ArticleNeurobiology of aging2012
Synaptic protein deficits are associated with dementia irrespective of extreme old age.
Article in Neurobiology of aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 36 citations in OpenAlex.
- Rapamycin Affects the Hippocampal SNARE Complex to Alleviate Cognitive Dysfunction Induced by Surgery in Aged Rats.Brain sciences · 2023Article
- Impact of the Cannabinoid System in Alzheimer's Disease.Current neuropharmacology · 2023Review
- Engagement of vascular early response genes typifies mild cognitive impairment.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Longitudinal CSF proteomics identifies NPTX2 as a prognostic biomarker of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021Article
- PET Neuroimaging of Alzheimer's Disease: Radiotracers and Their Utility in Clinical Research.Frontiers in aging neuroscience · 2021Review
- Distinctive alteration of presynaptic proteins in the outer molecular layer of the dentate gyrus in Alzheimer's disease.Brain communications · 2021Article
- Clinical Utility of the Pathogenesis-Related Proteins in Alzheimer's Disease.International journal of molecular sciences · 2020Review
- The Proteome of the Dentate Terminal Zone of the Perforant Path Indicates Presynaptic Impairment in Alzheimer Disease.Molecular & cellular proteomics : MCP · 2020Article
- The synaptic pathology of cognitive life .Dialogues in clinical neuroscience · 2019Review
- Moderate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer's disease at various cognitive stages.Scientific reports · 2018Article
- Religious Orders Study and Rush Memory and Aging Project.Journal of Alzheimer's disease : JAD · 2018Review
- Progressive Neuronal Pathology and Synaptic Loss Induced by Prediabetes and Type 2 Diabetes in a Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2017Article
- Association of Neuropathological Markers in the Parietal Cortex With Antemortem Cognitive Function in Persons With Mild Cognitive Impairment and Alzheimer Disease.Journal of neuropathology and experimental neurology · 2017Article
- SNAP-25a/b Isoform Levels in Human Brain Dorsolateral Prefrontal Cortex and Anterior Cingulate Cortex.Molecular neuropsychiatry · 2015Article
- Chronic adjunction of 1-deoxynojirimycin protects from age-related behavioral and biochemical changes in the SAMP8 mice.Age (Dordrecht, Netherlands) · 2015Article
- Perforant path synaptic loss correlates with cognitive impairment and Alzheimer's disease in the oldest-old.Brain : a journal of neurology · 2014Article
- Cognitive and social lifestyle: links with neuropathology and cognition in late life.Acta neuropathologica · 2014Review
- Deconstructing complexin function in activating and clamping Ca2+-triggered exocytosis by comparing knockout and knockdown phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Neuropathological approaches to cerebral aging and neuroplasticity.Dialogues in clinical neuroscience · 2013Review
- Cognitive decline and dementia in the oldest-old.Rambam Maimonides medical journal · 2012Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Recent evidence shows that despite high incidence of dementia in the very old, they exhibit significantly lower levels of Alzheimer's disease (AD) neuropathology relative to younger persons with dementia. The levels and distributions of some synaptic proteins have been found to be associated with dementia severity, even in the oldest-old, but the molecular and functional nature of these deficits have not been studied in detail. The objective of this study was to assess the relationship of dementia with gene and protein expression of a panel of synaptic markers associated with different synaptic functions in young-, middle-, and oldest-old individuals. The protein and messenger RNA (mRNA) levels of 7 synaptic markers (complexin-1, complexin-2, synaptophysin, synaptobrevin, syntaxin, synaptosomal-associated protein 25 (SNAP-25), and septin-5) were compared in the brains of nondemented and demented individuals ranging from 70 to 103 years of age. One hundred eleven brains were selected to have either no significant neuropathology or only AD-associated pathology (neuritic plaques [NPs] and neurofibrillary tangles [NFTs]). The cohort was then stratified into tertiles as young-old (70-81 years old), middle-old (82-88), and oldest-old (89-103). The brains of persons with dementia evidenced significantly lower levels of gene and protein expression of synaptic markers regardless of age. Importantly, dementia was associated with reductions in all measured synaptic markers irrespective of their role(s) in synaptic function. Although other dementia-associated hallmarks of AD neuropathology (neuritic plaques and neurofibrillary tangles) become less prominent with increasing age, synaptic marker abnormalities in dementia remain constant with increasing age and may represent an independent substrate of dementia spanning all ages.
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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.