Alzheimer`s disease (AD) is a neurodegenerative disorder that causes a progressive impairment of intellecutal functions. The neuropathology of AD is characterized by two different types of fibrillar deposits, senile plaques and neurofibrillary tangles. Amyloid-β-proteins (Aβ ) are the major constituents of senile plaques. The aggregation of soluble Aβ into insoluble amyloid fibrils is believed to be an important step in the pathogenesis of AD and the prevention of this process therefore seems to be a promising strategy for the treatment of AD. Laminin, which has been reported to accumulate in senile plaques, supports biological activities as cell adhesion, cell proliferation, neurite outgrowth. Some recent reports revealed that laminin inhibites both Aβ fibril formation and Aβ neurotoxicity in vitro. Moreover, some laminin-related peptides, which have the same biological activites like laminin, have recently been reported to inhibit Aβ fibril formation and/ or Aβ neurotoxicity. Recent reports have also shown that laminin can induce complete disaggregation of Aβ amyloid fibrils by the disassembly into protofibrils and subsequently into an amorphous aggregate. These results thus suggested that laminin or its related peptides may be effective as therapeutic agents to either prevent or slow down the progression of amyloidogenesis in Alzheimer ` s disease.
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