ArticleThe European journal of neuroscience2010
β-Secretase-1 elevation in aged monkey and Alzheimer's disease human cerebral cortex occurs around the vasculature in partnership with multisystem axon terminal pathogenesis and β-amyloid accumulation.
Article in The European journal of neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 65 citations in OpenAlex.
- Aberrant ɑSMA expression reveals broad mossy fiber reorganization integrating with tangle and plaque formation and mitoenergetic alteration in the human hippocampus.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Increase in BACE1 Phosphorylation in the Rat Hippocampus and Phytosphingosine in Plasma After Chronic Administration of Scopolamine.International journal of molecular sciences · 2026Article
- Bioinformatics-Driven Discovery of Aβ-Targeted Therapeutics and Diagnostic Biomarkers for Alzheimer's Disease.BioMed research international · 2026Article
- Neuritic Plaques - Gateways to Understanding Alzheimer's Disease.Molecular neurobiology · 2024Review
- Transformation of non-neuritic into neuritic plaques during AD progression drives cortical spread of tau pathology via regenerative failure.Acta neuropathologica communications · 2023Article
- The importance of social behavior in nonhuman primate studies of aging: A mini-review.Neuroscience and biobehavioral reviews · 2023Review
- Early Dendritic Dystrophy in Human Brains With Primary Age-Related Tauopathy.Frontiers in aging neuroscience · 2020Article
- Extracellular Sortilin Proteopathy Relative to β-Amyloid and Tau in Aged and Alzheimer's Disease Human Brains.Frontiers in aging neuroscience · 2020Article
- Premotor Cortical-Cerebellar Reorganization in a Macaque Model of Primary Motor Cortical Lesion and Recovery.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Lack of human-like extracellular sortilin neuropathology in transgenic Alzheimer's disease model mice and macaques.Alzheimer's research & therapy · 2018Article
- BACE1 elevation engendered by GGA3 deletion increases β-amyloid pathology in association with APP elevation and decreased CHL1 processing in 5XFAD mice.Molecular neurodegeneration · 2018Article
- Can brain impermeable BACE1 inhibitors serve as anti-CAA medicine?BMC neurology · 2017Article
- Sortilin Fragments Deposit at Senile Plaques in Human Cerebrum.Frontiers in neuroanatomy · 2017Article
- Extracellular matrix protein expression is brain region dependent.The Journal of comparative neurology · 2016Article
- Experimental microembolism induces localized neuritic pathology in guinea pig cerebrum.Oncotarget · 2015Article
- Non-neuronal and neuronal BACE1 elevation in association with angiopathic and leptomeningeal β-amyloid deposition in the human brain.BMC neurology · 2015Article
- Overexpression of mutant amyloid-β protein precursor and presenilin 1 modulates enteric nervous system.Journal of Alzheimer's disease : JAD · 2015Article
- Inverse correlation between Alzheimer's disease and cancer: implication for a strong impact of regenerative propensity on neurodegeneration?BMC neurology · 2014Article
- Can BACE1 inhibition mitigate early axonal pathology in neurological diseases?Journal of Alzheimer's disease : JAD · 2014Review
- The Alzheimer's β-secretase BACE1 localizes to normal presynaptic terminals and to dystrophic presynaptic terminals surrounding amyloid plaques.Acta neuropathologica · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is the most common dementia-causing disorder in the elderly; it may be related to multiple risk factors, and is characterized pathologically by cerebral hypometabolism, paravascular β-amyloid peptide (Aβ) plaques, neuritic dystrophy, and intra-neuronal aggregation of phosphorylated tau. To explore potential pathogenic links among some of these lesions, we examined β-secretase-1 (BACE1) alterations relative to Aβ deposition, neuritic pathology and vascular organization in aged monkey and AD human cerebral cortex. Western blot analyses detected increased levels of BACE1 protein and β-site-cleavage amyloid precursor protein C-terminal fragments in plaque-bearing human and monkey cortex relative to controls. In immunohistochemistry, locally elevated BACE1 immunoreactivity (IR) occurred in AD but not in control human cortex, with a trend for increased overall density among cases with greater plaque pathology. In double-labeling preparations, BACE1 IR colocalized with immunolabeling for Aβ but not for phosphorylated tau. In perfusion-fixed monkey cortex, locally increased BACE1 IR co-existed with intra-axonal and extracellular Aβ IR among virtually all neuritic plaques, ranging from primitive to typical cored forms. This BACE1 labeling localized to swollen/sprouting axon terminals that might co-express one or another neuronal phenotype markers (GABAergic, glutamatergic, cholinergic, or catecholaminergic). Importantly, these BACE1-labeled dystrophic axons resided near to or in direct contact with blood vessels. These findings suggest that plaque formation in AD or normal aged primates relates to a multisystem axonal pathogenesis that occurs in partnership with a potential vascular or metabolic deficit. The data provide a mechanistic explanation for why senile plaques are present preferentially near the cerebral vasculature.
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.