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• W1984918151 abstract "Alzheimer's disease (AD) is an epidemiologically complex disorder, in which both genetic and environmental factors play important roles contributing to disease susceptibility. Identification of these risk factors is crucial as they may provide new avenues for the identification of novel disease biomarkers as well as for the design of intervention approaches. Several novel AD susceptibility genes with small risk effects have been recently identified by employing genetic association analyses, in particular by those using a genome-wide approach. For most of the newly identified AD risk factors, however, the biological mechanisms driving these associations remain elusive, emphasizing the need for comprehensive functional characterization of these genes and for determining their relevance for AD pathogenesis. In addition, epidemiological and clinical studies have revealed that certain comorbidities often precede or cooccur with AD. These are often correlated with modifiable life-style factors potentially providing promising alternative routes to be exploited in treatment studies. For this special issue of the International Journal of Alzheimer's Disease, we invited investigators to contribute original research and review articles that stimulate efforts to identify novel molecular targets involved in AD pathogenesis. Eventually, we selected to include eight articles on the topic, which we believe to be of particular interest to the readers of the journal.The first set of four studies in this special issue elucidates a number of different genetic aspects of AD. The study by G. Hamilton et al. assessed the impact of recently identified AD genome-wide association signals on cognitive functioning in two birth cohorts from Scotland. Their strongest results implicate a haplotype at the TRAPPC6A locus in individuals lacking the APOEe4 allele. Less-pronounced effects on cognition are also observed for genetic variants in APP and BIN1. The study by L. Polito et al. investigated the potential role of SLC6A4, a serotonin transporter highly expressed in the brain, in contributing to AD risk. While they found nominally significant risk effects in their own case-control sample from Italy, combining these data with those from other groups yields a more ambiguous answer. The study by R. Dominici et al. followed a similar approach investigating the potential effects of DNA sequence variants in G protein-coupled receptor 3 (GPR3) in AD cases and controls from Italy. In agreement with recent genome-wide association studies, they found no evidence that GPR3 is involved in AD epidemiology. Finally,the paper by E. Blom et al. chose a more functionally orientated approach to AD genetics. The authors performed a genome-wide gene expression study in transgenic mouse models of AD, which suggested differences in expression patterns in genes of the Wnt pathway. Validation experiments in human brain samples confirm these findings and suggest that TCF7L2 and MYC show the largest expression differences in AD versus control subjects.The second set of studies focus on comorbidities and life-style factors that are associated with AD. In the paper by V. Leinonen et al., investigators assessed the well-known AD-related biomarkers, such as Aβ42, tau protein, and inflammatory components from the cerebrospinal fluid samples obtained from the patients of idiopathic normal pressure hydrocephalus (iNPH). As AD is the most important differential diagnosis for iNPH, brain biopsy samples obtained from NPH patients provide valuable information on pathogenic events taking place in early phase of AD. The paper by G. Pasinetti et al. summarizes the effects of caloric intake, dietary life-style and macronutrient composition on the risk of AD. More specifically, the investigators discuss how certain cardiovascular and diabetic conditions can induce an increased susceptibility for AD and provide potentialmechanisms through which this may occur. The paper by E. Tuminello et al. provides a comprehensive review related to the hypothesis of apolipoprotein E (protein: apoE; gene: APOE) antagonistic pleiotropy. The leading hypothesis is that the APOEe4 allele may be beneficial in earlier ages, while it leads to cognitive decline later in life. Finally, the last paper by V. Leduc et al. highlights the pleiotropic roles and the structure-function relationship of apoE particularly in the lipid homeostasis-related events in AD and cardiovascular diseases.Taken together, we believe that the articles included in this special issue of the International Journal of Alzheimer's Disease shed new light on a number of different aspects of AD pathogenesis. In concert with the work from hundreds of other AD laboratories worldwide, these exciting new data will hopefully translate into the identification of novel biomarkers and the development of new therapeutic strategies to efficiently diagnose and treat this devastating disorder.Mikko HiltunenLars BertramAleister J. Saunders" @default.
• W1984918151 created "2016-06-24" @default.
• W1984918151 creator A5004136948 @default.
• W1984918151 creator A5061553021 @default.
• W1984918151 creator A5082600086 @default.
• W1984918151 date "2011-01-01" @default.
• W1984918151 modified "2023-10-18" @default.
