Lactoferrin Immunoreactivity and Binding Sites in Neurons, Neuritic Plaques, and Neurofibrillary Tangles in Alzheimer’s Disease

Alzheimer’s disease (AD) is the major cause of dementia in the elderly and afflicts between two and four million persons in the United States alone (Cook-Deegan and Whitehouse, 1987). Although considerable advances in understanding the molecular biology of the principal molecular constituents of the characteristic brain lesions of this disorder have recently been made, little is formally known about the etiology and pathogenesis of AD. Previous evidence suggesting that aluminum or its compounds are causally involved (Crapper et al., 1973) or that a loss of cholinergic neurons is the primary neuropathologic feature (Davies and Maloney, 1976) has not been confirmed. It is generally accepted, however, that an understanding of the mechanisms involved in the initiation and formation of the pathognomic features of AD, the neuritic (amyloid) plaques (NP) and neurofibrillary tangles (NFT), will provide the essential basis for a rational approach to the treatment and prevention of this disease. The observations described here arise from a study of potential etiologic factors involved in the generation of NP and NFT.