habits in patients with dementia: a report from Alzheimer’s disease assessment units in northern Italy
No full textThe aim of this study was to characterize the driving
behavior of a sample of patients with dementia.
Demographic and clinical characteristics and parameters considered to be the most significant predictors of driving ability were collected. Of the total 198 patients enrolled, 172 were still driving. Many subjects (30-65%) were found to have modified their driving habits (reducing driving time and mileage, avoiding driving at night and during rush hours, sticking to familiar routes). The patients’ own rating of their driving ability was significantly higher than their care-givers’ rating (51% versus 29%). Crash history was not a significant variable. The patients’ restriction of their driving increased significantly (p<0.01) with age and increasing worsening of cognitive, functional and behavioral variables. In the absence of a gold standard for determining fitness to drive, the patients’ driving habits were self-regulated and, in particular, regulated by their caregivers. Age and
degree of dementia can be considered among the best predictors of driving safety
Driving ability in patients with dementia: report from Alzheimr's dementia assessment units in Northern Italy
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Mitochondrial alterations, oxidative stress and neuroinflammation in Alzheimer's disease
No full textAlzheimer's disease (AD) is a multifactorial disorder characterized by the progressive deterioration of neuronal networks. The primary cause and sequence of its progression are only partially understood but abnormalities in folding and accumulation of insoluble proteins such as beta-amyloid and Tau-protein are both associated with the pathogenesis of AD. Mitochondria play a crucial role in cell survival and death, and changes in mitochondrial structure and/or function are related to many human diseases. Increasing evidence suggests that compromised mitochondrial function contributes to the aging process and thus may increase the risk of AD. Dysfunctional mitochondria contribute to reactive oxygen species which can lead to extensive macromolecule oxidative damage and the progression of amyloid pathology. Oxidative stress and amyloid toxicity leave neurons chemically vulnerable. The mitochondrial toxicity induced by beta-amyloid is still not clear but may include numerous mechanisms, such as the increased permeability of mitochondrial membranes, the disruption of calcium homeostasis, the alteration of oxidative phosphorylation with a consequent overproduction of reactive oxygen species. Other mechanisms have been associated with the pathophysiology of AD. Inflammatory changes are observed in AD brain overall, particularly at the amyloid deposits, which are rich in activated microglia. Once stimulated, the microglia release a wide variety of pro-inflammatory mediators including cytokines, complement components and free radicals, all of which potentially contribute to further neuronal dysfunction and eventually death. Clinically, novel approaches to visualize early neuroinflammation in the human brain are needed to improve the monitoring and control of therapeutic strategies that target inflammatory and other pathological mechanisms. Similarly, there is growing interest in developing agents that modulate mitochondrial functio
