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Cited by 133Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

The DOI matches its Crossref record; 176 of the 177 references it cites were found in a registry or an index.

The Future of Precision Medicine in the Cure of Alzheimer’s Disease

Open access
Arafah, Azher, Khatoon, Saima, Rasool, Iyman, Khan, Andleeb, Rather, Mashoque Ahmad, Abujabal, Khaled Abdullah, Faqih, Yazid Abdullilah Hassan, Rashid, Hina, Rashid, Shahzada Mudasir, Bilal Ahmad, Sheikh, Alexiou, Athanasios, Rehman, Muneeb U.·2023·Biomedicines
DOI 10.3390/biomedicines11020335PMC PMC9953731
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Abstract

This decade has seen the beginning of ground-breaking conceptual shifts in the research of Alzheimer’s disease (AD), which acknowledges risk elements and the evolving wide spectrum of complicated underlying pathophysiology among the range of diverse neurodegenerative diseases. Significant improvements in diagnosis, treatments, and mitigation of AD are likely to result from the development and application of a comprehensive approach to precision medicine (PM), as is the case with several other diseases. This strategy will probably be based on the achievements made in more sophisticated research areas, including cancer. PM will require the direct integration of neurology, neuroscience, and psychiatry into a paradigm of the healthcare field that turns away from the isolated method. PM is biomarker-guided treatment at a systems level that incorporates findings of the thorough pathophysiology of neurodegenerative disorders as well as methodological developments. Comprehensive examination and categorization of interrelated and convergent disease processes, an explanation of the genomic and epigenetic drivers, a description of the spatial and temporal paths of natural history, biological markers, and risk markers, as well as aspects about the regulation, and the ethical, governmental, and sociocultural repercussions of findings at a subclinical level all require clarification and realistic execution. Advances toward a comprehensive systems-based approach to PM may finally usher in a new era of scientific and technical achievement that will help to end the complications of AD.

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Crossref · 10.3390/biomedicines11020335

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Figures

Figure 1 Biological indicators of AD’s histopathological changes.
Figure 1 Biological indicators of AD’s histopathological changes.CC BY · PubMed Central
Figure 2 Precision medicine approach to prevention of disease. Precision medicine in Alzheimer’s disease involves the use of biomarkers, such as genetic and imaging markers, to accurately diagnose and classify patients based on the specific subtype of the disease they have. This allows for more tailored treatment approaches and the development of targeted therapies.
Figure 2 Precision medicine approach to prevention of disease. Precision medicine in Alzheimer’s disease involves the use of biomarkers, such as genetic and imaging markers, to accurately diagnose and classify patients based on the specific subtype of the disease they have. This allows for more tailored treatment approaches and the development of targeted therapies.CC BY · PubMed Central
Figure 3 Neuroinflammation: A key initiating component in the development of AD. Signaling of neurotrophins is impaired. By inducing microglia to release proinflammatory cytokines (IL-1β and TNF-α) and blocking the production of anti-inflammatory cytokines such as TGF-β1, Aβ oligomers cause neuroinflammation and neuronal death in the AD brain. TNF-α promotes g-secretase activity and prevents microglia from phagocytizing Aβ, which promotes Aβ build up and microglia-mediated neuroinflammation. Through the production of ROS and RNS, proinflammatory microglial activities also accelerate the death of neurons. Eventually, neuroinflammatory phenomena may play a role in the pathogenesis of AD by impairing neurotrophin signaling. This includes decreasing the synthesis of TGF-β1 and impairing the NGF metabolic pathway, which is characterized by a decreased conversion of proNGF to biologically active mNGF and a higher rate of mNGF degradation aided by MMP-9. Aβ, amyloid beta; IL-1b, interleukin-1 beta; MMP-9, metalloprotease-9; NGF, nerve growth factor; mNGF, mature nerve growth factor; proNGF, precursor of the nerve growth factor; RNS, reactive nitrogen species; ROS, reactive oxygen species; TGF-β, transforming growth factor-beta; TNF-α, tumor necrosis factor-alpha.
Figure 3 Neuroinflammation: A key initiating component in the development of AD. Signaling of neurotrophins is impaired. By inducing microglia to release proinflammatory cytokines (IL-1β and TNF-α) and blocking the production of anti-inflammatory cytokines such as TGF-β1, Aβ oligomers cause neuroinflammation and neuronal death in the AD brain. TNF-α promotes g-secretase activity and prevents microglia from phagocytizing Aβ, which promotes Aβ build up and microglia-mediated neuroinflammation. Through the production of ROS and RNS, proinflammatory microglial activities also accelerate the death of neurons. Eventually, neuroinflammatory phenomena may play a role in the pathogenesis of AD by impairing neurotrophin signaling. This includes decreasing the synthesis of TGF-β1 and impairing the NGF metabolic pathway, which is characterized by a decreased conversion of proNGF to biologically active mNGF and a higher rate of mNGF degradation aided by MMP-9. Aβ, amyloid beta; IL-1b, interleukin-1 beta; MMP-9, metalloprotease-9; NGF, nerve growth factor; mNGF, mature nerve growth factor; proNGF, precursor of the nerve growth factor; RNS, reactive nitrogen species; ROS, reactive oxygen species; TGF-β, transforming growth factor-beta; TNF-α, tumor necrosis factor-alpha.CC BY · PubMed Central

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Research works printed but not linked: 1

  1. (2011). National Research Council (US) Committee on A Framework for Developing a New Taxonomy of Disease toward Precision Medicine: Building a Knowledge Network for Biomedical Research and a New Taxonomy of Disease; The National Academies Collection: Reports Funded by National Institutes of Health, National Academies Press (US).

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Authors
Arafah, A., Khatoon, S., Rasool, I., Khan, A., Rather, M. A., Abujabal, K. A., Faqih, Y. A. H., Rashid, H., Rashid, S. M., Bilal Ahmad, S., Alexiou, A., & Rehman, M. U.
Affiliations
  • King Saud bin Abdulaziz University for Health Sciences (SA)
  • Jamia Hamdard (IN)
  • Government Medical College (IN)
  • Jazan University (SA)
  • University of South Florida (US)
  • Department of Pharmacy, Abu Areish General Hospital, Abu Areish 45911, Saudi Arabia
  • Department of Emergency and Accident, Abu Areish General Hospital, Abu Areish 45911, Saudi Arabia
  • Sher-e-Kashmir University of Agricultural Sciences and Technology of Kashmir (IN)
  • Division of Veterinary Biochemistry, Faculty of Veterinary Sciences and Animal Husbandry, Sher-e-Kashmir University of Agricultural Sciences and Technology (SKUAST-K), Srinagar 190006, India
  • Novel Global Community Educational Foundation, Hebersham, NSW 2770, Australia
Corresponding author
  • Arafah, Azher
  • Khan, Andleeb
  • Rehman, Muneeb U.
ORCID
Venue
Biomedicines
Publisher
MDPI AG
Published
2023-01-25
Volume
11
Issue
2
Pages
335
ISSN
2227-9059 (ISSN-L)
DOI
10.3390/biomedicines11020335
PMC
PMC9953731
OpenAlex
W4317934405
Cited by
133
References
176
Citations by year
2026: 31 · 2025: 54 · 2024: 41 · 2023: 7
FWCI
4.75
Type
journal article
Language
en
Open access
Licence
Locations
  • Biomedicines (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Deputyship for Research and Innovation, Ministry of Education in Saudi Arabia (ISP22-19)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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, precision medicine, neurodegenerative diseases, biomarkers, risk factors, pathophysiology, epigenetics, systems biology, disease natural history

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