ReviewExperimental neurology2014
Focality, stochasticity and neuroanatomic propagation in ALS pathogenesis.
Review in Experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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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.
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Who cites it
48 citing papers in PubMed, 103 citations in OpenAlex.
- Data-Driven SuStaIn Model of Disability Progression in Amyotrophic Lateral Sclerosis.Annals of clinical and translational neurology · 2026Article
- Scalable assay to identify inhibitors of prion-like propagation of protein misfolding as potential therapeutics for neurodegeneration.Protein science : a publication of the Protein Society · 2026Article
- ALS and Huntington Disease: Unraveling the Connections between TDP-43 and Huntingtin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Review
- The role of microglia in the prion-like transmission of protein aggregates in neurodegeneration.Brain communications · 2025Review
- The causal association between epilepsy and amyotrophic lateral sclerosis: A two-sample Mendelian randomization study.Brain and behavior · 2024Article
- Clinical spreading of muscle weakness in amyotrophic lateral sclerosis (ALS): a study in 910 patients.Journal of neurology · 2024Observational
- Frontotemporal dementia-like disease progression elicited by seeded aggregation and spread of FUS.Molecular neurodegeneration · 2024Article
- Astrocyte-Neuron Interactions Contributing to Amyotrophic Lateral Sclerosis Progression.Advances in neurobiology · 2024Review
- The impact of upper and lower motor neuron burden on diagnostic certainty, and clinical course of spinal-onset amyotrophic lateral sclerosis: a cluster-based approach.Journal of neurology · 2023Article
- Different patterns of spreading direction and motor neurons involvement in a cohort of limb-onset amyotrophic lateral sclerosis patients from Southern Italy: Potential implication on disease course or progression?Brain and behavior · 2023Article
- Clinical Profiles and Patterns of Neurodegeneration in Amyotrophic Lateral Sclerosis: A Cluster-Based Approach Based on MR Imaging Metrics.AJNR. American journal of neuroradiology · 2023Article
- Distinct patterns of progressive gray and white matter degeneration in amyotrophic lateral sclerosis.Human brain mapping · 2022Article
- Stochasticity, Entropy and Neurodegeneration.Brain sciences · 2022Article
- Nitric oxide inhibits endothelial cell apoptosis by inhibiting cysteine-dependent SOD1 monomerization.FEBS open bio · 2022Article
- Pharyngeal electrical stimulation in amyotrophic lateral sclerosis: a pilot study.Therapeutic advances in neurological disorders · 2022Article
- Motor cortical patterns of upper motor neuron pathology in amyotrophic lateral sclerosis: A 3 T MRI study with iron-sensitive sequences.NeuroImage. Clinical · 2022Article
- C-Boutons and Their Influence on Amyotrophic Lateral Sclerosis Disease Progression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Fast Progression in Amyotrophic Lateral Sclerosis Is Associated With Greater TDP-43 Burden in Spinal Cord.Journal of neuropathology and experimental neurology · 2021Article
- Review
- Global alterations to the choroid plexus blood-CSF barrier in amyotrophic lateral sclerosis.Acta neuropathologica communications · 2020Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) phenotypes such as limb ALS, bulbar ALS, primary lateral sclerosis and primary muscular atrophy are highly heterogeneous and exist on a continuum. These are largely determined by the neuroanatomy of the underlying pathological changes, which can be clinically imputed. Deconstructing these early in disease, before temporal-spatial summation induces complexity, shows that ALS begins focally at a seemingly random location and progresses contiguously. This suggests that focality and anatomic propagation of pathology are significant parts of pathogenesis-disease propagates over space as well as progresses over time. Focality and neuroanatomic propagation can explain how dominant genetic traits manifest with heterogeneous phenotypes, since the anatomic site of outbreak is a prime determinant of phenotype. Focality and neuroanatomic propagation can also explain why frontotemporal dementia (FTD), a neurodegeneration closely related to ALS, has heterogeneous phenotypes, since here too the anatomic site of the outbreak is a prime determinant of phenotype. There are two distinct types of neuroanatomic propagation: contiguous propagation, which occurs side-to-side regionally through the extracellular matrix independent of synaptic connection; and network propagation, which occurs end-to-end dependent on synaptic connections and axonal transmission in connected neuronal networks. The molecular basis of neuroanatomic propagation is unknown, although prion-like misfolding and templating of pathogenic proteins is a compelling unifying hypothesis.
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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.