ArticleFrontiers in neuroanatomy2013
Neurites containing the neurofilament-triplet proteins are selectively vulnerable to cytoskeletal pathology in Alzheimer's disease and transgenic mouse models.
Article in Frontiers in neuroanatomy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 21 citations in OpenAlex.
- Functional analysis of late-onset Alzheimer's disease risk genes in Caenorhabditis elegans identifies regulators of neuronal aging.Translational neurodegeneration · 2026Article
- Are neurodegenerative diseases late-onset neurodevelopmental disorders? Tracing the developmental origins of neuronal vulnerability.Frontiers in neuroscience · 2026Review
- GFAPβ and GFAPδ Isoforms Expression in Mesenchymal Stem Cells, MSCs Differentiated Towards Schwann-like, and Olfactory Ensheathing Cells.Current issues in molecular biology · 2025Article
- Specific neuronal subpopulations in the rat basolateral amygdala express high levels of nonphosphorylated neurofilaments.The Journal of comparative neurology · 2021Article
- Cell Type-Specific Human APP Transgene Expression by Hippocampal Interneurons in the Tg2576 Mouse Model of Alzheimer's Disease.Frontiers in neuroscience · 2019Article
- Age, but Not Amyloidosis, Induced Changes in Global Levels of Histone Modifications in Susceptible and Disease-Resistant Neurons in Alzheimer's Disease Model Mice.Frontiers in aging neuroscience · 2019Article
- Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer's disease mice.BMC anesthesiology · 2018Article
- High plasticity of axonal pathology in Alzheimer's disease mouse models.Acta neuropathologica communications · 2017Article
- Locus coeruleus cellular and molecular pathology during the progression of Alzheimer's disease.Acta neuropathologica communications · 2017Article
- Quantitative Comparison of Dense-Core Amyloid Plaque Accumulation in Amyloid-β Protein Precursor Transgenic Mice.Journal of Alzheimer's disease : JAD · 2017Article
- Combination treatment with leptin and pioglitazone in a mouse model of Alzheimer's disease.Alzheimer's & dementia (New York, N. Y.) · 2017Article
- Defining the earliest pathological changes of Alzheimer's disease.Current Alzheimer research · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid-β plaque accumulation in Alzheimer's disease (AD) is associated with dystrophic neurite (DN) formation and synapse loss in principal neurons, but interneuron pathology is less clearly characterized. We compared the responses of neuronal processes immunoreactive for either neurofilament triplet (NF(+)) or calretinin (CR(+)) to fibrillar amyloid (Aβ) plaques in human end-stage and preclinical AD, as well as in APP/PS1 and Tg2576 transgenic mouse AD models. Neurites traversing the Aβ plaque core, edge, or periphery, defined as 50, 100, and 150% of the plaque diameter, respectively, in human AD and transgenic mouse tissue were compared to age-matched human and wild-type mouse controls. The proportion of NF(+) neurites exhibiting dystrophic morphology (DN) was significantly larger than the proportion of dystrophic CR(+) neurites in both human AD and transgenic mice (p < 0.01). Additionally, the number of NF(+), but not CR(+), DNs, correlated with Aβ plaque size. We conclude that CR(+) interneurons appear to be more resistant than NF(+) neurons to AD-mediated cytoskeletal pathology.
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.