Affiliations: [a] Protein Design and Immunotherapy Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biociències, Universitat Autònoma de Barcelona, Bellaterra, Barcelona, Spain
| [b] Department of Clinical Chemistry and Transfusion Medicine, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden
Correspondence:
[*]
Correspondence to: Laia Montoliu-Gaya and Sandra Villegas, Protein Design and Immunotherapy Group,
Departament de Bioquímica i Biologia Molecular, Facultat de Biociències, Universitat Autònoma de
Barcelona, 08193 Bellaterra, Barcelona, Spain. Tel.: +34 935814258; Fax: +34 935811264; E-mail:
Laia.Montoliu.Gaya@gu.se (L. Montoliu-Gaya) and Sandra.Villegas@uab.cat (S. Villegas).
Abstract: Alzheimer’s disease (AD), the most common type of dementia worldwide, is characterized by high levels of amyloid-β (Aβ) peptide and hyperphosphorylated tau protein. Genetically, the ɛ4 allele of apolipoprotein E (ApoE) has been established as the major risk factor for developing late-onset AD (LOAD), the most common form of the disease. Although the role ApoE plays in AD is still not completely understood, a differential role of its isoforms has long been known. The current review compiles the involvement of ApoE isoforms in amyloid-β protein precursor transcription, Aβ aggregation and clearance, synaptic plasticity, neuroinflammation, lipid metabolism, mitochondrial function, and tau hyperphosphorylation. Due to the complexity of LOAD, an accurate description of the interdependence among all the related molecular mechanisms involved in the disease is needed for developing successful therapies.
