Publications by authors named "W Robberecht"

Article Synopsis
  • Humans appear more prone to neurodegeneration than similarly aged primates, and it's unclear if this trait is unique to modern humans or shared with other hominids.
  • The study explored the potential impact of Neanderthal DNA on neurodegenerative disorders and examined the role of natural selection on genetic variants linked to these diseases using advanced statistical methods.
  • Findings indicated that there is no significant evidence that Neanderthal DNA or positively-selected genetic variants contribute to the genetic risk of Alzheimer's, ALS, or Parkinson's disease, helping to clarify the evolutionary background of these disorders in modern humans.
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Article Synopsis
  • - Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative disease marked by the loss of motor neurons, often leading to death from respiratory failure within 3 to 5 years, with a significant genetic component influencing its risk.
  • - A study analyzed telomere length using genetic data from 6,195 ALS patients and controls, revealing that individuals with ALS had 20% longer telomeres compared to controls after adjusting for age and sex, and this finding was validated using brain samples.
  • - Interestingly, shorter telomeres were associated with a 10% increase in median survival among ALS patients, suggesting that telomere length may play a role in the disease's progression and overall survival chances.
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Article Synopsis
  • * This study compares people with SOD1-related ALS to those without SOD1 variants, using extensive data from both groups to analyze age at symptom onset and survival time.
  • * Findings indicate that certain SOD1 variants are tied to younger ages of onset and unique survival patterns, suggesting that onset and survival can be independent in SOD1-ALS cases, highlighting the need for further research on rare variants.
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There is a strong genetic contribution to Amyotrophic lateral sclerosis (ALS) risk, with heritability estimates of up to 60%. Both Mendelian and small effect variants have been identified, but in common with other conditions, such variants only explain a little of the heritability. Genomic structural variation might account for some of this otherwise unexplained heritability.

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