160 research outputs found
Ubiquitin reactive dystrophic axons have a widespread distribution in Creutzfeldt-Jakob disease
Ubiquitin reactive neurites in cerebral cortex of subjects with Huntington's chorea: a possible correlate of dementia?
Balance features in Alzheimer's disease and amnestic mild cognitive impairment
Abstract. We evaluated alterations of balance by stabilometry in patients with amnestic mild cognitive impairment (aMCI) and
with mild-moderate Alzheimer’s disease (AD). Fifteen patients with aMCI and 15 with mild AD were recruited according to the
current diagnostic criteria. Fifteen healthy subjects of the same age range were recruited as controls. Stabilometry was carried out
using a commercial 4 load cell platform. Statistical analysis of between group differences was performed using one-way analysis
of variance for parametric data and Kruskal-Wallis tests for non-parametric data. Spearman correlation coefficients were used
to investigate the association between cognitive test scores and stabilometric data. All stabilometry measures were significantly
altered in mild AD patients compared to normal controls. Antero-posterior sway was found to be the most sensitive parameter,
since it correlated with the ADAS-cog orientation subscale in AD patients, and also discriminated between aMCI and normal
controls. Our study shows that impairment in balance is a feature not only of AD, but also of aMCI. The alterations found suggest
that a progressive failure of the vestibular system, possibly linked to reduced hippocampal performance, may be responsible for
such a feature. Further research must be focused on studying the predictive value of stabilometry in the conversion of aMCI
Amnestic mild cognitive impairment and conversion to Alzheimer's disease: insulin resistance and glycoxidation as early biomarker clusters.
Autopsy studies have indicated brain accumulation of amyloid-β peptides as a common pathogenetic hallmark of amnestic cognitive impairment (aMCI) and overt Alzheimer's disease (AD). The pathogenesis of AD is still debated but recent reports have even designated AD as type III diabetes. This study aims to assess plasma levels of malondialdehyde, pentosidine, and insulin resistance in a group of aMCI patients, AD subjects, and age- and gender-matched controls, to confirm, beyond the accumulation of amyloid-β, the presence of a metabolic disorder, as a causative/contributive factor for AD. Patients were recruited and diagnosed as aMCI (n = 180), AD (n = 84), and age- and gender-matched controls (n = 62) at three different Italian memory clinics. Plasma insulin and glucose, plasma pentosidine and malondialdehyde (MDA), HOMA-IR and QUICKI score for insulin sensitivities indexes were collected at the basal visit. Plasma MDA levels were higher in the aMCI group who converted to AD compared to controls, stable aMCI subjects, and AD subjects (p < 0.01) respectively, while plasma pentosidine was higher compared to controls. The aMCI group showed a significant correlation between HOMA-IR, QUICKI, insulin, and MDA (p < 0.02). aMCI might be considered the early biochemical active disease stage where glycoxidation, hyperinsulinemia, and pro-amyloidogenic status are at the highest rate while overt AD might indicate the glycoxidative cascade dwindling, ending a process possibly started two decades earlier. © 2015 - IOS Press and the authors
Alternative, non-secretase processing of Alzheimer's beta-amyloid precursor protein during apoptosis by caspase-6 and -8.
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