ReviewFrontiers in aging neuroscience2023
Emerging Alzheimer's disease therapeutics: promising insights from lipid metabolism and microglia-focused interventions.
Review in Frontiers in aging neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 30 citations in OpenAlex.
- Revisiting TREM2: from multi-omics signaling networks to clinical translation.Frontiers in immunology · 2026Review
- Ageing, Neurodegeneration and the Endocannabinoid System.Current topics in behavioral neurosciences · 2026Review
- Obesity and Cognitive Function: Leptin Role Through Blood-Brain Barrier and Hippocampus.Molecular neurobiology · 2025Review
- Alzheimer's disease patient brain extracts induce multiple pathologies in novel vascularized neuroimmune organoids for disease modeling and drug discovery.Molecular psychiatry · 2025Article
- The flexible stalk domain of sTREM2 modulates its interactions with brain-based phospholipids.eLife · 2025Article
- Neuronal Death and Biomolecular Condensates: Are There Any New Treatment Options for Alzheimer's Disease?Cells · 2025Review
- Expression of Reelin, Aβ1-42, Tau and FTH1 in Idiopathic Epiretinal Membranes: Exploring the Link Between Reelin and Neurodegenerative Biomarkers.Biomolecules · 2025Article
- Are Hippocampal Hypoperfusion and ATP Depletion Prime Movers in the Genesis of Alzheimer's Disease? A Review of Recent Pertinent Observations from Molecular Biology.International journal of molecular sciences · 2025Review
- HIV Protein TAT Dysregulates Multiple Pathways in Human iPSCs-Derived Microglia.Life (Basel, Switzerland) · 2025Article
- Neuroinflammation in Alzheimer disease.Nature reviews. Immunology · 2025Review
- Article
- A Comparison of the Brain Parameters of Thais with Normal Cognition, Mild Cognitive Impairment, and Dementia.Brain sciences · 2025Article
- Alzheimer's Disease Protein Targets: Comprehensive Review and Future Directions.Current pharmaceutical design · 2025Review
- Predicting biological activity and design of 5-HTJournal of molecular modeling · 2024Article
- Article
- Novel Therapeutic Strategies in Alzheimer's Disease: Pitfalls and Challenges of Anti-Amyloid Therapies and Beyond.Journal of clinical medicine · 2024Review
- Joint association of serum sodium and frailty with mild cognitive impairment among hospitalized older adults with chronic diseases: a cross-sectional study.Frontiers in nutrition · 2024Article
- Unraveling the molecular links: Alzheimer's disease-induced mechanisms of memory impairment: A narrative review.Journal of Alzheimer's disease reportsReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
More than 55 million people suffer from dementia, with this number projected to double every 20 years. In the United States, 1 in 3 aged individuals dies from Alzheimer's disease (AD) or another type of dementia and AD kills more individuals than breast cancer and prostate cancer combined. AD is a complex and multifactorial disease involving amyloid plaque and neurofibrillary tangle formation, glial cell dysfunction, and lipid droplet accumulation (among other pathologies), ultimately leading to neurodegeneration and neuronal death. Unfortunately, the current FDA-approved therapeutics do not reverse nor halt AD. While recently approved amyloid-targeting antibodies can slow AD progression to improve outcomes for some patients, they are associated with adverse side effects, may have a narrow therapeutic window, and are expensive. In this review, we evaluate current and emerging AD therapeutics in preclinical and clinical development and provide insight into emerging strategies that target brain lipid metabolism and microglial function - an approach that may synergistically target multiple mechanisms that drive AD neuropathogenesis. Overall, we evaluate whether these disease-modifying emerging therapeutics hold promise as interventions that may be able to reverse or halt AD progression.
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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 Socratic graph.