Our earlier studies in vitro indicated that expression of TGFβ2 was induced by toxic amyloid βs (Aβs) in both glial and neuronal cells and increased levels of TGFβ2 triggered a neuronal cell death pathway related to Alzheimer's disease (AD) by binding to the extracellular domain of amyloid β precursor protein (APP). In this study we have demonstrated by immunohistochemical analysis that the levels of TGFβ2 are elevated in cells mainly consisting of neurons of both the hippocampi and cerebral cortices of human AD brains. This result indicates that upregulation of the TGFβ2 level is a common pathological feature of AD brains and suggests that it may be closely linked to the development of neuronal death related to AD.
|Number of pages||8|
|Journal||International Journal of Neuroscience|
|Publication status||Published - 2010 Apr|
- Alzheimer's disease
- Neuronal death
ASJC Scopus subject areas