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Neurology International
Special Issues
Pathogenesis and Therapeutic Intervention of Alzheimer's Disease
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Pathogenesis and Therapeutic Intervention of Alzheimer's Disease

A Special Issue of Neurology International (ISSN 2035-8377) belonging to the section "Movement Disorders and Neurodegenerative Diseases".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 478

Editor

Dr. Chanchal Sharma

E-Mail Website
Guest Editor
School of Chemistry, Chemical Engineering and Biotechnology, Nanyang Technological University, Singapore, Singapore
Interests: Alzheimer’s disease; neuroinflammation; microglia; gene therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer's Disease (AD) is the most common cause of dementia. Neuronal death occurs via several mechanisms, including oxidative stress, excitotoxicity, energy depletion, inflammation, and apoptosis, particularly in brain regions that are essential for cognitive and memory functions. Although no therapeutic approach has achieved complete success in the treatment of AD, the early detection and management of AD with appropriate drugs is crucial for improving prognosis. An enhanced understanding of the molecular mechanisms that underlie neuronal cell death and glial homeostasis could pave the way for novel therapeutic strategies. Several treatments have progressed to the clinical stage, including acetylcholinesterase inhibitors, nerve growth factors, nonsteroidal anti-inflammatory drugs (NSAIDs), estrogen, and compounds such as antioxidants, neuronal calcium channel blockers, and anti-apoptotic agents. More recently, it has been suggested that the gut microbiome could influence the function of the brain. Additionally, the application of artificial intelligence in the identification of novel AD-related genes has provided new opportunities for research and therapeutic development.

You may choose our Joint Special Issue in Biomedicines.

Dr. Chanchal Sharma
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Neurology International is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • dementia
  • Alzheimer’s disease
  • neuroinflammation
  • microglia
  • gene therapy
  • stem cells
  • blood–brain barrier
  • oxidative stress
  • gut-microbiome
  • diet
  • artificial intelligence

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Published Papers (1 paper)

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Review

17 pages, 382 KB  
Review
Anti-Amyloid Monoclonal Antibodies in Early Alzheimer Disease: Lecanemab and Donanemab
by Ülkü Figen Demir and Fatmanur Karakuş Dilbaz
Neurol. Int. 2026, 18(9), 171; https://doi.org/10.3390/neurolint18090171 - 11 Sep 2026
Abstract
Background/Objectives: Alzheimer disease (AD) causes progressive cognitive and functional loss and substantial caregiver and healthcare burden. Anti-amyloid monoclonal antibodies represent a shift toward biology-directed treatment in biomarker-confirmed early symptomatic AD, but modest clinical effects must be balanced against amyloid-related imaging abnormalities (ARIA), intensive [...] Read more.
Background/Objectives: Alzheimer disease (AD) causes progressive cognitive and functional loss and substantial caregiver and healthcare burden. Anti-amyloid monoclonal antibodies represent a shift toward biology-directed treatment in biomarker-confirmed early symptomatic AD, but modest clinical effects must be balanced against amyloid-related imaging abnormalities (ARIA), intensive monitoring, and implementation burden. Heterogeneity in trial populations, endpoints, dosing, stopping rules, and follow-up complicates interpretation. This narrative review critically integrates efficacy, safety, durability, biomarker, and implementation evidence for lecanemab and donanemab while preserving study-family relationships and avoiding unsupported cross-trial superiority claims. Methods: For this revised narrative review, a targeted PubMed/MEDLINE search covering the period from database inception was initially conducted before manuscript submission and was subsequently updated through 21 August 2026, supplemented by reference-list and citation tracking. Search terms combined Alzheimer disease with lecanemab, donanemab, anti-amyloid monoclonal antibody, ARIA, APOE, amyloid PET, open-label extension, real-world, clinical meaningfulness, implementation, and access. Sixty-two sources were purposively selected for a comprehensive narrative synthesis; no meta-analysis or formal certainty grading was performed. Results: Pivotal trials demonstrated statistically significant but modest average slowing of decline: Clarity AD showed a 0.45-point between-group difference in CDR-SB worsening at 18 months, and TRAILBLAZER-ALZ 2 showed a 3.25-point iADRS difference in the low/medium-tau population at 76 weeks. ARIA-E occurred in 12.6% of lecanemab-treated and 24.0% of donanemab-treated participants in the pivotal trials, with higher risk in APOE ε4 carriers. Extensions and biomarker analyses suggest persistent biological effects but are less secure for causal inference, and real-world evidence is currently more mature for lecanemab. Conclusions: Both antibodies substantially reduce amyloid and modestly slow average clinical decline in selected patients, but neither restores lost function, greater amyloid clearance does not establish greater individual benefit, and cross-trial superiority cannot be inferred. Treatment requires biomarker-guided selection, APOE-informed risk counseling, serial MRI, infusion and ARIA-management capacity, and shared decision-making that incorporates cost, access, and patient/caregiver burden. Full article
(This article belongs to the Special Issue Pathogenesis and Therapeutic Intervention of Alzheimer's Disease)
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