ArticleNeurobiology of aging2018
Early Alzheimer-type lesions in cognitively normal subjects.
Article in Neurobiology of aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Celebrating neuropathology's contributions to Alzheimer's Disease Research Centers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Tau PET positivity in individuals with and without cognitive impairment varies with age, amyloid-β status, APOE genotype and sex.Nature neuroscience · 2025Article
- Sex- and region-dependent neuroinflammation in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Chemiexcitation: Mammalian Photochemistry in the DarkPhotochemistry and photobiology · 2023Review
- Hypothesis review: Alzheimer's overture guidelines.Brain pathology (Zurich, Switzerland) · 2023Review
- Neurodegenerative Diseases: Implications of Environmental and Climatic Influences on Neurotransmitters and Neuronal Hormones Activities.International journal of environmental research and public health · 2022Review
- Effect of olfactory bulb pathology on olfactory function in normal aging.Brain pathology (Zurich, Switzerland) · 2022Article
- Evidence of traumatic brain injury in headbutting bovids.Acta neuropathologica · 2022Article
- The mechanism and efficacy of GLP-1 receptor agonists in the treatment of Alzheimer's disease.Frontiers in endocrinology · 2022Review
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
- Comparative neuropathology in aging primates: A perspective.American journal of primatology · 2021Review
- Risk of early-onset dementia among persons with tinnitus: a retrospective case-control study.Scientific reports · 2021Article
- Alzheimer's disease and type 2 diabetes mellitus: Pathophysiologic and pharmacotherapeutics links.World journal of diabetes · 2021Review
- Rosmarinic acid suppresses tau phosphorylation and cognitive decline by downregulating the JNK signaling pathway.NPJ science of food · 2021Article
- Aging: What We Can Learn From Elephants.Frontiers in aging · 2021Review
- Common Protective Strategies in Neurodegenerative Disease: Focusing on Risk Factors to Target the Cellular Redox System.Oxidative medicine and cellular longevity · 2020Review
- Extracellular Sortilin Proteopathy Relative to β-Amyloid and Tau in Aged and Alzheimer's Disease Human Brains.Frontiers in aging neuroscience · 2020Article
- Early Dendritic Dystrophy in Human Brains With Primary Age-Related Tauopathy.Frontiers in aging neuroscience · 2020Article
- Aberrant White Matter Microstructure as a Potential Diagnostic Marker in Alzheimer's Disease by Automated Fiber Quantification.Frontiers in neuroscience · 2020Article
- Bridging the Gap between Alzheimer's Disease and Alzheimer's-like Diseases in Animals.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Amyloid deposits and tau-immunoreactive neurofibrillary tangles, together with neuronal and synaptic loss, are the neuropathological hallmarks of Alzheimer's disease (AD). Both proteins are present in the normal brain during aging. However, the temporal sequence of their involvement in the onset of AD pathology remains controversial. To define whether amyloid β protein deposits or tau protein lesions appear first during normal brain aging, we performed an immunohistological study on serial sections from 105 autopsy brains (age range: 40-104 years) from patients free of clinical signs of cognitive decline, using anti-tau (AT8) and anti-amyloid (4G8) antibodies in the hippocampus, entorhinal cortex, inferior temporal cortex (Brodmann area 20), prefrontal cortex (Brodmann area 9), occipital cortex (Brodmann areas 17 and 18), and in the brainstem. All cases older than 48 years displayed at least a few neurofibrillary tangles, which appeared more frequently in the entorhinal than in the transentorhinal cortex. Tau pathology in these areas preceded tau inclusions in the brainstem. Furthermore, the first site of the apparition of tau pathology is inconsistent, being the entorhinal cortex in most cases, and in fewer cases, the transentorhinal region. There was no case presenting with amyloid deposition in the absence of neurofibrillary tangles, lending evidence to the fact that neurofibrillary tangles appear earlier than amyloid plaques during normal brain aging. However, the role of amyloid in promoting tau deposition cannot be excluded in some cases but may not represent the sole mechanism of disease induction and progression.
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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.