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Alzheimer’s Disease

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Neuroscience in the 21st Century

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Abstract

Alzheimer’s disease (AD) represents the most prevalent form of senile dementias. The disease is characterized by the occurrence of extracellular plaques, intracellular neurofibrillary tangles, a loss of neurons and synapses, hippocampus and cerebral atrophy and memory loss. Extracellular plaques consist mainly of β-amyloid peptides (Aβ), which are generated through proteolytical cleavage of the larger amyloid precursor protein (APP). Mutations in the APP gene as well as in the two presenilin genes (PSEN1/PSEN2) are responsible for the majority of familial AD (FAD) cases. All these mutations lead to an enhanced Aβ deposition, favoring mostly the generation of the longer Aβ variant containing 42 amino acids (Aβ42). In this chapter, we will briefly summarize the clinical features of AD, mild cognitive impairment being a transitional stage between the cognitive changes during normal aging and AD, as well as information on AD genetics and main pathological hallmarks. In addition, transgenic animal models, as well as current and future therapy options, will be addressed and risk factors such as diabetes will be discussed.

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Abbreviations

AD:

Alzheimer’s disease

ADAM:

A disintegrin and metalloprotease

APH-1:

Anterior pharynx defective 1

ApoE:

Apolipoprotein E

APP:

Amyloid precursor protein

ATP:

Adenosine triphosphate

Aβ:

Amyloid beta

BACE 1:

Beta-site APP cleaving enzyme 1

BDNF:

Derived neurotrophic factor

CA1:

Cornu ammonis 1

CAA:

Cerebral amyloid angiopathy

CNS:

Central nervous system

CSF:

Cerebrospinal fluid

CT:

Computer tomography

Cu:

Copper

DMII:

Type 2 diabetes mellitus

DS:

Down syndrome

FAD:

Familial Alzheimer’s disease

FDG:

Fluorodeoxyglucose

GSK-3β:

Glycogen synthase kinase-3β

IDE:

Insulin degrading enzyme

IGF-1:

Insulin-like growth factor-1

LOAD:

Late-onset Alzheimer’s disease

MAP:

Microtubule-associated protein

MCI:

Mild cognitive impairment

MMSE:

Mini mental state examination

MRI:

Magnetic resonance imaging

NFT:

Neurofibrillary tangles

NMDA:

N-methyl-D-aspartate

NSAID:

Nonsteroidal anti-inflammatory drug

PEN-2:

Presenilin enhancer 2

PET:

Positron emission tomography

PHF:

Paired helical filaments

PIB:

Pittsburgh compound B

PSEN1:

Presenilin 1

PSEN2:

Presenilin 2

ROS:

Reactive oxygen species

VEGF:

Vascular endothelial growth factor

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Authors and Affiliations

  1. Department of Psychiatry and Psychotherapy, University Medical Center Göttingen (UMG), Georg-August-University Göttingen, Göttingen, Germany

    Oliver Wirths, Yvonne Bouter & Thomas A. Bayer

Authors
  1. Oliver Wirths
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  2. Yvonne Bouter
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  3. Thomas A. Bayer
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Corresponding author

Correspondence to Oliver Wirths .

Editor information

Editors and Affiliations

  1. Rockefeller University Lab. Neurobiology & Behaviour, New York, NY, USA

    Donald W. Pfaff

  2. National Institutes of Health (NIH), National Institute of Drug Abuse (NIDA), Rockville, MD, USA

    Nora D. Volkow

  3. Department of Psychiatry, University of California, San Francisco, San Francisco, CA, USA

    John Rubenstein

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Wirths, O., Bouter, Y., Bayer, T.A. (2021). Alzheimer’s Disease. In: Pfaff, D.W., Volkow, N.D., Rubenstein, J. (eds) Neuroscience in the 21st Century. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-6434-1_114-4

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  • DOI: https://doi.org/10.1007/978-1-4614-6434-1_114-4

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  • Publisher Name: Springer, New York, NY

  • Print ISBN: 978-1-4614-6434-1

  • Online ISBN: 978-1-4614-6434-1

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Chapter history

  1. Latest

    Alzheimer’s Disease
    Published:
    31 March 2022

    DOI: https://doi.org/10.1007/978-1-4614-6434-1_114-4

  2. Original

    Alzheimer’s Disease
    Published:
    29 March 2016

    DOI: https://doi.org/10.1007/978-1-4614-6434-1_114-3

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