ArticleBiological psychiatry2015
Resilience of precuneus neurotrophic signaling pathways despite amyloid pathology in prodromal Alzheimer's disease.
Article in Biological psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 47 citations in OpenAlex.
- Pretangle tau pathology accrual in the default mode network during the progression of Alzheimer's disease.Molecular neurodegeneration advances · 2026Article
- Spliceosome protein alterations differentiate hubs of the default mode connectome during the progression of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2025Article
- U1-70K and U1A and tau pathogenesis in demented and non-demented individuals with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The Role and Pathogenesis of Tau Protein in Alzheimer's Disease.Biomolecules · 2025Review
- Pterostilbene: A natural neuroprotective stilbene with anti-Alzheimer's disease properties.Journal of pharmaceutical analysis · 2025Review
- Revealing the potential therapeutic mechanism ofFrontiers in medicine · 2024Article
- Oligomeric, phosphorylated, and truncated tau and spliceosome pathology within the entorhinal-hippocampal connectome across stages of Alzheimer's disease.The Journal of comparative neurology · 2023Article
- Vesicular Glutamate Transporter Changes in the Cortical Default Mode Network During the Clinical and Pathological Progression of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Article
- A Two-Stage Model for Predicting Mild Cognitive Impairment to Alzheimer's Disease Conversion.Frontiers in aging neuroscience · 2022Article
- Expression profiling of precuneus layer III cathepsin D-immunopositive pyramidal neurons in mild cognitive impairment and Alzheimer's disease: Evidence for neuronal signaling vulnerability.The Journal of comparative neurology · 2020Article
- Atrophy of Basal Forebrain Initiates with Tau Pathology in Individuals at Risk for Alzheimer's Disease.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Frontal cortex chitinase and pentraxin neuroinflammatory alterations during the progression of Alzheimer's disease.Journal of neuroinflammation · 2020Article
- Article
- Frontal cortex and striatal cellular and molecular pathobiology in individuals with Down syndrome with and without dementia.Acta neuropathologica · 2019Article
- Nerve Growth Factor Pathobiology During the Progression of Alzheimer's Disease.Frontiers in neuroscience · 2019Review
- Pretangle pathology within cholinergic nucleus basalis neurons coincides with neurotrophic and neurotransmitter receptor gene dysregulation during the progression of Alzheimer's disease.Neurobiology of disease · 2018Article
- Autophagy and Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Implications.Frontiers in aging neuroscience · 2018Review
- Conformational characterization of nerve growth factor-β reveals that its regulatory pro-part domain stabilizes three loop regions in its mature part.The Journal of biological chemistry · 2017Article
- Neocortical and hippocampal TREM2 protein levels during the progression of Alzheimer's disease.Neurobiology of aging · 2017Article
- Analyzing the genes related to Alzheimer's disease via a network and pathway-based approach.Alzheimer's research & therapy · 2017Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundReduction of precuneus choline acetyltransferase activity co-occurs with greater beta-amyloid (Aβ) in Alzheimer's disease (AD). Whether this cholinergic deficit is associated with alteration in nerve growth factor (NGF) signaling and its relation to Aβ plaque and neurofibrillary tangle (NFT) pathology during disease onset is unknown.
methodsPrecuneus NGF upstream and downstream signaling levels relative to Aβ and NFT pathology were evaluated using biochemistry and histochemistry in 62 subjects with a premortem diagnosis of non-cognitively impaired (NCI; n = 23), mild cognitive impairment (MCI; n = 21), and mild to moderate AD (n = 18).
resultsImmunoblots revealed increased levels of proNGF in AD subjects but not MCI subjects, whereas cognate receptors were unchanged. There were no significant differences in protein level for the downstream survival kinase-signaling proteins Erk and phospho-Erk among groups. Apoptotic phospho-JNK, phospho-JNK/JNK ratio, and Bcl-2 were significantly elevated in AD subjects. Soluble Aβ1-42 and fibrillar Aβ measured by [(3)H] Pittsburgh compound-B ([(3)H]PiB) binding were significantly higher in AD subjects compared with MCI and NCI subjects. The density of plaques showed a trend to increase, but only 6-CN-PiB-positive plaques reached significance in AD subjects. AT8-positive, TOC-1-positive, and Tau C3-positive NFT densities were unchanged, whereas only AT8-positive neuropil thread density was statistically higher in AD subjects. A negative correlation was found between proNGF, phospho-JNK, and Bcl-2 levels and phospho-JNK/JNK ratio and cognition, whereas proNGF correlated positively with 6-CN-PiB-positive plaques during disease progression.
conclusionsData indicate that precuneus neurotrophin pathways are resilient to amyloid toxicity during the onset of AD.
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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.