• W1984918151 title "Genetic Risk Factors: Their Function and Comorbidities in Alzheimer's Disease" @default.
• W1984918151 cites W134453782 @default.
• W1984918151 cites W139660127 @default.
• W1984918151 cites W1414030173 @default.
• W1984918151 cites W1417309998 @default.
• W1984918151 cites W1463980068 @default.
• W1984918151 cites W148236777 @default.
• W1984918151 cites W1482753335 @default.
• W1984918151 cites W1490077018 @default.
• W1984918151 cites W149726692 @default.
• W1984918151 cites W1501035907 @default.
• W1984918151 cites W152398027 @default.
• W1984918151 cites W1528661679 @default.
• W1984918151 cites W1529259401 @default.
• W1984918151 cites W1534314329 @default.
• W1984918151 cites W1539503465 @default.
• W1984918151 cites W1548248031 @default.
• W1984918151 cites W1559121591 @default.
• W1984918151 cites W1561957445 @default.
• W1984918151 cites W1563058663 @default.
• W1984918151 cites W1563590122 @default.
• W1984918151 cites W1576181724 @default.
• W1984918151 cites W1576642143 @default.
• W1984918151 cites W1577502861 @default.
• W1984918151 cites W1584077124 @default.
• W1984918151 cites W1591191431 @default.
• W1984918151 cites W1602771322 @default.
• W1984918151 cites W1603930029 @default.
• W1984918151 cites W1607399348 @default.
• W1984918151 cites W1636209651 @default.
• W1984918151 cites W1636888051 @default.
• W1984918151 cites W1644155731 @default.
• W1984918151 cites W1659662945 @default.
• W1984918151 cites W1711248712 @default.
• W1984918151 cites W1718169955 @default.
• W1984918151 cites W1758002729 @default.
• W1984918151 cites W1768446746 @default.
• W1984918151 cites W1855728914 @default.
• W1984918151 cites W1874453010 @default.
• W1984918151 cites W1896684749 @default.
• W1984918151 cites W1916894088 @default.
• W1984918151 cites W192876098 @default.
• W1984918151 cites W1936478256 @default.
• W1984918151 cites W1942904161 @default.
• W1984918151 cites W1953255974 @default.
• W1984918151 cites W1963021413 @default.
• W1984918151 cites W1963756656 @default.
• W1984918151 cites W1963791487 @default.
• W1984918151 cites W1964309555 @default.
• W1984918151 cites W1965135336 @default.
• W1984918151 cites W1965141016 @default.
• W1984918151 cites W1965263019 @default.
• W1984918151 cites W1965353755 @default.
• W1984918151 cites W1965780119 @default.
• W1984918151 cites W1966556007 @default.
• W1984918151 cites W1966650637 @default.
• W1984918151 cites W1967607566 @default.
• W1984918151 cites W1967789041 @default.
• W1984918151 cites W1967940232 @default.
• W1984918151 cites W1968012352 @default.
• W1984918151 cites W1968258479 @default.
• W1984918151 cites W1968409213 @default.
• W1984918151 cites W1968866732 @default.
• W1984918151 cites W1970045462 @default.
• W1984918151 cites W1970168335 @default.
• W1984918151 cites W1970816926 @default.
• W1984918151 cites W1971552792 @default.
• W1984918151 cites W1971763706 @default.
• W1984918151 cites W1972833727 @default.
• W1984918151 cites W1973026127 @default.
• W1984918151 cites W1973241402 @default.
• W1984918151 cites W1974754952 @default.
• W1984918151 cites W1974873409 @default.
• W1984918151 cites W1975040221 @default.
• W1984918151 cites W1975391685 @default.
• W1984918151 cites W1976046032 @default.
• W1984918151 cites W1976313368 @default.
• W1984918151 cites W1976725721 @default.
• W1984918151 cites W1976755866 @default.
• W1984918151 cites W1977141171 @default.
• W1984918151 cites W1977431443 @default.
• W1984918151 cites W1977949510 @default.
• W1984918151 cites W1978306592 @default.
• W1984918151 cites W1978684823 @default.
• W1984918151 cites W1978707951 @default.
• W1984918151 cites W1979543098 @default.
• W1984918151 cites W1979995395 @default.
• W1984918151 cites W1980375888 @default.
• W1984918151 cites W1981068018 @default.
• W1984918151 cites W1981487663 @default.
• W1984918151 cites W1982420401 @default.

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