ReviewCurrent Alzheimer research2016
Defining the earliest pathological changes of Alzheimer's disease.
Review in Current Alzheimer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled 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.
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
59 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Blood pressure and Alzheimer's disease: A review of meta-analysis.Frontiers in neurology · 2022Pooled it
- Bay leaves: the neuroprotective dietary spice via inhibition of amyloid-like aggregation.Metabolic brain disease · 2025Article
- Unraveling the Mystery of Hemoglobin in Hypoxia-Accelerated Neurodegenerative Diseases.Biomolecules · 2025Review
- Article
- Unveiling the Protective Roles of Melatonin on Glial Cells in the Battle Against Alzheimer's Disease-Insights from In Vivo and In Vitro Studies.Molecular neurobiology · 2025Review
- Neutrophil-to-Lymphocyte Ratio in the Alzheimer's Disease Continuum.International journal of molecular sciences · 2025Review
- Quantitative magnetic resonance imaging in Alzheimer's disease: a narrative review.Quantitative imaging in medicine and surgery · 2025Review
- Exploring the Efficacy and Target Genes ofCurrent issues in molecular biology · 2025Article
- Predicting risk of impending cognitive decline in asymptomatic individuals with early Alzheimer's disease: Insights from cortical diffusion MRI.Imaging neuroscience (Cambridge, Mass.) · 2025Article
- Early emergence of motivational and hedonic feeding deficits in the TgF344-AD rat model of Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Elevated plasma p-tau231 is associated with reduced generalization and medial temporal lobe dynamic network flexibility among healthy older African Americans.Alzheimer's research & therapy · 2024Article
- Neuroinflammation in Neurodegenerative Disorders: Current Knowledge and Therapeutic Implications.International journal of molecular sciences · 2024Review
- mTOR signaling and Alzheimer's disease: What we know and where we are?CNS neuroscience & therapeutics · 2024Review
- Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.Frontiers in aging neuroscience · 2024Review
- Brain metabolites are associated with sleep architecture and cognitive functioning in older adults.Brain communications · 2024Article
- Review
- Review
- The Role of the JAK/STAT Signaling Pathway in the Pathogenesis of Alzheimer's Disease: New Potential Treatment Target.International journal of molecular sciences · 2023Review
- The effects of GPER on age-associated memory impairment induced by decreased estrogen levels.Frontiers in molecular biosciences · 2023Review
- Microstructural mapping of dentate gyrus pathology in Alzheimer's disease: A 16.4 Tesla MRI study.NeuroImage. Clinical · 2023Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prospects for effectively treating well-established dementia, such as Alzheimer's disease (AD), are slim, due to the destruction of key brain pathways that underlie higher cognitive function. There has been a substantial shift in the field towards detecting conditions such as AD in their earliest stages, which would allow preventative or therapeutic approaches to substantially reduce risk and/or slow the progression of disease. AD is characterized by hallmark pathological changes such as extracellular Aβ plaques and intracellular neurofibrillary pathology, which selectively affect specific subclasses of neurons and brain circuits. Current evidence indicates that Aβ plaques begin to form many years before overt dementia, a gradual and progressive pathology which offers a potential target for early intervention. Early Aβ changes in the brain result in localized damage to dendrites, axonal processes and synapses, to which excitatory synapses and the processes of projection neurons are highly vulnerable. Aβ pathology is replicated in a range of transgenic models overexpressing mutant human familial AD genes (e.g. APP and presenilin 1). Studying the development of aberrant regenerative and degenerative changes in neuritic processes associated with Aβ plaques may represent the best opportunity to understand the relationship between the pathological hallmarks of AD and neuronal damage, and to develop early interventions to prevent, slow down or mitigate against Aβ pathology and/or the neuronal alterations that leads to cognitive impairment.
Indexed as
Identifiers
What OpenQuestion holds
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.