Wang, Y., Jia, S., Tseng, B., Drewe, J. and Cai, S.X. (2007) Dipeptidyl Aspartyl Fluoromethylketones as Potent Caspase Inhibitors: Peptidomimetic Replacement of the P2 Amino Acid by 2-Aminoaryl Acids and Other Non-Natural Amino Acids. Bioorganic & Medicinal Chemistry Letters, 17, 6178-6182.
http://dx.doi.org/10.1016/j.bmcl.2007.09.030

has been cited by the following article:

• TITLE: Activated Caspase-3 and Neurodegeneration and Synaptic Plasticity in Alzheimer’s Disease

  AUTHORS: Anna Płóciennik, Michał Prendecki, Ewelina Zuba, Marcin Siudzinski, Jolanta Dorszewska

  KEYWORDS: Caspase-3, MicroRNA, Apoptosis, Synaptic Plasticity, Experimental Models, AD

  JOURNAL NAME: Advances in Alzheimer's Disease, Vol.4 No.3, August 28, 2015

  ABSTRACT: In Alzheimer’s disease (AD) there is a loss of neurons in different areas of the brain, including hippocampus, temporal and frontal cortex. Molecular mechanism of neuronal death in AD is not clear. It seems that apoptosis is a major form of neuronal cell death in this neurodegenerative disease. Neurons in both experimental animals and AD brains showed apoptotic changes, including DNA fragmentation, microRNA expression and caspase-3 activation. Activated caspase-3 may lead to amyloid precursor protein (APP) cleavage, extracellular senile plaques (SPs) and intracellular neurofibrillary tangles (NFTs) formation and neuronal loss, and it contributes to synaptic plasticity and cognitive dysfunction, especially in early stage of AD. Moreover, changes of caspase-3 activity were observed after therapy with memantine (NMDA receptor antagonist), donepezil and ladostigil (acetylcholinesterase inhibitors) in AD patients. It has been shown that both mementine and acetylcholinesterase inhibitors protect neurons from the caspase-3 activation. It seems that caspase-3 may be a potential diagnostic factor and target for pharmacotherapy of AD patients.