CoChat
Sign Up
Cited by 154Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchCholinesterase and Neurodegenerative Diseases

The DOI matches its Crossref record; 158 of the 158 references it cites were found in a registry or an index.

Current progress, challenges and future prospects of diagnostic and therapeutic interventions in Alzheimer's disease

Open access
Rajasekhar, K., Govindaraju, Thimmaiah·2018·RSC Advances
DOI 10.1039/c8ra03620aPMC PMC9081849
Open this paper in CoChat — free accountOpen PDF

Abstract

The diverse pathological mechanisms and their implications for the development of effective diagnostic and therapeutic interventions in Alzheimer's disease are presented with current progress, challenges and future prospects.

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 · 10.1039/c8ra03620a

Cites

158 of 158 references verified0 citation errors · 0 not checkable

Statistics

Figures

Fig. 1 (a) Characteristic features of the pathology of AD in the human brain and recent statistics showing the dramatic and rapid rise of AD as a global epidemic. (b) Multiple pathological pathways of AD.
Fig. 1 (a) Characteristic features of the pathology of AD in the human brain and recent statistics showing the dramatic and rapid rise of AD as a global epidemic. (b) Multiple pathological pathways of AD.CC BY-NC · PubMed Central
Fig. 2 Molecular tools and techniques available for the detection of biomarkers in AD.
Fig. 2 Molecular tools and techniques available for the detection of biomarkers in AD.CC BY-NC · PubMed Central
Fig. 3 Red and NIR (far-red) fluorescent probes for diagnosis of AD. (a) Absorption and emission (λex = 537 nm) spectra of the probe TC in the presence and absence (dotted lines) of Aβ42 fibrillar aggregates. Inset: molecular structure of TC. (b) Photographs of TC and samples of TC + Aβ42 fibrillar aggregates illuminated with visible and UV light (365 nm) and TC + Aβ42 fibrillar aggregates illuminated with a green laser (532 nm), which gives a red beam in the sample solution. (c) Normalized fluorescence intensity (NFI) of CQ upon interaction with various protein aggregates, biomacromolecules and polymorphic Aβ species. (d) Dual staining of human brain cross-sections using CQ and ThT (100 nM CQ: 1.57 mM thioflavin T). (e) CQ stains Aβ plaques and congophilic angiopathy in human brain tissue with Congo red as control. (f) Molecular structure of the probe CQ and selective staining of Aβ plaques in human brain tissue. CQ selectively stains Aβ plaques in brain tissue in AD even in the presence of NFTs of Tau. This figure has been adapted from ref. 49 and 50 with permission from Nature Publishing Group and Elsevier, respectively.
Fig. 3 Red and NIR (far-red) fluorescent probes for diagnosis of AD. (a) Absorption and emission (λex = 537 nm) spectra of the probe TC in the presence and absence (dotted lines) of Aβ42 fibrillar aggregates. Inset: molecular structure of TC. (b) Photographs of TC and samples of TC + Aβ42 fibrillar aggregates illuminated with visible and UV light (365 nm) and TC + Aβ42 fibrillar aggregates illuminated with a green laser (532 nm), which gives a red beam in the sample solution. (c) Normalized fluorescence intensity (NFI) of CQ upon interaction with various protein aggregates, biomacromolecules and polymorphic Aβ species. (d) Dual staining of human brain cross-sections using CQ and ThT (100 nM CQ: 1.57 mM thioflavin T). (e) CQ stains Aβ plaques and congophilic angiopathy in human brain tissue with Congo red as control. (f) Molecular structure of the probe CQ and selective staining of Aβ plaques in human brain tissue. CQ selectively stains Aβ plaques in brain tissue in AD even in the presence of NFTs of Tau. This figure has been adapted from ref. 49 and 50 with permission from Nature Publishing Group and Elsevier, respectively.CC BY-NC · PubMed Central
Fig. 4 Molecular structures of thioflavin T, thioflavin S, PET probes and SPECT probe for the detection and imaging of Aβ and Tau aggregates.
Fig. 4 Molecular structures of thioflavin T, thioflavin S, PET probes and SPECT probe for the detection and imaging of Aβ and Tau aggregates.CC BY-NC · PubMed Central
Fig. 5 Aggregation inhibitors based on small molecules and natural products.
Fig. 5 Aggregation inhibitors based on small molecules and natural products.CC BY-NC · PubMed Central
Fig. 6 Peptidomimetic modulators. Cyclic hybrid peptoids (a) as autophagy modulators (b). (c) Schematic representation of inhibition and dissolution of Aβ42 aggregates by the peptidomimetic inhibitor P5. (d) Structure of P5. (e) Growth curve of yeast (autophagy model) with Aβ toxicity. P5 rescues yeast cells from Aβ toxicity. (f) Degradation of toxic GFP-βA by P5 in a WT GFP-βA yeast model. This figure has been adapted from ref. 88 and 89 with permission from Wiley and Nature Publishing Group, respectively.
