Publications by authors named "Alper Kilci"

Article Synopsis
  • The study addresses the limitations in Alzheimer's disease research due to the absence of effective animal models that reflect key disease features such as amyloid deposition, tau aggregation, inflammation, and neurodegeneration.
  • Researchers created a dual transgenic mouse model (APPNL-G-F/PS19 MAPTP301S) that exhibited significant pathologies including amyloid plaques, tau pathology, and inflammation at just 6 months of age.
  • The findings indicate that amyloid presence worsens tau pathology and inflammation, with specific brain regions showing stronger microglial inflammation and an increase in N-methyladenosine (mA), a modification linked to Alzheimer's, suggesting potential implications for understanding AD's mechanisms.
View Article and Find Full Text PDF

The study for the pathophysiology study of Alzheimer's disease (AD) has been hampered by lack animal models that recapitulate the major AD pathologies, including extracellular β-amyloid (Aβ) deposition, intracellular aggregation of microtubule associated protein tau (MAPT), inflammation and neurodegeneration. We now report on a double transgenic APP MAPT mouse that at 6 months of age exhibits robust Aβ plaque accumulation, intense MAPT pathology, strong inflammation and extensive neurodegeneration. The presence of Aβ pathology potentiated the other major pathologies, including MAPT pathology, inflammation and neurodegeneration.

View Article and Find Full Text PDF

The study for the pathophysiology study of Alzheimer's disease (AD) has been hampered by lack animal models that recapitulate the major AD pathologies, including extracellular β-amyloid (Aβ) deposition, intracellular aggregation of microtubule associated protein tau (MAPT), inflammation and neurodegeneration. We now report on a double transgenic APP MAPT mouse that at 6 months of age exhibits robust Aβ plaque accumulation, intense MAPT pathology, strong inflammation and extensive neurodegeneration. The presence of Aβ pathology potentiated the other major pathologies, including MAPT pathology, inflammation and neurodegeneration.

View Article and Find Full Text PDF