Cited by 13Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchCholinesterase and Neurodegenerative Diseases

A Chronological Review of Potential Disease-Modifying Therapeutic Strategies for Alzheimer’s Disease

Ettcheto, Miren, Busquets, Oriol, Espinosa-Jiménez, Triana, Verdaguer, Ester, Auladell, Carme, Camins, Antoni·2020·Current Pharmaceutical Design

Abstract

Late-onset Alzheimer's disease (LOAD) is a neurodegenerative disorder that has become a worldwide health problem. This pathology has been classically characterized for its affectation on cognitive function and the presence of depositions of extracellular amyloid β-protein (Aβ) and intracellular neurofibrillary tangles (NFT) composed of hyperphosphorylated Tau protein. To this day, no effective treatment has been developed. Multiple strategies have been proposed over the years with the aim of finding new therapeutic approaches, such as the sequestration of Aβ in plasma or the administration of anti-inflammatory drugs. Also, given the significant role of the insulin receptor in the brain in the proper maintenance of cognitive function, drugs focused on the amelioration of insulin resistance have been proposed as potentially useful and effective in the treatment of AD. In the present review, taking into account the molecular complexity of the disease, it has been proposed that the most appropriate therapeutic strategy is a combinatory treatment of several drugs that will regulate a wide spectrum of the described altered pathological pathways.

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Crossref · 10.2174/1381612826666200211121416

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139 of 139 references verified0 citation errors · 0 not checkable

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  • γ-secretase inhibitors such as tarenflurbil, avagacestat, and semagacestat lower amyloid beta synthesis by preventing gamma secretase enzyme from functioning.

    “This includes γ-secretase inhibitors, such as tarenflurbil (7, Figure 5) [155,156], avagacestat (labeled as 6, Figure 5) [157,158], and semagacestat (5, Figure 5) [159,160]. Their purpose is to lower the synthesis of amyloid beta by preventing the gamma secretase enzyme from functioning.”

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Authors
Ettcheto, M., Busquets, O., Espinosa-Jiménez, T., Verdaguer, E., Auladell, C., & Camins, A.
Affiliations
Instituto de Salud Carlos III (ES)
Corresponding author
Camins, Antoni
Venue
Current Pharmaceutical Design
Published
2020-05-06
Volume
26
Issue
12
Pages
1286-1299
ISSN
1381-6128 (ISSN-L)
OpenAlex
W3006191596
Cited by
13
References
139
Citations by year
2024: 1 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 3
FWCI
0.38
Type
journal article
Language
en
Open access
closed
Locations
  • Current Pharmaceutical Design (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Spanish Ministry of Science and Innovation (SAF2017- 84283-R, PI2016/01)
  • CIBERNED (CB06/05/0024)
  • Generalitat de Catalunya (2017SGR625)
  • Ministry of Science, Innovation and Universities (FPU18/05729)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Pharmacology › Cholinesterase and Neurodegenerative Diseases
Keywords
Alzheimer's disease, disease-modifying therapy, amyloid-beta, neurofibrillary tangles, tau hyperphosphorylation, anti-inflammatory agents, insulin resistance, insulin receptor, combination therapy, neurodegeneration
MeSH terms
Alzheimer Disease, Humans, Insulin Resistance, Amyloid beta-Peptides, tau Proteins

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