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β-amyloid Peptides and Amyloid Plaques in Alzheimer’s Disease

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Neurotherapeutics

Abstract

Many lines of evidence support that β-amyloid (Aβ) peptides play an important role in Alzheimer’s disease (AD), the most common cause of dementia. But despite much effort the molecular mechanisms of how Aβ contributes to AD remain unclear. While Aβ is generated from its precursor protein throughout life, the peptide is best known as the main component of amyloid plaques, the neuropathological hallmark of AD. Reduction in Aβ has been the major target of recent experimental therapies against AD. Unfortunately, human clinical trials targeting Aβ have not shown the hoped-for benefits. Thus, doubts have been growing about the role of Aβ as a therapeutic target. Here we review evidence supporting the involvement of Aβ in AD, highlight the importance of differentiating between various forms of Aβ, and suggest that a better understanding of Aβ’s precise pathophysiological role in the disease is important for correctly targeting it for potential future therapy.

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Acknowledgments

We are grateful for funding support from MultiPark, the Swedish Research Council, and the European Research Council.

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Authors and Affiliations

  1. Department of Experimental Medical Science, Lund University, Lund, Sweden

    Gunnar K. Gouras & Tomas T. Olsson

  2. Clinical Memory Research Unit, Clinical Sciences Malmö, Lund University, Lund, Sweden

    Oskar Hansson

  3. Memory Clinic, Skåne University Hospital, Skåne, Sweden

    Oskar Hansson

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  1. Gunnar K. Gouras
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  2. Tomas T. Olsson
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  3. Oskar Hansson
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Correspondence to Gunnar K. Gouras or Oskar Hansson.

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Gouras, G.K., Olsson, T.T. & Hansson, O. β-amyloid Peptides and Amyloid Plaques in Alzheimer’s Disease. Neurotherapeutics 12, 3–11 (2015). https://doi.org/10.1007/s13311-014-0313-y

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