Evidence mapPaperPMID 42084750Full record

ReviewJournal of neurology2026

A new era in neuropharmacology: assessing the efficacy and safety of novel anti-amyloid and non-amyloid drug targets for Alzheimer's disease.

Mohamed M Hafez, Haidy A Abbas, Nabil A Shoman, Ayman A Soubh, Omnia Aly, Mohamed F Sallam, Mahmoud Seliem, Fady A Malaak

Abstract readReview
In one paragraph

Review in Journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Mohamed M HafezDepartment of Biochemistry, Faculty of Pharmacy, Ahram Canadian University, Giza, Egypt. mmhafez@acu.edu.eg.
Haidy A AbbasDepartment of Pharmacognosy, Faculty of Pharmacy, Ahram Canadian University, Giza, Egypt.
Nabil A ShomanDepartment of Pharmaceutics and Pharmaceutical Technology, Faculty of Pharmacy, Ahram Canadian University, Giza, Egypt.
Ayman A SoubhDepartment of Pharmacology and Toxicology, School of Life and Medical Sciences, University of Hertfordshire Hosted By Global Academic Foundation, New Administrative Capital, Cairo, Egypt.
Omnia AlyDepartment of Medical Biochemistry, National Research Centre, Cairo, Egypt.
Mohamed F SallamDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Ahram Canadian University, Giza, Egypt.
Mahmoud SeliemDepartment of Biochemistry, Faculty of Pharmacy, Ahram Canadian University, Giza, Egypt.
Fady A MalaakDepartment of Pharmaceutics and Pharmaceutical Technology, Faculty of Pharmacy, Ahram Canadian University, Giza, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer disease (AD) is the most common cause of dementia in the world with the prevalence expected to increase threefold to 152.8 million people by 2050. The current medications provide a short-term ameliorative effect, and this requires development of disease-modifying treatments, which address the biological pathogenesis.

methodsThis review assesses the changing neuropharmacological environment offering a critical analysis of anti-amyloid monoclonal antibodies and investigates the so-called expanding frontier of non-amyloid targets. It also examines the approaches of clinical trials and the trend of biomarker-based patient selection and precision medicine.

resultsAlthough β-site APP-cleaving enzyme 1 (BACE1) and secretase inhibitors did not achieve success in clinical trials because of mechanism-based toxicity and cognitive impairment, new monoclonal antibodies such as lecanemab and donanemab have shown high amyloid plaque clearance and reduced cognitive deterioration. Nevertheless, the treatments are associated with amyloid-related imaging abnormalities (ARIA). In addition to amyloid, studies are focusing on tau hyperphosphorylation, neuroinflammation through triggering receptor on myeloid cells 2 (TREM2) and NLR family pyrin domain containing 3 (NLRP3) and growth factor-mediated synaptic plasticity through brain-derived neurotrophic factor (BDNF).

conclusionsAD treatment has entered the new era that demands a paradigm shift from monotherapies to multi-target cocktails. The future lies in precision neuropharmacology, where genetic stratification and individual biomarker analysis are used to provide the correct treatment at the most appropriate biological stage.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAntibodies, MonoclonalNeuropharmacologyAnimalsHumansAmyloid beta-PeptidesAntibodies, MonoclonalAlzheimer’s diseaseAnti-amyloid monoclonal antibodiesBiomarkersNeuroinflammationPrecision neuropharmacologyTau-centric therapies

Identifiers

PMID42084750
PMCPMC13144244

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.