Increased Expression of Presenilin 2 Inhibits Protein Synthesis

Gamliel, Amir; Teicher, Carmit; Michaelson, Daniel M.; Pradier, Laurent; Hartmann, Tobias; Beyreuther, Konrad; Stein, Reuven

doi:10.1006/mcne.2001.1068

Cited by 8 publications

(2 citation statements)

References 67 publications

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“…Our primary keyword search revealed (Table 6) that both a presenilin excess (Vezina et al, 1999; Gamliel et al, 2002; Prat et al, 2002) and deficiency (Herreman et al, 1999; Dewachter et al, 2002; Chen et al, 2008; Aoki et al, 2009; Yun et al, 2014) elevate the risk of familial AD, whereas PSEN1 underexpression can also reduce the risk of some complications of this disease. On the basis of these data, we propose 15 aforementioned SNPs as candidate markers of familial AD (Table 6).…”

Section: Resultsmentioning

confidence: 99%

Candidate SNP Markers of Familial and Sporadic Alzheimer's Diseases Are Predicted by a Significant Change in the Affinity of TATA-Binding Protein for Human Gene Promoters

Пономаренко

Chadaeva

Рассказов

et al. 2017

Front. Aging Neurosci.

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While year after year, conditions, quality, and duration of human lives have been improving due to the progress in science, technology, education, and medicine, only eight diseases have been increasing in prevalence and shortening human lives because of premature deaths according to the retrospective official review on the state of US health, 1990-2010. These diseases are kidney cancer, chronic kidney diseases, liver cancer, diabetes, drug addiction, poisoning cases, consequences of falls, and Alzheimer's disease (AD) as one of the leading pathologies. There are familial AD of hereditary nature (~4% of cases) and sporadic AD of unclear etiology (remaining ~96% of cases; i.e., non-familial AD). Therefore, sporadic AD is no longer a purely medical problem, but rather a social challenge when someone asks oneself: “What can I do in my own adulthood to reduce the risk of sporadic AD at my old age to save the years of my lifespan from the destruction caused by it?” Here, we combine two computational approaches for regulatory SNPs: Web service SNP_TATA_Comparator for sequence analysis and a PubMed-based keyword search for articles on the biochemical markers of diseases. Our purpose was to try to find answers to the question: “What can be done in adulthood to reduce the risk of sporadic AD in old age to prevent the lifespan reduction caused by it?” As a result, we found 89 candidate SNP markers of familial and sporadic AD (e.g., rs562962093 is associated with sporadic AD in the elderly as a complication of stroke in adulthood, where natural marine diets can reduce risks of both diseases in case of the minor allele of this SNP). In addition, rs768454929, and rs761695685 correlate with sporadic AD as a comorbidity of short stature, where maximizing stature in childhood and adolescence as an integral indicator of health can minimize (or even eliminate) the risk of sporadic AD in the elderly. After validation by clinical protocols, these candidate SNP markers may become interesting to the general population [may help to choose a lifestyle (in childhood, adolescence, and adulthood) that can reduce the risks of sporadic AD, its comorbidities, and complications in the elderly].

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Section: Resultsmentioning

confidence: 99%

Candidate SNP Markers of Familial and Sporadic Alzheimer's Diseases Are Predicted by a Significant Change in the Affinity of TATA-Binding Protein for Human Gene Promoters

Пономаренко

Chadaeva

Рассказов

et al. 2017

Front. Aging Neurosci.

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“…Lipin codes for a nuclear protein that plays a key role in nutrient sensing and adipocyte development (Peterfy et al 2001, Huffman et al 2002. Presenilin 2 contributes to Alzheimer's disease risk, and has been implicated in the processing of amyloid precursors (Edbauer et al 2002), control of apoptosis (Alves da Costa et al 2002), and protein synthesis (Gamliel et al 2002). Although presenilin is expressed in liver (Benkovic et al 1997), its function there has not been studied.…”

Section: Discussionmentioning

confidence: 99%

Expressions of hepatic genes, especially IGF-binding protein-1, correlating with serum corticosterone in microarray analysis

Cheng¹,

Birely²,

Lum³

et al. 2004

Journal of Molecular Endocrinology

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Microarray technology was evaluated for usefulness in assessing relationships between serum corticosterone and hepatic gene expression. Nine pairs of female Swiss mice were chosen to provide a wide range of serum corticosterone ratios; cDNA microarray analysis (∼8000 genes) was performed on their livers. A statistical method based on calculation of 99% confidence intervals discovered 32 genes which varied significantly among the livers. Five of these ratios correlated significantly with serum corticosterone ratio, including tyrosine aminotransferase, stress-induced protein, pleiotropic regulator 1 and insulin-like growth factor-binding protein-1; the latter has a potential role in cancer development. Secondly, linear regression of gene expression vs corticosterone ratios was screened for those with r ≥ 0·8 (P<0·01), yielding 141 genes, including some known to be corticosterone regulated and others of interest as possible glucocorticoid targets. Half of these significant correlations involved data sets where no microarray ratio exceeded±1·5. These results showed that microarray may be used to survey tissues for changes in gene expression related to serum hormones, and that even small changes in expression can be of statistical significance in a study with adequate numbers of replicate samples.

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Mutant presenilin 2 increased oxidative stress and p53 expression in neuronal cells

Nguyen

Lee

Hwang

et al. 2007

Biochemical and Biophysical Research Communications

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Increased Expression of Presenilin 2 Inhibits Protein Synthesis

Cited by 8 publications

References 67 publications

Candidate SNP Markers of Familial and Sporadic Alzheimer's Diseases Are Predicted by a Significant Change in the Affinity of TATA-Binding Protein for Human Gene Promoters

Candidate SNP Markers of Familial and Sporadic Alzheimer's Diseases Are Predicted by a Significant Change in the Affinity of TATA-Binding Protein for Human Gene Promoters

Expressions of hepatic genes, especially IGF-binding protein-1, correlating with serum corticosterone in microarray analysis

Mutant presenilin 2 increased oxidative stress and p53 expression in neuronal cells

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