ReviewExperimental neurology2013
Axonal degeneration in Alzheimer's disease: when signaling abnormalities meet the axonal transport system.
Review in Experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 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
129 citing papers in PubMed, 1 synthesis or guideline pooled it, 220 citations in OpenAlex.
- Sex-specific DNA methylation differences in Alzheimer's disease pathology.Acta neuropathologica communications · 2021Pooled it
- Early axonal degeneration linked to clinical decline in Alzheimer's disease progression revealed with diffusion MRI.The Journal of clinical investigation · 2026Trial
- An integratediScience · 2026Article
- Alzheimer's disease: from molecular pathways to therapies.Molecular biomedicine · 2026Review
- Vascular stiffness predicts plasma markers of neurodegeneration among older African Americans.The journal of prevention of Alzheimer's disease · 2026Observational
- Axonal Degeneration Across the Alzheimer's Disease Spectrum: A Longitudinal MRI and Fluid Biomarker Study.medRxiv : the preprint server for health sciences · 2025Article
- Imaging myelin degradation in ex vivo prefrontal cortex tissue blocks in Alzheimer's disease and chronic traumatic encephalopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Protein aggregation and neurodegenerative disease: Structural outlook for the novel therapeutics.Proteins · 2025Review
- SARM1: The Checkpoint of Axonal Degeneration in the Nervous System Disorders.Molecular neurobiology · 2025Review
- Proteostasis and Its Role in Disease Development.Cell biochemistry and biophysics · 2025Review
- Optineurin-facilitated axonal mitochondria delivery promotes neuroprotection and axon regeneration.Nature communications · 2025Article
- Systems-Level Interactome Mapping Reveals Actionable Protein Network Dysregulation Across the Alzheimer's Disease Spectrum.Research square · 2025Article
- Programmed neurite degeneration in human central nervous system neurons driven by changes in NADCell death & disease · 2025Article
- Aging and Alzheimer's: the critical role of mitochondrial dysfunction and synaptic alterations.Frontiers in synaptic neuroscience · 2025Review
- Molecular mechanisms underlying the neuroprotective effects of polyphenols: implications for cognitive function.EXCLI journal · 2025Review
- Synaptotagmin 4 Supports Spontaneous Axon Sprouting after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Microtubules, Membranes, and Movement: New Roles for Stathmin-2 in Axon Integrity.Journal of neuroscience research · 2024Review
- Review
- Optineurin-facilitated axonal mitochondria delivery promotes neuroprotection and axon regeneration.bioRxiv : the preprint server for biology · 2024Article
- SARM1 Promotes Neurodegeneration and Memory Impairment in Mouse Models of Alzheimer's Disease.Aging and disease · 2024Article
69 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is characterized by progressive, age-dependent degeneration of neurons in the central nervous system. A large body of evidence indicates that neurons affected in AD follow a dying-back pattern of degeneration, where abnormalities in synaptic function and axonal connectivity long precede somatic cell death. Mechanisms underlying dying-back degeneration of neurons in AD remain elusive but several have been proposed, including deficits in fast axonal transport (FAT). Accordingly, genetic evidence linked alterations in FAT to dying-back degeneration of neurons, and FAT defects have been widely documented in various AD models. In light of these findings, we discuss experimental evidence linking several AD-related pathogenic polypeptides to aberrant activation of signaling pathways involved in the phosphoregulation of microtubule-based motor proteins. While each pathway appears to affect FAT in a unique manner, in the context of AD, many of these pathways might work synergistically to compromise the delivery of molecular components critical for the maintenance and function of synapses and axons. Therapeutic approaches aimed at preventing FAT deficits by normalizing the activity of specific protein kinases may help prevent degeneration of vulnerable neurons in AD.
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.