Alzheimer’s disease (AD) is the most common age-dependent disease of dementia, and there is currently no cure
available. This hallmark pathologies of AD are the presence of amyloid plaques and neurofibrillary tangles. Although
the exact etiology of AD remains a mystery, studies over the past 30 have shown that abnormal generation or
accumulation of β-amyloid peptides (Aβ) is likely to be a predominant early event in AD pathological development.
Aβ is generated from amyloid precursor protein (APP) via proteolytic cleavage by β-site APP cleaving enzyme 1
(BACE1). Chemical inhibition of BACE1 has been shown to reduce Aβ in animal studies and in human trials. While
BACE1 inhibitors are currently being tested in clinical trials to treat AD patients, it is highly important to understand
whether BACE1 inhibition will significantly impact cognitive functions in AD patients. This review summarizes the
recent studies on BACE1 synaptic functions. This knowledge will help to guide the proper use of BACE1 inhibitors
in AD therapy.

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• Role of BACE1 in Alzheimer’s synaptic function