Relationship between proinflammatory cytokines (Il-1beta, Il-18) and leukocyte telomere length in mild cognitive impairment and Alzheimer's disease.

Inflammation plays a crucial role in Alzheimer's disease (AD). AD neurodegeneration and concurrent involvement of the peripheral immune system may promote leukocyte division and telomere shortening. We examined genotypes and plasma levels of two proinflammatory cytokines, IL-1beta and IL-18, and leukocyte telomere length (LTL) in patients with mild cognitive impairment (MCI) and AD.

Correction to: Comprehension of written texts for the assessment of clinical competence and decision making in people with mild to moderate Alzheimer disease.

The above article was published online with missing author. The additional author is Michele Scandola.

Comprehension of written texts for the assessment of clinical competence and decision making in people with mild to moderate Alzheimer disease.

Background: Clinical competence is the term used to describe an individual's capacity to express a choice regarding their participation in clinical procedures or experimental studies. Understanding the information provided is a prerequisite but consent forms are often lengthy and complicated. Alzheimer's disease patients may be vulnerable in written comprehension, due to cognitive deficits, but unfortunately to date, a specific evaluation of this ability is not included in periodical assessments.

Leukocyte telomere length in mild cognitive impairment and Alzheimer's disease patients.

Numerous studies have reported an association between shortened leukocyte telomere length (LTL) and increased risk of Alzheimer's disease (AD). In this study we investigated the relationship between LTL and AD development, including in the analysis patients with amnestic mild cognitive impairment (aMCI), a clinical entity considered prodromal of AD. LTL (T/S ratio) was measured in patients with AD (n=61) or aMCI (n=46), and compared with LTL of age-matched controls (n=56).