ReviewProceedings of the Japan Academy. Series B, Physical and biological sciences2017
The past, present, and future of disease-modifying therapies for Alzheimer's disease.
Review in Proceedings of the Japan Academy. Series B, Physical and biological sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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.
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.
Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- A Narrative Review of Amyloid-β Monoclonal Antibodies for Alzheimer Disease: How Amyloid Species Engagement May Affect Clinical Outcomes.The neurologist · 2026Review
- Tau and β-Amyloid Relevant Pathology as a Central Therapeutic Target in Alzheimer's Disease.Biomolecules · 2026Review
- Improving current understanding of cognitive impairment in patients with a spinal cord injury: A UK-based clinician survey.The journal of spinal cord medicine · 2025Article
- Review
- Therapeutic potential of aromatic plant extracts in Alzheimer's disease: Comprehensive review of their underlying mechanisms.CNS neuroscience & therapeutics · 2023Review
- Aducanumab and Its Effects on Tau Pathology: Is This the Turning Point of Amyloid Hypothesis?International journal of molecular sciences · 2022Review
- Ocular Vascular Changes: Choroidal Thickness as an Early Biomarker for Alzheimer's Disease?Journal of personalized medicine · 2021Article
- Gene Therapy Strategy for Alzheimer's and Parkinson's Diseases Aimed at Preventing the Formation of Neurotoxic Oligomers in SH-SY5Y Cells.International journal of molecular sciences · 2021Article
- Drug Development for Psychotropic, Cognitive-Enhancing, and Disease-Modifying Treatments for Alzheimer's Disease.The Journal of neuropsychiatry and clinical neurosciences · 2021Article
- Trends in the public health significance, definitions of disease, and implications for prevention of Alzheimer's disease.Current epidemiology reports · 2020Article
- Presenilin1 exerts antiproliferative effects by repressing the Wnt/β-catenin pathway in glioblastoma.Cell communication and signaling : CCS · 2020Article
- Upregulation of Prickle2 Ameliorates Alzheimer's Disease-Like Pathology in a Transgenic Mouse Model of Alzheimer's Disease.Frontiers in cell and developmental biology · 2020Article
- Icaritin Improves Memory and Learning Ability by Decreasing BACE-1 Expression and the Bax/Bcl-2 Ratio in Senescence-Accelerated Mouse Prone 8 (SAMP8) Mice.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Biomarkers of Alzheimer Disease.The journal of applied laboratory medicine · 2020Article
- Oleocanthal-Rich Extra-Virgin Olive Oil Restores the Blood-Brain Barrier Function through NLRP3 Inflammasome Inhibition Simultaneously with Autophagy Induction in TgSwDI Mice.ACS chemical neuroscience · 2019Article
- BACE-1 and γ-Secretase as Therapeutic Targets for Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Amyloid-β oligomers suppress subunit-specific glutamate receptor increase during LTP.Alzheimer's & dementia (New York, N. Y.) · 2019Article
- Granisetron Alleviates Alzheimer's Disease Pathology in TgSwDI Mice Through Calmodulin-Dependent Protein Kinase II/cAMP-Response Element Binding Protein Pathway.Journal of Alzheimer's disease : JAD · 2019Article
- Dreaming of a New World Where Alzheimer's Is a Treatable Disorder.Frontiers in aging neuroscience · 2019Article
- NGP 555, a γ-secretase modulator, shows a beneficial shift in the ratio of amyloid biomarkers in human cerebrospinal fluid at safe doses.Alzheimer's & dementia (New York, N. Y.) · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of disease-modifying therapies for Alzheimer's disease (AD) is an urgent issue. Progress in the understanding of AD pathophysiology based on the amyloid hypothesis has led to the development of numerous candidate disease-modifying therapies over the past 15 years. The therapeutic target, amyloid β (Aβ), starts to accumulate in AD brains long before the onset of cognitive decline. γ-secretase inhibitors, γ-secretase modulators, and β-secretase inhibitors aim to reduce the production of toxic Aβ species by modifying the processing of amyloid precursor protein. Another strategy is to eliminate accumulated Aβ by active or passive immunotherapeutic approaches. Therapeutic strategies targeting tau protein are also currently emerging. Despite these efforts, successful disease-modifying therapies for AD have not yet been developed. Recently, very early interventional trials targeting preclinical stages of AD have begun; the paradigm shift in AD therapies from cure to prevention could be key to the success of disease modification.
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Registered trials
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 OpenQuestion graph.