作者: Nathan C. Denham , James A. R. Nicoll , Delphine Boche
DOI: 10.1007/978-1-4419-7061-9_14
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摘要: Alzheimer’s disease (AD) was first described more than 100 years ago; however, the mechanisms underlying its pathogenesis are still poorly understood. Current theories suggest a pivotal role for protein amyloid-β (Aβ) and many of novel treatments AD focus on Aβ. In this chapter, we discuss evidence that Aβ underpins cognitive decline as result direct indirect toxicity peptide synapses in cerebral cortex hippocampus. Furthermore, will follow promise immunisation holds to alter natural history AD, from beginnings animal models current research humans. The success seen mice preventing both synapse loss reducing functional is yet be matched humans serious adverse events patients stopped initial vaccination approach. Research, continuing human aiming provide greater understanding immune response potential effects or reversing impairment.