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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 31 out of 100. Treatments

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Alzheimer’s disease (AD) is characterized by progressive accumulation of amyloid-β (Aβ) peptides, initiating a pathological cascade from soluble monomers to toxic oligomers, protofibrils, fibrils, and ultimately extracellular amyloid plaques that contribute to synaptic dysfunction and neuronal degeneration. Aβ is generated through sequential cleavage of amyloid precursor protein by β- and γ-secretases, releasing peptides into the brain and cerebrospinal fluid. Therapeutic monoclonal antibodies have been developed to target distinct Aβ species along this aggregation pathway. Agents such as solanezumab and bapineuzumab primarily bind monomeric Aβ, while aducanumab, gantenerumab, crenezumab, and SAR228810 target aggregated forms, and lecanemab preferentially recognizes protofibrils. Donanemab selectively targets deposited amyloid plaques. Recent regulatory approvals of aducanumab, lecanemab, and donanemab demonstrate significant plaque reduction and modest slowing of cognitive decline in early AD, supporting the amyloid hypothesis. However, multiple clinical failures highlight limitations including late-stage intervention, inadequate targeting of neurotoxic oligomers, and safety concerns such as amyloid-related imaging abnormalities. Future therapeutic strategies emphasize early intervention, improved targeting of soluble toxic species, enhanced brain penetration, and biomarker-guided patient selection. Collectively, monoclonal antibodies validate Aβ as a therapeutic target while underscoring the need to optimize timing, specificity, and clinical impact in AD treatment.

What this study adds

Evidence grade: Low

Regulatory approvals of aducanumab, lecanemab and donanemab show significant plaque reduction and modest slowing of cognitive decline in early Alzheimer disease, supporting the amyloid hypothesis. Multiple clinical failures highlight limitations including late-stage intervention, inadequate targeting of neurotoxic oligomers, and safety concerns such as ARIA.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Bhati, S. S., & Tanwar, S. S. (2026). Therapeutic monoclonal antibodies targeting amyloid beta in Alzheimer disease current evidence clinical outcomes limitations and future directions. Discover Neuroscience. https://doi.org/10.1186/s13064-026-00295-0

Vancouver

Bhati SS, Tanwar SS. Therapeutic monoclonal antibodies targeting amyloid beta in Alzheimer disease current evidence clinical outcomes limitations and future directions. Discover Neuroscience. 2026. doi:10.1186/s13064-026-00295-0.

BibTeX

@article{bhati2026-0a449f11,
  author  = {Bhati, Sampat Singh and Tanwar, Sampat Singh},
  title   = {{Therapeutic monoclonal antibodies targeting amyloid beta in Alzheimer disease current evidence clinical outcomes limitations and future directions}},
  journal = {Discover Neuroscience},
  year    = {2026},
  doi     = {10.1186/s13064-026-00295-0},
  url     = {https://doi.org/10.1186/s13064-026-00295-0}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

Key findings

Why it matters

Regulatory approvals of aducanumab, lecanemab and donanemab show significant plaque reduction and modest slowing of cognitive decline in early Alzheimer disease, supporting the amyloid hypothesis. Multiple clinical failures highlight limitations including late-stage intervention, inadequate targeting of neurotoxic oligomers, and safety concerns such as ARIA.

Study details

How this study scored 31/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 0 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 5 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomized / blinded 0 of 2; Times cited 1 of 7; Citations per year 0 of 5; Impact for its field and year 3 of 6; Cited by studies here 0 of 6; Still being cited 0 of 4; Senior author's track record 1 of 4; Institution's track record 0 of 3; Multicenter collaboration 0 of 3; Indexed in PubMed 1 of 2; Free to read 2 of 2. Total 31 of 100.31 of 100 points earned69 not earned

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Discover Neuroscience)
Journal's citation record 0 / 4 Discover Neuroscience: journal h-index 6 (OpenAlex, 2026-10-29)
Study design 0 / 12 No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence 1 / 5 Rated “low” in our summary
Peer-review validation 10 / 10 Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent 5 / 5 2026 — within 1 year(s) of the newest study here
Sample size 0 / 4 Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported 0 / 3 No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people 0 / 3 Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomized / blinded 0 / 2 No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 1 / 7 Cited 1 times (OpenAlex, 2026-10-10)
Citations per year 0 / 5 0.5 citations a year over 2 year(s) since 2026
Impact for its field and year 3 / 6 Cited 4.2× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 0 / 6 No other study in this library cites it
Still being cited 0 / 4 Cited 1 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 1 / 4 Last-listed author Sampat Singh Tanwar: h-index 6 (OpenAlex, whole career)
Institution's track record 0 / 3 Shri Vaishnav Vidyapeeth Vishwavidyalaya, Indore: institution h-index 49 (OpenAlex)
Multicenter collaboration 0 / 3 OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed 1 / 2 Not in PubMed, but has a DOI
Free to read 2 / 2 Free to read
Total 31 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

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