ReviewFrontiers in aging neuroscience2017
Perspective Insights into Disease Progression, Diagnostics, and Therapeutic Approaches in Alzheimer's Disease: A Judicious Update.
Review in Frontiers in aging neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 44 citations in OpenAlex.
- Autophagy: From Molecular Mechanisms to Disease Regulation and Therapeutic Strategies.Current issues in molecular biology · 2026Review
- Iron dyshomeostasis in neuropsychiatric disorders.Frontiers in psychiatry · 2026Review
- Review
- Article
- Brain Iron Metabolism, Redox Balance and Neurological Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Hippocampal Iron Accumulation Impairs Synapses and Memory via Suppressing Furin Expression and Downregulating BDNF Maturation.Molecular neurobiology · 2022Article
- The emerging role of furin in neurodegenerative and neuropsychiatric diseases.Translational neurodegeneration · 2022Review
- Can healthy lifestyle reduce disease progression of Alzheimer's during a global pandemic of COVID-19?Ageing research reviews · 2021Review
- Brain Atrophy and White Matter Damage Linked to Peripheral Bioenergetic Deficits in the Neurodegenerative Disease FXTAS.International journal of molecular sciences · 2021Article
- Repetitive Transcranial Magnetic Stimulation in the Treatment of Alzheimer's Disease and Other Dementias.Healthcare (Basel, Switzerland) · 2021Review
- Vitamin K2 Modulates Organelle Damage and Tauopathy Induced by Streptozotocin and Menadione in SH-SY5Y Cells.Antioxidants (Basel, Switzerland) · 2021Article
- Biocomputational Screening of Natural Compounds against Acetylcholinesterase.Molecules (Basel, Switzerland) · 2021Article
- Hepcidin overexpression in astrocytes alters brain iron metabolism and protects against amyloid-β induced brain damage in mice.Cell death discovery · 2020Article
- Expedition into Taurine Biology: Structural Insights and Therapeutic Perspective of Taurine in Neurodegenerative Diseases.Biomolecules · 2020Review
- The potential of neurofilaments analysis using dry-blood and plasma spots.Scientific reports · 2020Article
- Advances in the Biosynthetic Pathways and Application Potential of Plasmalogens in Medicine.Frontiers in cell and developmental biology · 2020Review
- Xeno-miRNA in Maternal-Infant Immune Crosstalk: An Aid to Disease Alleviation.Frontiers in immunology · 2020Review
- Combinatorial Treatment Using Umbilical Cord Perivascular Cells and Aβ Clearance Rescues Vascular Function Following Transient Hypertension in a Rat Model of Alzheimer Disease.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Plasmalogens and Alzheimer's disease: a review.Lipids in health and disease · 2019Review
- Exosome Determinants of Physiological Aging and Age-Related Neurodegenerative Diseases.Frontiers in aging neuroscience · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the progressive accumulation of β-amyloid fibrils and abnormal tau proteins in and outside of neurons. Representing a common form of dementia, aggravation of AD with age increases the morbidity rate among the elderly. Although, mutations in the ApoE4 act as potent risk factors for sporadic AD, familial AD arises through malfunctioning of APP, PSEN-1, and-2 genes. AD progresses through accumulation of amyloid plaques (Aβ) and neurofibrillary tangles (NFTs) in brain, which interfere with neuronal communication. Cellular stress that arises through mitochondrial dysfunction, endoplasmic reticulum malfunction, and autophagy contributes significantly to the pathogenesis of AD. With high accuracy in disease diagnostics, Aβ deposition and phosphorylated tau (p-tau) are useful core biomarkers in the cerebrospinal fluid (CSF) of AD patients. Although five drugs are approved for treatment in AD, their failures in achieving complete disease cure has shifted studies toward a series of molecules capable of acting against Aβ and p-tau. Failure of biologics or compounds to cross the blood-brain barrier (BBB) in most cases advocates development of an efficient drug delivery system. Though liposomes and polymeric nanoparticles are widely adopted for drug delivery modules, their use in delivering drugs across the BBB has been overtaken by exosomes, owing to their promising results in reducing disease 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 OpenQuestion graph.