Cited by 97Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Cellular Receptors of Amyloid β Oligomers (AβOs) in Alzheimer’s Disease

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Mroczko, Barbara, Groblewska, Magdalena, Litman-Zawadzka, Ala, Kornhuber, Johannes, Lewczuk, Piotr·2018·International Journal of Molecular Sciences

Abstract

It is estimated that Alzheimer’s disease (AD) affects tens of millions of people, comprising not only suffering patients, but also their relatives and caregivers. AD is one of age-related neurodegenerative diseases (NDs) characterized by progressive synaptic damage and neuronal loss, which result in gradual cognitive impairment leading to dementia. The cause of AD remains still unresolved, despite being studied for more than a century. The hallmark pathological features of this disease are senile plaques within patients’ brain composed of amyloid beta (Aβ) and neurofibrillary tangles (NFTs) of Tau protein. However, the roles of Aβ and Tau in AD pathology are being questioned and other causes of AD are postulated. One of the most interesting theories proposed is the causative role of amyloid β oligomers (AβOs) aggregation in the pathogenesis of AD. Moreover, binding of AβOs to cell membranes is probably mediated by certain proteins on the neuronal cell surface acting as AβO receptors. The aim of our paper is to describe alternative hypotheses of AD etiology, including genetic alterations and the role of misfolded proteins, especially Aβ oligomers, in Alzheimer’s disease. Furthermore, in this review we present various putative cellular AβO receptors related to toxic activity of oligomers.

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  • Misfolded Aβ and tau proteins accumulate in the AD brain in a neurodegenerative cascade leading to cognitive decline and dementia.

    “Misfolded Aβ and tau proteins accumulate in the AD brain in a neurodegenerative cascade leading to cognitive decline and dementia [4,5,6,7,8,9].”
  • Cognitive deficits in mild cognitive impairment patients and decreased executive and reasoning abilities in Alzheimer's disease are caused by oxidative damage of small Aβ oligomers to synaptic membranes.

    “Cognitive deficits in MCI patients and decreased executive and reasoning abilities in AD are caused by the oxidative damage of small Aβ oligomers to the synaptic membranes [83,84,85].”

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Authors
Mroczko, B., Groblewska, M., Litman-Zawadzka, A., Kornhuber, J., & Lewczuk, P.
Affiliations
  • Medical University of Białystok (PL)
  • University Clinical Hospital In Bialystok (PL)
  • Department of Neurodegeneration Diagnostics, Medical University of Białystok, 15-089 Białystok, Poland
  • Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
Corresponding author
Mroczko, Barbara
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2018-06-27
Volume
19
Issue
7
Pages
1884
ISSN
1422-0067 (ISSN-L)
OpenAlex
W2810634108
Cited by
97
References
230
Citations by year
2026: 9 · 2025: 6 · 2024: 15 · 2023: 16 · 2022: 22 · 2021: 15 · 2020: 8 · 2019: 5 · 2018: 1
FWCI
0.95
Type
journal article
Language
en
Open access
Locations
  • International Journal of Molecular Sciences (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • OPUS Repository (Kooperativer Bibliotheksverbund Berlin-Brandenburg) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Uniwersytet Medyczny w Bialymstoku (N/ST/ZB/18/002/1198)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, amyloid-beta oligomers, amyloid-beta aggregation, neurofibrillary tangles, tau protein, amyloid plaques, misfolded proteins, protein misfolding, genetic alterations
MeSH terms
Alzheimer Disease, Animals, Humans, Amyloid beta-Peptides, Neurofibrillary Tangles, Protein Aggregation, Pathological

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