The DOI matches its Crossref record; 168 of the 168 references it cites were found in a registry or an index.
Amyloid Beta in Aging and Alzheimer’s Disease
Open accessAbstract
Alzheimer’s disease (AD), is a progressive neurodegenerative disease that affects behavior, thinking, learning, and memory in elderly individuals. AD occurs in two forms, early onset familial and late-onset sporadic; genetic mutations in PS1, PS2, and APP genes cause early onset familial AD, and a combination of lifestyle, environment and genetic factors causes the late-onset sporadic form of the disease. However, accelerated disease progression is noticed in patients with familial AD. Disease-causing pathological changes are synaptic damage, and mitochondrial structural and functional changes, in addition to increased production and accumulation of phosphorylated tau (p-tau), and amyloid beta (Aβ) in the affected brain regions in AD patients. Aβ is a peptide derived from amyloid precursor protein (APP) by proteolytic cleavage of beta and gamma secretases. APP is a glycoprotein that plays a significant role in maintaining neuronal homeostasis like signaling, neuronal development, and intracellular transport. Aβ is reported to have both protective and toxic effects in neurons. The purpose of our article is to summarize recent developments of Aβ and its association with synapses, mitochondria, microglia, astrocytes, and its interaction with p-tau. Our article also covers the therapeutic strategies that reduce Aβ toxicities in disease progression and discusses the reasons for the failures of Aβ therapeutics.
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
1 retracted
Kuruva, C. S., Mańczak, M., Yin, X., Ogunmokun, G., Reddy, A. P., & Reddy, P. H. (2017) · Human Molecular Genetics · doi:10.1093/hmg/ddx226 · Cited by 71
Self-citationRetractedHealth benefits of physical activity: the evidence
Warburton, D. E. R. (2006) · Canadian Medical Association Journal · doi:10.1503/cmaj.051351 · Cited by 8,007
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
Goate, A., Chartier-Harlin, M.-C., Mullan, M., Brown, J., Crawford, F., Fidani, L., Giuffra, L., Haynes, A., Irving, N., James, L., et al. (1991) · Nature · doi:10.1038/349704a0 · Cited by 4,659
The neuropathological diagnosis of Alzheimer's disease
DeTure, M. A., & Dickson, D. W. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0333-5 · Cited by 3,329
The molecular pathology of Alzheimer's disease
Selkoe, D. J. (1991) · Neuron · doi:10.1016/0896-6273(91)90052-2 · Cited by 2,708
Amyloid deposition as the central event in the aetiology of Alzheimer’s disease
Hardy, J., & Allsop, D. (1991) · Trends in Pharmacological Sciences · doi:10.1016/0165-6147(91)90609-v · Cited by 2,538
Inflammation as a central mechanism in Alzheimer's disease
Kinney, J. W., Bemiller, S. M., Murtishaw, A. S., Leisgang, A. M., Salazar, A. M., & Lamb, B. T. (2018) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1016/j.trci.2018.06.014 · Cited by 2,253
Oxidative stress and the amyloid beta peptide in Alzheimer’s disease
Cheignon, C., Tomas, M., Bonnefont-Rousselot, D., Faller, P., Hureau, C., & Collin, F. (2018) · Redox Biology · doi:10.1016/j.redox.2017.10.014 · Cited by 2,185
Amyloid Precursor Protein Processing and Alzheimer's Disease
O'Brien, R. J., & Wong, P. C. (2011) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-061010-113613 · Cited by 2,061
Cited by
Alzheimer’s disease as type 3 diabetes: understanding the link and implications
Kciuk, M., Kruczkowska, W., Gałęziewska, J., Wanke, K., Kałuzińska-Kołat, Ż., Aleksandrowicz, M., & Kontek, R. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252211955 · Cited by 98
Amyloid-β and Tau in Alzheimer’s disease: pathogenesis, mechanisms, and interplay
Abdulkhaliq, A. A., Kim, B., Almoghrabi, Y. M., Khan, J., Ajoolabady, A., Ren, J., Bahijri, S., Tuomilehto, J., Borai, A., & Pratico, D. (2026) · Cell Death & Disease · doi:10.1038/s41419-025-08186-8 · Cited by 87
Kazemeini, S., Nadeem-Tariq, A., Shih, R., Rafanan, J., Ghani, N., & Vida, T. A. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252111720 · Cited by 41
Islam, M. A., Sultana, O. F., Bandari, M., Kshirsagar, S., Manna, P. R., & Reddy, P. H. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102459 · Cited by 28
Self-citationAdvances in nanotechnology for targeted drug delivery in neurodegenerative diseases
Rafieezadeh, D. (2025) · American Journal of Neurodegenerative Disease · doi:10.62347/qhvi3317 · Cited by 20
Metadata
- Authors
- Sehar, U., Rawat, P., Reddy, A. P., Kopel, J., & Reddy, P. H.
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2022-10-26
- Volume
- 23
- Issue
- 21
- Pages
- 12924
- ISSN
- 1422-0067 (ISSN-L)
- OpenAlex
- W4307280821
- Cited by
- 361
- References
- 168
- FWCI
- 35.68
- 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: Amyloid Beta in Aging and Alzheimer’s Disease. https://app.cochat.ai/papers/10.3390/ijms232112924
- The paper
- Sehar, U., Rawat, P., Reddy, A. P., Kopel, J., & Reddy, P. H. (2022). Amyloid Beta in Aging and Alzheimer’s Disease. International Journal of Molecular Sciences. https://doi.org/10.3390/ijms232112924
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.
