Facial expression recognition in Alzheimer’s disease: A systematic review

Introduction: It is well established that behavioral variant frontotemporal dementia can impair social and emotional function. However, there is no consensus regarding how Alzheimer’s disease can affect facial expression recognition. We aim to systematically review all the literature addressing this issue over the last 10 years.

Method: We conducted a search based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). The search for literature was undertaken on 19 September 2017, using Pubmed, SciELO, BIREME, and Thomson Reuters Web of Science electronic databases. The key terms for the search were: Alzheimer’s disease, dementia, and facial expression recognition.

Results: We screened 173 articles, and 22 of them were selected. The most common methodology involved showing participants photographs of people expressing the six basic emotions—fear, anger, sadness, disgust, surprise, and happiness. Results were ambiguous. Among people with mild Alzheimer’s disease, happiness was easier to recognize than the other five basic emotions, with sadness and anger the most difficult to recognize. In addition, the intensity level of the emotions presented seems to be important, and facial expression recognition is related to specific cognitive capacities, including executive function and visuoperceptual abilities. Impairment in facial expression recognition does not appear to be a consistent neuropsychological finding in Alzheimer’s disease.

Conclusions: The lack of standardized assessment instruments and the heterogeneity of the methods and samples used across studies hamper comparisons. Future researches should investigate facial expression recognition through more ecological and standardized methods.     

Modelling hypercholesterolaemia in rats using high cholesterol diet

Hypercholesterolaemia is a complex condition with multiple causes, including both lifestyle and genetic aspects. It is also a risk factor for cardiovascular diseases (CVDs), which are responsible for 172 million deaths/year. Although the reasons for hypercholesterolaemia are known, there are many critical questions that remain to be answered so that new therapeutics can be developed. In order to elucidate the pathobiology of this condition, animal models can mimic the pathology of human hypercholesterolaemia. One example of an animal model is induced by the hypercholesterolaemic diet in Wistar rats. The present review first summarizes the current understanding of the metabolic profile involved in hypercholesterolaemia in humans. Next it comments about the lack of consensus as to which hypercholesterolaemia induction protocol should be used. The present work aimed to review experimental studies that induced hypercholesterolaemia in Wistar rats it was not intended to judge the “best” model, since they all achieved the goal of inducing an increase in serum cholesterol.     

Genetic Analysis of Hereditary Ataxias in Peru Identifies SCA10 Families with Incomplete Penetrance

The Cerebellum - Relative frequency of hereditary ataxias remains unknown in many regions of Latin America. We described the relative frequency in spinocerebellar ataxias (SCA) due to (CAG)n and to...     

Screening the full leucocyte receptor complex genomic region revealed associations with pemphigus that might be explained by gene regulation

Pemphigus foliaceus (PF) is a blistering autoimmune skin disease rare in most of the world but endemic in certain regions of Brazil. PF is characterized by the detachment of epidermal cells and the presence of autoantibodies against desmoglein 1. In previous studies, we have shown that genetic polymorphisms and variable expression levels of certain leucocyte receptor complex (LRC) genes were associated with PF. However, the role of the LRC on PF susceptibility remained to be investigated. Here, we analysed 527 tag single nucleotide polymorphisms (SNPs) distributed within the 1·5 Mb LRC. After quality control, a total of 176 SNPs were analysed in 229 patients with PF and 194 controls. Three SNPs were associated with differential susceptibility to PF. The intergenic variant rs465169 [odds ratio (OR) = 1·50; P = 0·004] is located in a region that might regulate several immune-related genes, including VSTM1, LILRB1/2, LAIR1/2, LILRA3/4 and LENG8. The rs35336528 (OR = 3·44; P = 0·009) and rs1865097 (OR = 0·57; P = 0·005) SNPs in LENG8 and FCAR genes, respectively, were also associated with PF. Moreover, we found four haplotypes with SNPs within the KIR3DL2/3, LAIR2 and LILRB1 genes associated with PF (P < 0·05), which corroborate previously reported associations. Thus, our results confirm the importance of the LRC for differential susceptibility to PF and reveal new markers that might influence expression levels of several LRC genes, as well as candidates for further functional studies.