The DOI matches its Crossref record; 306 of the 306 references it cites were found in a registry or an index.
Advances in developing novel therapeutic strategies for Alzheimer’s disease
Open accessAbstract
Alzheimer's Disease (AD), the most prevalent neurodegenerative disease of aging, affects one in eight older Americans. Nearly all drug treatments tested for AD today have failed to show any efficacy. There is a great need for therapies to prevent and/or slow the progression of AD. The major challenge in AD drug development is lack of clarity about the mechanisms underlying AD pathogenesis and pathophysiology. Several studies support the notion that AD is a multifactorial disease. While there is abundant evidence that amyloid plays a role in AD pathogenesis, other mechanisms have been implicated in AD such as tangle formation and spread, dysregulated protein degradation pathways, neuroinflammation, and loss of support by neurotrophic factors. Therefore, current paradigms of AD drug design have been shifted from single target approach (primarily amyloid-centric) to developing drugs targeted at multiple disease aspects, and from treating AD at later stages of disease progression to focusing on preventive strategies at early stages of disease development. Here, we summarize current strategies and new trends of AD drug development, including pre-clinical and clinical trials that target different aspects of disease (mechanism-based versus non-mechanism based, e.g. symptomatic treatments, lifestyle modifications and risk factor management).
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.
Integrity signals
Registry
Cites
Statistics
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.
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
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., Klunk, W. E., Koroshetz, W. J., Manly, J. J., Mayeux, R., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.005 · Cited by 18,657
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Albert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., Gamst, A., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.008 · Cited by 10,152 · cited 2×
“AD biomarkers include key proteins that reflect AD pathology such as amyloid and tau, as well as biomarkers of neuronal injury and regional patterns of abnormalities detected by various imaging modalities that provide indirect evidence of disease development and progression [293, 294].”
Background2016 Alzheimer's disease facts and figures
Alzheimer's Association (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.03.001 · Cited by 5,069
Clinical and biomarker changes in dominantly inherited Alzheimer's disease
Bateman, R. J., Xiong, C., Benzinger, T. L. S., Fagan, A. M., Goate, A., Fox, N. C., Marcus, D. S., Cairns, N. J., Xie, X., Blazey, T. M., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1202753 · Cited by 3,814
Ngandu, T., Lehtisalo, J., Solomon, A., Levälahti, E., Ahtiluoto, S., Antikainen, R., Bäckman, L., Hänninen, T., Jula, A., Laatikainen, T., et al. (2015) · The Lancet · doi:10.1016/s0140-6736(15)60461-5 · Cited by 3,689
Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy
Liu, C.-C., Kanekiyo, T., Xu, H., & Bu, G. (2013) · Nature Reviews Neurology · doi:10.1038/nrneurol.2012.263 · Cited by 3,459
Shepherd, J., Blauw, G. J., Murphy, M. B., Bollen, E. L., Buckley, B. M., Cobbe, S. M., Ford, I., Gaw, A., Hyland, M., Jukema, J. W., et al. (2002) · The Lancet · doi:10.1016/s0140-6736(02)11600-x · Cited by 3,378
2013 Alzheimer's disease facts and figures
Alzheimer's Association, Thies, W., & Bleiler, L. (2013) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2013.02.003 · Cited by 3,328
Cited by
The Semantics of Microglia Activation: Neuroinflammation, Homeostasis, and Stress
Woodburn, S. C., Bollinger, J. L., & Wohleb, E. S. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02309-6 · Cited by 783
Neuro-inflammation and anti-inflammatory treatment options for Alzheimer’s disease
Ozben, T., & Ozben, S. (2019) · Clinical Biochemistry · doi:10.1016/j.clinbiochem.2019.04.001 · Cited by 381
Dhapola, R., Hota, S. S., Sarma, P., Bhattacharyya, A., Medhi, B., & Reddy, D. H. (2021) · Inflammopharmacology · doi:10.1007/s10787-021-00889-6 · Cited by 383
The Pivotal Role of NF-kB in the Pathogenesis and Therapeutics of Alzheimer’s Disease
Sun, E., Motolani, A., Campos, L., & Lu, T. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23168972 · Cited by 361
APOE2: protective mechanism and therapeutic implications for Alzheimer’s disease
Li, Z., Shue, F., Zhao, N., Shinohara, M., & Bu, G. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00413-4 · Cited by 306
Metadata
- Authors
- Cao, J., Hou, J., Ping, J., & Cai, D.
- Venue
- Molecular Neurodegeneration
- Published
- 2018-12
- Volume
- 13
- Issue
- 1
- Pages
- 64-64
- ISSN
- 1750-1326 (ISSN-L)
- OpenAlex
- W2905504149
- Cited by
- 285
- References
- 306
- FWCI
- 21.38
- Type
- journal article
- Language
- en
- Open access
- gold
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
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Advances in developing novel therapeutic strategies for Alzheimer’s disease. https://app.cochat.ai/papers/10.1186/s13024-018-0299-8
- The paper
- Cao, J., Hou, J., Ping, J., & Cai, D. (2018). Advances in developing novel therapeutic strategies for Alzheimer’s disease. Molecular Neurodegeneration. https://doi.org/10.1186/s13024-018-0299-8
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
