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Alzheimer's disease and Aβ toxicity: from top to bottom

Nature Reviews Neuroscience volume 2, pages 595–598 (2001)Cite this article

Abstract

Evidence implicating the β-amyloid protein (Aβ) in the pathogenesis of Alzheimer's disease has steadily accumulated. However, the mechanism by which Aβ causes dementia is unknown. Here we argue that a more integrated, top–down approach to brain function is needed to assess the role of Aβ in Alzheimer's disease, and that more attention should be paid to the effects of Aβ on synaptic function rather than on cell death.

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Figure 1: Pathways in neurons, astrocytes and microglia that are implicated in β-amyloid toxicity.
Figure 2: Effects of β-amyloid on pathways that control synaptic plasticity in dendrites.

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Authors and Affiliations

  1. Department of Pathology, The University of Melbourne, Victoria 3010, Australia

    David H. Small & Su San Mok

  2. Department of Physiology, The University of Melbourne, Victoria 3010, Australia

    Joel C. Bornstein

  3. David H. Small

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  1. David H. Small
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Related links

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DATABASE LINKS

Alzheimer's disease

APP

α7 nAChR

ERK/MAP kinase

tau

Bax

cdk

E2F1

ERAB

FADD

FAS/TNFR

IL1β

iNOS

JNK

L-VGCC

m-CSF

NFκB

p35

p75NTR

RAGE

Rb

TNFα

MIT ENCYCLOPEDIA OF COGNITIVE SCIENCES

Computational neuroscience

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Small, D., Mok, S. & Bornstein, J. Alzheimer's disease and Aβ toxicity: from top to bottom. Nat Rev Neurosci 2, 595–598 (2001). https://doi.org/10.1038/35086072

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