Alzheimer’s disease: pathogenesis, diagnostics, and therapeutics
Open accessAbstract
Abstract: Currently, 47 million people live with dementia globally, and it is estimated to increase more than threefold (∼131 million) by 2050. Alzheimer’s disease (AD) is one of the major causative factors to induce progressive dementia. AD is a neurodegenerative disease, and its pathogenesis has been attributed to extracellular aggregates of amyloid β (Aβ) plaques and intracellular neurofibrillary tangles made of hyperphosphorylated τ-protein in cortical and limbic areas of the human brain. It is characterized by memory loss and progressive neurocognitive dysfunction. The anomalous processing of APP by β-secretases and γ-secretases leads to production of Aβ 40 and Aβ 42 monomers, which further oligomerize and aggregate into senile plaques. The disease also intensifies through infectious agents like HIV. Additionally, during disease pathogenesis, the presence of high concentrations of Aβ peptides in central nervous system initiates microglial infiltration. Upon coming into vicinity of Aβ, microglia get activated, endocytose Aβ, and contribute toward their clearance via TREM2 surface receptors, simultaneously triggering innate immunoresponse against the aggregation. In addition to a detailed report on causative factors leading to AD, the present review also discusses the current state of the art in AD therapeutics and diagnostics, including labeling and imaging techniques employed as contrast agents for better visualization and sensing of the plaques. The review also points to an urgent need for nanotechnology as an efficient therapeutic strategy to increase the bioavailability of drugs in the central nervous system. Keywords: amyloid beta, amyloidogenesis, amyloid precursor proteins, β-secretases, γ-secretases, tau phosphorylation
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AD pathogenesis is mainly identified by extracellular aggregates of amyloid β peptides and formation of intracellular neurofibrillary tangles.
“AD pathogenesis is mainly identified by extracellular aggregates of amyloid β (Aβ) peptides and the formation of intracellular neurofibrillary tangles. 51”
From Therapeutic Properties and Pharmacological Activities of Asiaticoside and Madecassoside: A Review (2023) · cites this paper as [51]
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- Authors
- Tiwari, S., Atluri, V., Kaushik, A., Yndart, A., & Nair, M.
- Affiliations
- Florida International University (US)
- Corresponding author
- Tiwari, Sneham
- Atluri, Venkata
- Kaushik, Ajeet
- Yndart, Adriana
- Nair, Madhavan
- Venue
- International Journal of Nanomedicine
- Publisher
- Informa UK Limited
- Published
- 2019-07
- Volume
- Volume 14
- Pages
- 5541-5554
- ISSN
- 1176-9114 (ISSN-L)
- 1178-2013
- PMC
- PMC6650620
- OpenAlex
- W2958665365
- Cited by
- 1,308
- References
- 19
- Citations by year
- 2026: 141 · 2025: 231 · 2024: 306 · 2023: 243 · 2022: 198 · 2021: 133 · 2020: 46 · 2019: 9
- FWCI
- 11.30
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Nanomedicine (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (acceptedVersion)
- Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
- Funders
- Florida Department of Health (8AZ04)
- Florida International University
- University Graduate School, Florida International University
- National Institutes of Health
- National Institute on Drug Abuse (R01DA034547)
- 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, amyloid plaques, tau hyperphosphorylation, neurofibrillary tangles, amyloid precursor protein, beta-secretase, gamma-secretase, amyloidogenesis, microglial activation, TREM2, HIV, Alzheimer's disease therapeutics, nanotechnology drug delivery
- MeSH terms
- Alzheimer Disease, Blood-Brain Barrier, Humans, Amyloid beta-Peptides, Nanotechnology, Epigenesis, Genetic, Plaque, Amyloid
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