The DOI matches its Crossref record; 248 of the 250 references it cites were found in a registry or an index.
Disease modifying therapy for AD?1
Open accessAbstract
Alzheimer's disease (AD) is the most common form of dementia in industrialized nations. If more effective therapies are not developed that either prevent AD or block progression of the disease in its very early stages, the economic and societal cost of caring for AD patients will be devastating. Only two types of drugs are currently approved for the treatment of AD: inhibitors of acetyl cholinesterase, which symptomatically enhance cognitive state to some degree but are not disease modifying; and the adamantane derivative, memantine. Memantine preferentially blocks excessive NMDA receptor activity without disrupting normal receptor activity and is thought to be a neuroprotective agent that blocks excitotoxicty. Memantine therefore may have a potentially disease modifying effect in multiple neurodegenerative conditions. An improved understanding of the pathogeneses of AD has now led to the identification of numerous therapeutic targets designed to alter amyloid beta protein (Abeta) or tau accumulation. Therapies that alter Abeta and tau through these various targets are likely to have significant disease modifying effects. Many of these targets have been validated in proof of concept studies in preclinical animal models, and some potentially disease modifying therapies targeting Abeta or tau are being tested in the clinic. This review will highlight both the promise of and the obstacles to developing such disease modifying AD therapies.
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.
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?
The cited source says what the claim attributes to it.
In the citing paper
“AD disease-modifying strategies are designed to target abnormal Aβ aggregates, clear, and delay or prevent the formation of aggregates [33].”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [33]
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
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
Hardy, J., & Selkoe, D. J. (2002) · Science · doi:10.1126/science.1072994 · Cited by 13,864
Alzheimer's disease: the amyloid cascade hypothesis
Hardy, J. A., & Higgins, G. A. (1992) · Science · doi:10.1126/science.1566067 · Cited by 7,484
Alzheimer's Disease: Genes, Proteins, and Therapy
Selkoe, D. J. (2001) · Physiological Reviews · doi:10.1152/physrev.2001.81.2.741 · Cited by 6,063
Inflammation and Alzheimer’s disease
Akiyama, H. (2000) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00124-x · Cited by 4,514
Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound‐B
Klunk, W. E., Engler, H., Nordberg, A., Wang, Y., Blomqvist, G., Holt, D. P., Bergström, M., Savitcheva, I., Huang, G., Estrada, S., et al. (2004) · Annals of Neurology · doi:10.1002/ana.20009 · Cited by 4,496
Amyloid plaque core protein in Alzheimer disease and Down syndrome.
Masters, C. L., Simms, G., Weinman, N. A., Multhaup, G., McDonald, B. L., & Beyreuther, K. (1985) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.82.12.4245 · Cited by 4,431
Vassar, R., Bennett, B. D., Babu-Khan, S., Kahn, S., Mendiaz, E. A., Denis, P., Teplow, D. B., Ross, S., Amarante, P., Loeloff, R., et al. (1999) · Science · doi:10.1126/science.286.5440.735 · Cited by 3,876 · cited 1×
“…membrane bound aspartyl protease responsible for b-secretase cleavage of APP (BACE, memapsin, b-secretase) (Hussain et al. 1999; Sinha et al. 1999; Vassar et al. 1999; Yan et al. 1999). b-secretase is an excellent theoretical target as it is the rate limiting enzyme in Ab production, but it has…”
BackgroundAssociation of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17
Hutton, M., Lendon, C. L., Rizzu, P., Baker, M., Froelich, S., Houlden, H., Pickering-Brown, S., Chakraverty, S., Isaacs, A., Grover, A., et al. (1998) · Nature · doi:10.1038/31508 · Cited by 3,498
Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse
Schenk, D., Barbour, R., Dunn, W., Gordon, G., Grajeda, H., Guido, T., Hu, K., Huang, J., Johnson-Wood, K., Khan, K., et al. (1999) · Nature · doi:10.1038/22124 · Cited by 3,160
Lee, V. M.-Y., Goedert, M., & Trojanowski, J. Q. (2001) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.24.1.1121 · Cited by 2,480
Flagged first, then by citations
2 of the 250 references couldn’t be matched to a known paper.
