Alzheimer disease is a progressive and unrelenting neurodegenerative disorder causing incremental cognitive decline due to increasing neuropathologic changes including amyloid-containing neuritic plaques, aggregated hyperphosphorylated tau as neurofibrillary tangles, dystrophic neurites, gliosis, and synaptic and neuronal loss. These changes have been established findings for many years, and the impression is that they are permanent and fixed. What has emerged in recent years using transgenic mouse models containing mutant genes causal of Alzheimer disease is that these neuropathologic fixtures can indeed be altered and changed, and they have even been shown to regress.
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