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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Age of Onset

 
 
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Disease relevance of Age of Onset

 

Psychiatry related information on Age of Onset

 

High impact information on Age of Onset

  • A related challenge is to determine the degree to which each pathogenic variant impairs ABCR function, as genotype-phenotype analyses indicate that age of onset and disease severity correlate with different ABCA4 alleles [11].
  • Unlike MODY3 families, the Finnish families with low insulin have an age-of-onset typical for NIDDM (mean = 58 years) [12].
  • The steep inverse correlation between age of onset and CAG number suggests a higher sensitivity to polyglutamine length than in the other polyglutamine expansion diseases [13].
  • Maturity-onset diabetes of the young, a form of NIDDM with an early age of onset and autosomal dominant inheritance, can result from mutations in glucokinase, a key enzyme of glucose metabolism in beta cells and the liver [14].
  • We have assessed 360 HD individuals from 259 unrelated families and found a highly significant correlation (r = 0.70, p = 10(-7)) between the age of onset and the repeat length, which accounts for approximately 50% of the variation in the age of onset [15].
 

Chemical compound and disease context of Age of Onset

  • Retrospective study of 129 patients treated with dopamine substitution showed that the occurrence of response variations is related to the duration of therapy and not to the nature of the predominant symptom (tremor or hypokinesia and rigidity) or the age of onset of the disease [16].
  • Further heterogeneity is being demonstrated within each of these broad groups of disorders--within insulin-dependent diabetes using the HLA antigens and immunologic studies, and within noninsulin-dependent diabetes using such criteria as obesity, insulin response, age of onset and chlorpropamide-primed alcohol-induced flushing [17].
  • Results: No significant evidence of association between alleles of the serotonin transporter gene and pulmonary hypertension was detected, nor did we observe a relationship with age of onset in familial and idiopathic disease [18].
  • Although we confirm the previously reported correlation between the CAG repeat length and the early onset of the neurological disease, we describe a significant correlation between repeat length and the age of onset of gynecomastia as well as biological indexes of androgen insensitivity [19].
  • In the present studies, we have extended previous work by determining maturational patterns of the deiodinating pathways in several thyroid hormone-responsive rat tissues, possible modulation of those patterns by glucocorticoids, and the age of onset of responsivity of the deiodinases to hypothyroidism [20].
 

Biological context of Age of Onset

 

Anatomical context of Age of Onset

 

Associations of Age of Onset with chemical compounds

  • The age of onset of mammary tumors was also earlier after neonatal steroid treatment [31].
  • The male MZ/DZ concordance difference for composite diagnosis but not for Alcohol Dependence could be accounted for statistically by differences in age of onset between MZ and DZ probands [32].
  • Interestingly, we detected in the same region overlapping linkages with three QTLs: age of onset of CHD (LOD = 2.03), HDL cholesterol (LOD = 1.48) and LDL/HDL ratio (LOD = 1.34) [33].
  • The low doses of 17beta-estradiol and progesterone each resulted in an earlier age of onset and a higher incidence of mammary tumors; this also occurred after both combined estrogen-progesterone treatments [34].
  • Otherwise, clinical characteristics of PD in the kindred, including variance in onset age and incidence of tremor and levodopa responsiveness, are similar to those of PD in the community [35].
 

Gene context of Age of Onset

  • While the biological basis for the association of APOE epsilon4 with AD is not known, age of onset and A beta deposition are positively correlated with epsilon4 allele dosage in some cases, suggesting that this risk may also be mediated directly or indirectly through A beta [36].
  • The wide variability in the age of onset of ILD in patients with SFTPC mutations may be related to environmental insults that ultimately overwhelm the homeostatic cytoprotective response [37].
  • Inheritance of specific apolipoprotein E (apoE) alleles determines, in large part, the risk and mean age of onset of late-onset familial and sporadic Alzheimer disease [38].
  • In contrast, Tg(Dpl)ZrchI mice showed cerebellar granule and Purkinje cell loss; the age of onset of ataxia was inversely proportional to the levels of Dpl protein [39].
  • Analysis of additional members of a pedigree known to segregate a Met239Val mutation in PS-2 revealed that the age of onset of symptoms is highly variable (range 45-88 years) [40].
 

Analytical, diagnostic and therapeutic context of Age of Onset

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