Research works printed but not linked: 2
- Black S., 2006, Efficacy and safety ofMPC‐7869 (R.‐flurbiprofen), a selective Abeta42 loering agent in mild Alzheimer's disease: results of a 12‐month phase 2 trial and 1‐year follow on study, Neurology, 66, A347
- Seabrook T. J., 2006, Dendrimeric Abeta1–15 is an effective immunogen in wildtype and APP‐tg mice, Neurobiol. Aging.
Cited by
Sorted by citations
Items 101–119 of 119
Cutler, N. R., Sramek, J. J., Murphy, M. F., Riordan, H., Bieck, P. R., & Carta, A. (2010) · doi:10.1002/9781444318579.ch6
What does it take to stay healthy past 100?
Price, J. L. (2008) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2008.04.011
Luzardo, M. D. (2013) · Revista da Graduação
Summary, Perspective and Direction for Future Research
Farooqui, A. A. (2016) · Springer eBooks · doi:10.1007/978-3-319-15889-1_10
Golde, T. E., Lessard, C. B., & Ran, Y. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-802173-6.00005-8
Self-citationCroft, C. L. (2016) · Research Portal (King's College London)
The Roles of GxxxG Motif and γ-Secretase Components in APP Processing
Kim, S., Han, S., & Nam, H. G. (2009)
An Innovative Framework for Integrative Rehabilitation in Dementia
Bragin, V., & Bragin, I. (2022) · IntechOpen eBooks · doi:10.5772/intechopen.101863
Current awareness in geriatric psychiatry
(2007) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.1629
Therapeutic antibodies as a Wright Brothers' airplane: Clinical proof-of-concept
Saido, T. C. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-28979-8.00015-2
Özkurt, Ç., Köse, S., Karasu, Ç., Kortholt, A., & Kelicen‐Uğur, P. (2025) · Research Square · doi:10.21203/rs.3.rs-7094261/v1
Determinants of Treatment Willingness and Willingness-to-Pay for Lecanemab in China
Tan, A., Wang, Z., Aumont, É., Li, A., Qin, X., Yang, X., Feng, W., Yang, J., Li, X., Xiao, J. F., et al. (2025) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0000000000000689
Grapevine Stilbenoids: Bioavailability and Neuroprotection
Waffo‐Téguo, P., Krisa, S., Pawlus, A. D., Richard, T., Monti, J., & Mérillon, J. (2025) · Springer eBooks · doi:10.1007/978-3-642-36202-6_74-1
Özkurt, Ç., Köse, S., Karasu, Ç., Kortholt, A., & Kelicen‐Uğur, P. (2026) · Neurochemical Research · doi:10.1007/s11064-026-04792-w
Metadata
- Authors
- Golde, T. E.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Golde, Todd E.
- ORCID
- Golde, Todd E.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2006-10-02
- Volume
- 99
- Issue
- 3
- Pages
- 689-707
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2056442085
- Cited by
- 117
- References
- 250
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 2 · 2022: 2 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 1 · 2017: 3 · 2016: 5 · 2015: 3 · 2014: 3 · 2013: 5 · 2012: 6
- FWCI
- 2.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association
- National Institutes of Health
- National Institute on Aging
- 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, disease-modifying therapy, amyloid-beta, tau protein, acetylcholinesterase inhibitors, memantine, NMDA receptor, neuroprotection, excitotoxicity, therapeutic target, clinical trials, dementia
- MeSH terms
- Alzheimer Disease, Animals, Humans, Immunotherapy, Peptide Hydrolases, Phosphorylation, Protease Inhibitors, Amyloid beta-Peptides, Neurofibrillary Tangles, tau Proteins, Protein Folding, Molecular Chaperones, Alzheimer Vaccines
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
