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    Traumatic Brain Injury Alters the Metabolism and Facilitates Alzheimer’s Disease in a Murine Model

    A majority of Alzheimer’s disease (AD) cases are sporadic without known cause. People who suffered from traumatic brain injury (TBI) are more likely to develop neurodegeneration and cognitive impairments. Howe...

    Dandan Lou, Yao Du, Daochao Huang, Fang Cai, Yun Zhang, Tinyu Li in Molecular Neurobiology (2018)

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    Ethanol Alters APP Processing and Aggravates Alzheimer-Associated Phenotypes

    The majority of Alzheimer’s disease (AD) cases are sporadic with unknown causes. Many dietary factors including excessive alcohol intake have been reported to increase the risk to develop AD. The effect of alc...

    Daochao Huang, Mengjiao Yu, Shou Yang, Dandan Lou, Weitao Zhou in Molecular Neurobiology (2018)

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    Regulation of SET Gene Expression by NFkB

    SET is elevated and mislocalized in the neuronal cytoplasm in brains of Alzheimer’s disease (AD) and Down syndrome (DS) patients. Cytoplasm SET leads to inhibition of protein phosphatase 2A and is involved in ...

    Yi Feng, **aoyong Li, Weitao Zhou, Dandan Lou, Daochao Huang in Molecular Neurobiology (2017)

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    Sp1 Regulates Human Huntingtin Gene Expression

    Huntington’s disease (HD) is a hereditary neurodegenerative disorder resulting from the expansion of a polyglutamine tract in the huntingtin protein. The expansion of cytosine–adenine–guanine repeats results i...

    Ruitao Wang, Yawen Luo, Philip T. T. Ly, Fang Cai in Journal of Molecular Neuroscience (2012)

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    BACE1 Gene Promoter Single-Nucleotide Polymorphisms in Alzheimer’s Disease

    Alzheimer’s disease (AD) is the most neurodegenerative disorder leading to dementia. Neuritic plaque formation in brains is a hallmark of AD pathogenesis. Amyloid β protein (Aβ) is the central component of neu...

    Weihui Zhou, Fang Cai, Yu Li, George S. Yang in Journal of Molecular Neuroscience (2010)