Publications by authors named "Mehmet Murat Koseoglu"

Article Synopsis
  • A hexanucleotide repeat expansion in the C9orf72 gene is linked to familial and some sporadic cases of ALS and frontotemporal dementia.
  • Inducible pluripotent stem cells from C9orf72+ ALS patients show that while their neuronal progenitor cells can differentiate into neurons, these C9+ neurons re-express cell cycle proteins and exhibit signs of aging or senescence after 12 weeks.
  • The study indicates that C9+ neurons produce high levels of specific inflammatory molecules and reactive oxygen species, which may contribute to neuronal dysfunction in ALS and frontotemporal dementia.
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Neurological diseases comprise more than a thousand ailments that adversely affect the brain and nervous system. When grouped together, these neurological conditions impact an estimated 100 million individuals in the United States and up to a billion people worldwide, making drug discovery efforts imperative. However, recent research and development efforts for these neurological diseases, including Alzheimer's disease and amyotrophic lateral sclerosis, have been exceedingly disappointing and typify the challenges associated with translating and cell-based discoveries to successful preclinical models and subsequent human clinical trials.

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Aberrant neuronal cell cycle re-entry (CCR) is a phenomenon that precedes and may mechanistically lead to a majority of the neuronal loss observed in Alzheimer's disease (AD). Recent developments concerning the regulation of aberrant neuronal CCR in AD suggest that there are potential intracellular signaling "hotspots" in AD, cancer, and brain insulin resistance, the latter of which is characteristically associated with AD. Critically, these common signaling nodes across different human diseases may represent currently untapped therapeutic opportunities for AD.

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