Transcriptional Changes in Alzheimer's Disease

摘要: Alzheimer’s disease (AD) is the most common form of dementia, affecting millions aging people worldwide with no known cure. Pathological analyses have identified extracellular β-amyloid plaques and intracellular neurofibrillary tangles hyperphosphorylated tau as core features, but key causal biochemical pathways remain elusive. In fact, functional genomic suggest a number other cellular changes occurring early in disease, including synaptic bio-energetic dysfunction, well role for neuron–glia interactions. Given complexity AD limitations our current knowledge, field research would benefit from taking hypothesis-independent approaches that allow one to view data systems biology framework. This paradigm shift transcriptional permit consolidation large body often-conflicting transcriptional, proteomic, screening results into testable theories progression. this chapter, we will first review studies use postmortem human brain, animal model systems, peripheral tissue, addressing biological these degrade Next, discuss recent more multifaceted designs, how such lend support some theories. Finally, using systems-level approach study could help scientists further clarify what goes wrong brain at various stages progression be beneficial development targeted therapies.