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• W59742045 abstract "Independent of the etiology, i.e. whether genetic or non-genetic, Alzheimer disease (AD) is characterized histopathologically by the intraneuronal accumulation of paired helical filaments (PHF), forming neurofibrillary tangles, neuropil threads and dystrophic neurites surrounding the extracellular deposits of β-amyloid, the second major lesion. The clinical expression of AD correlates with the presence of neurofibrillary degeneration; β-amyloidosis alone does not produce the disease clinically. Thus, arresting neurofibrillary degeneration offers a promising key target for therapeutic intervention of AD. In this chapter the molecular pathology, the mechanisms of neurofibrillary degeneration and therapeutic strategies to arrest this brain lesion in AD are briefly reviewed." @default.
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• W59742045 date "1997-01-01" @default.
• W59742045 modified "2023-09-26" @default.
• W59742045 title "Alzheimer Neurofibrillary Degeneration: A Feasible and Key Target for Therapeutics" @default.
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• W59742045 doi "https://doi.org/10.1007/978-1-4612-4116-4_6" @default.
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