CoChat
Sign Up
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
Open this paper in CoChat — free accountOpen PDF

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.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3390/biomedicines11020335

Cites

176 of 177 references verified1 citation errors · 0 not checkable

Statistics

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

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

1 retracted

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).

Cited by

Sorted by citations

See all 133

Related

See all

Metadata

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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review