Abstract：
:The proteolytical processing of the amyloid precursor protein (APP) gives rise to beta-amyloid peptides, which accumulate in brains of Alzheimer's disease (AD) patients. Different soluble or insoluble higher molecular weight forms of beta-amyloid peptides have been postulated to trigger a complex pathological cascade that may cause synaptic dysfunction, inflammatory processes, neuronal loss, cognitive impairment, and finally the onset of the disease. The generation of beta-amyloid peptides requires the proteolytical cleavage of APP by an aspartyl protease named beta-site APP-cleaving enzyme 1 (BACE1). The expression and enzymatic activity of BACE1 are increased in brains of AD patients. Here we discuss the importance of a number of recently identified transcription factors as well as post-transcriptional modifications and activation of intracellular signaling molecules for the regulation of BACE1 expression in brain. Importantly, some of these factors are known to be involved in the inflammatory and chronic stress responses of the brain, which are compromised during aging. Moreover, recent evidence indicates that beneficial effects of non-steriodal anti-inflammatory drugs on the progression of AD are mediated--at least in part--by effects on the peroxisome proliferator-activated receptor-gamma response element present in the BACE1 promoter. The identification of the cell type-specific expression and activation of NF-kappaB, Sp1 and YY1 transcription factors may provide a basis to specifically interfere with BACE1 expression and, thereby, to lower the concentrations of beta-amyloid peptides, which may prevent neuronal cell loss and cognitive decline in AD patients.
journal_name
Prog Neurobioljournal_title
Progress in neurobiologyauthors
Rossner S,Sastre M,Bourne K,Lichtenthaler SFdoi
10.1016/j.pneurobio.2006.06.001subject
Has Abstractpub_date
2006-06-01 00:00:00pages
95-111issue
2eissn
0301-0082issn
1873-5118pii
S0301-0082(06)00056-6journal_volume
79pub_type
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journal_title：Progress in neurobiology
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journal_title：Progress in neurobiology
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journal_title：Progress in neurobiology
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journal_title：Progress in neurobiology
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