Fig. 6 Peptidomimetic modulators. Cyclic hybrid peptoids (a) as autophagy modulators (b). (c) Schematic representation of inhibition and dissolution of Aβ42 aggregates by the peptidomimetic inhibitor P5. (d) Structure of P5. (e) Growth curve of yeast (autophagy model) with Aβ toxicity. P5 rescues yeast cells from Aβ toxicity. (f) Degradation of toxic GFP-βA by P5 in a WT GFP-βA yeast model. This figure has been adapted from ref. 88 and 89 with permission from Wiley and Nature Publishing Group, respectively.CC BY-NC · PubMed Central
Fig. 7 Multifunctional peptidomimetic modulators. (a) Schematic representation showing modulation of the multifaceted toxicity of Aβ by the multifunctional modulator P6. (b) Molecular structure of P6. (c) P6 rescues plasmid DNA (pBR322) from damage by ROS generated by the Aβ42 + CuII + Asc system. (d) P6 rescues PC12 cells from toxicity induced by metal-induced Aβ42 aggregates. This figure has been adapted from ref. 98 with permission from the American Chemical Society.
Fig. 7 Multifunctional peptidomimetic modulators. (a) Schematic representation showing modulation of the multifaceted toxicity of Aβ by the multifunctional modulator P6. (b) Molecular structure of P6. (c) P6 rescues plasmid DNA (pBR322) from damage by ROS generated by the Aβ42 + CuII + Asc system. (d) P6 rescues PC12 cells from toxicity induced by metal-induced Aβ42 aggregates. This figure has been adapted from ref. 98 with permission from the American Chemical Society.CC BY-NC · PubMed Central
Fig. 8 (a) Small-molecule-based metal chelators and hybrid multifunctional modulators (HMMs). (b) Schematic representation of inhibition of the multifaceted toxicity of Aβ and mitochondrial damage by an HMM. (c) Molecular structure of an HMM (TGR 86). (d) TGR86 rescues PC12 cells from toxicity induced by metal-induced Aβ42 aggregates. TGR86 rescues the mitochondrial membrane potential of PC12 cells from the metal-induced toxicity of Aβ42. (e) Microscopic images and (f) quantification of fluorescence at 540 nm (λex = 511 nm). This figure has been adapted from ref. 105 with permission from the American Chemical Society.
Fig. 8 (a) Small-molecule-based metal chelators and hybrid multifunctional modulators (HMMs). (b) Schematic representation of inhibition of the multifaceted toxicity of Aβ and mitochondrial damage by an HMM. (c) Molecular structure of an HMM (TGR 86). (d) TGR86 rescues PC12 cells from toxicity induced by metal-induced Aβ42 aggregates. TGR86 rescues the mitochondrial membrane potential of PC12 cells from the metal-induced toxicity of Aβ42. (e) Microscopic images and (f) quantification of fluorescence at 540 nm (λex = 511 nm). This figure has been adapted from ref. 105 with permission from the American Chemical Society.CC BY-NC · PubMed Central
Fig. 9 (a) Active and passive immunotherapy. (b) Liposome-based active immunisation and interaction of anti-Aβ antibodies with Aβ. This figure has been adapted from ref. 120, 123 and 124 with permission from Nature Publishing Group (120 and 124) and BioMed Central (123).
Fig. 9 (a) Active and passive immunotherapy. (b) Liposome-based active immunisation and interaction of anti-Aβ antibodies with Aβ. This figure has been adapted from ref. 120, 123 and 124 with permission from Nature Publishing Group (120 and 124) and BioMed Central (123).CC BY-NC · PubMed Central
Fig. 10 Molecular structures of inhibitors of β-secretase, γ-secretase and kinases that are undergoing clinical trials.
Fig. 10 Molecular structures of inhibitors of β-secretase, γ-secretase and kinases that are undergoing clinical trials.CC BY-NC · PubMed Central
Fig. 11 Molecular structures of modulators of inflammation that are undergoing clinical trials.
Fig. 11 Molecular structures of modulators of inflammation that are undergoing clinical trials.CC BY-NC · PubMed Central
Fig. 12 (a) Cholinergic inhibitors and NMDA antagonist for treating AD. Molecular docking of donepezil (b) and memantine (c) with AChE and NMDA receptors, respectively. This figure has been adapted from ref. 156 with permission from Nature Publishing Group.
Fig. 12 (a) Cholinergic inhibitors and NMDA antagonist for treating AD. Molecular docking of donepezil (b) and memantine (c) with AChE and NMDA receptors, respectively. This figure has been adapted from ref. 156 with permission from Nature Publishing Group.CC BY-NC · 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

