ReviewAmerican journal of Alzheimer's disease and other dementias2010
Review: disruption of the postsynaptic density in Alzheimer's disease and other neurodegenerative dementias.
Review in American journal of Alzheimer's disease and other dementias, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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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
54 citing papers in PubMed.
- Review
- IMPAIRED BRIDGING OF TEMPORAL DISCONTINUITIES IN OLDER ADULT HIV-1 TG RATS.bioRxiv : the preprint server for biology · 2026Article
- From the past to the present: evolving theories in the pathophysiology of normal pressure hydrocephalus.Journal of neurology, neurosurgery, and psychiatry · 2026Review
- Common and rare variant analyses implicateNPJ dementia · 2026Article
- Loss of excitatory inputs and decreased tonic and evoked activity of locus coeruleus neurons in aged P301S mice.Neurobiology of disease · 2025Article
- Loss of excitatory inputs and decreased tonic and evoked activity of locus coeruleus neurons in aged P301S mice.bioRxiv : the preprint server for biology · 2025Article
- Differential impact of eicosapentaenoic acid and docosahexaenoic acid in an animal model of Alzheimer's disease.Journal of lipid research · 2024Article
- Introducing TEC-LncMir for prediction of lncRNA-miRNA interactions through deep learning of RNA sequences.Briefings in bioinformatics · 2024Article
- The effect of paeoniflorin on the rewarding effect of methamphetamine and the associated cognitive impairment in mice.Metabolic brain disease · 2024Article
- Genome-wide scan of Flortaucipir PET levels findsmedRxiv : the preprint server for health sciences · 2024Article
- Cognitive synaptopathy: synaptic and dendritic spine dysfunction in age-related cognitive disorders.Frontiers in aging neuroscience · 2024Review
- BMECs Ameliorate High Glucose-Induced Morphological Aberrations and Synaptic Dysfunction via VEGF-Mediated Modulation of Glucose Uptake in Cortical Neurons.Cellular and molecular neurobiology · 2023Article
- Article
- Tauopathy and alcohol consumption interact to alter locus coeruleus excitatory transmission and excitability in male and female mice.Alcohol (Fayetteville, N.Y.) · 2023Article
- Identification of key genes and signaling pathways associated with dementia with Lewy bodies and Parkinson's disease dementia using bioinformatics.Frontiers in neurology · 2023Article
- Co-expression network analysis of human tau-transgenic mice reveals protein modules associated with tau-induced pathologies.iScience · 2022Article
- Comparison of Cerebral Cortex Transcriptome Profiles in Ischemic Stroke and Alzheimer's Disease Models.Clinical nutrition research · 2022Article
- Neuronal pentraxins as biomarkers of synaptic activity: from physiological functions to pathological changes in neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Activation of α7 nicotinic acetylcholine receptor ameliorates HIV-associated neurology and neuropathology.Brain : a journal of neurology · 2021Article
- DL0410 ameliorates cognitive disorder in SAMP8 mice by promoting mitochondrial dynamics and the NMDAR-CREB-BDNF pathway.Acta pharmacologica Sinica · 2021Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The most common causes of neurodegenerative dementia include Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD). We believe that, in all 3, aggregates of pathogenic proteins are pathological substrates which are associated with a loss of synaptic function/plasticity. The synaptic plasticity relies on the normal integration of glutamate receptors at the postsynaptic density (PSD). The PSD organizes synaptic proteins to mediate the functional and structural plasticity of the excitatory synapse and to maintain synaptic homeostasis. Here, we will discuss the relevant disruption of the protein network at the PSD in these dementias and the accumulation of the pathological changes at the PSD years before clinical symptoms. We suggest that the functional and structural plasticity changes of the PSD may contribute to the loss of molecular homeostasis within the synapse (and contribute to early symptoms) in these dementias.
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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.