Few public health problems have captured the attention of the biomedical
and lay communities alike as has Alzheimer disease (AD). As the new millennium
begins, it is becoming increasingly clear that a great many people will escape
other major causes of mortality to reach the age when neurodegenerative diseases,
particularly AD, become highly prevalent. To avoid an exacerbation of the
personal and societal tragedy that AD already represents, clinicians and researchers
must accurately define its cause and early pathogenesis and develop effective
interventions, preferably agents that prevent the onset of symptoms. The study
by Näslund et al1 in this issue of THE
JOURNAL provides compelling evidence that the accumulation of small protein
fragments called amyloid β-peptides (Aβ) in brain regions subserving
memory and cognition is a very early pathogenic event that precedes both neurological
impairment and the development of the other proteinaceous lesion of AD, the
neurofibrillary tangle. Moreover, the authors show that the conversion from
a presymptomatic to a symptomatic state and the subsequent progression of
dementia correlate significantly with a dramatic increase in brain Aβ
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