Show all 158 references

Research works printed but not linked: 7

  1. Steele, 2013, Postdoc J., 1, 21
  2. Newberg, 2006, J. Nucl. Med., 47, 748
  3. Hung, 2017, J. Biomed. Sci., 24, 47, 10.1186/s12929-017-0355-7 · DOI · Paper page
  4. Mark, 2002, Curr. Opin. Drug Discovery Dev., 2, 417
  5. Guo, 2013, Neural Regener. Res., 8, 2003
  6. Zhang, 2014, Front. Cell. Neurosci., 8, 427
  7. Dolan, 2010, Curr. Opin. Drug Discovery Dev., 13, 595

Cited by

Sorted by citations

See all 154

Related

Metadata

Authors
Rajasekhar, K., & Govindaraju, T.
Affiliations
Jawaharlal Nehru Centre for Advanced Scientific Research (IN)
Corresponding author
Govindaraju, Thimmaiah
ORCID
Venue
RSC Advances
Publisher
Royal Society of Chemistry (RSC)
Published
2018
Volume
8
Issue
42
Pages
23780-23804
ISSN
2046-2069 (ISSN-L)
DOI
10.1039/c8ra03620a
PMC
PMC9081849
OpenAlex
W2811135471
Cited by
150
References
158
Citations by year
2026: 4 · 2025: 16 · 2024: 27 · 2023: 20 · 2022: 17 · 2021: 24 · 2020: 25 · 2019: 13 · 2018: 4
FWCI
2.17
Type
journal article
Language
en
Open access
Licence
Locations
  • RSC Advances (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
  • Department of Science and Technology, Ministry of Science and Technology (DST/SJF/CSA-02/2015-2016)
  • Sheikh Saqr Laboratory
  • Jawaharlal Nehru Centre for Advanced Scientific Research
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
  • Health Sciences › Medicine › Pharmacology (medical) › Cholinesterase and Neurodegenerative Diseases
Keywords
Alzheimer's disease, Alzheimer's disease pathogenesis, early diagnosis, therapeutic interventions, drug development, neurotoxicity, clinical trials

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