Publications by authors named "R M Liscic"

Many potential immune therapeutic targets are similarly affected in adult-onset neurodegenerative diseases, such as Alzheimer's (AD) disease, Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and frontotemporal dementia (FTD), as well as in a seemingly distinct Niemann-Pick type C disease with primarily juvenile onset. This strongly argues for an overlap in pathogenic mechanisms. The commonly researched immune targets include various immune cell subsets, such as microglia, peripheral macrophages, and regulatory T cells (Tregs); the complement system; and other soluble factors.

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Amyotrophic lateral sclerosis (ALS) and Frontotemporal Degeneration (FTD) are neurodegenerative disorders, related by deterioration of motor and cognitive functions and short survival. Aside from cases with an inherited pathogenic mutation, the causes of the disorders are still largely unknown and no effective treatment currently exists. It has been shown that FTD may coexist with ALS and this overlap occurs at clinical, genetic, and molecular levels.

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Article Synopsis
  • ALS and FTLD are closely related neurodegenerative disorders characterized by declining motor and cognitive abilities, with unclear causes and currently no effective treatments.
  • FTLD can occur alongside ALS, with both conditions sharing common neuropathological features, especially involving the abnormal TDP-43 protein.
  • New research into the genetic factors and potential therapies, including drugs targeting specific proteins and gene therapies, is ongoing and may lead to effective treatment options in the future.
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Article Synopsis
  • ALS and FTD are serious neurodegenerative disorders that lead to declining motor and cognitive abilities, with no current effective treatments apart from a couple of drugs, like Riluzole.
  • Most ALS cases are sporadic, but a genetic mutation (SOD1) is common in familial ALS, while C9ORF72 mutations are the most frequently identified in both ALS and FTD.
  • Research is ongoing into the molecular mechanisms behind these diseases, focusing on proteins like TDP-43 and SOD1, which may lead to new therapeutic strategies.
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