Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Tau protein accumulation is one of the characteristic features of Alzheimer's disease (AD).
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Alzheimer's disease (AD) is pathologically characterized by deposition of amyloid plaques (comprising amyloid β [Aβ] protein) and neurofibrillary tangles (comprising tau protein), and neuronal death.
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Glutamate transporter-1 (GLT-1) dynamics are implicated in excitotoxicity and Alzheimer's disease (AD) progression.
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The eye is closely connected to the brain, providing a unique window to detect pathological changes in the brain.
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Activation of the NLRP3 pathway was observed in the mouse organotypic slice culture (OSC) model following stimulation with LPS and nigericin or exposure to tau seeds.
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Neuronal excitatory synapses are primarily located on small dendritic protrusions called spines.
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43/100
We found a significant reduction in PSD-95-actin association in synaptosomes from middle-aged APP/PS1 mice compared to wild-type (WT) mice.
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Tau interacts with α-Synuclein (α-Syn) and co-localizes with it in the Lewy bodies, influencing α-Syn pathology in Parkinson's disease (PD).
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Neurodegenerative diseases represent the most common cause of dementia.
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Alzheimer's Disease (AD) is a progressive neurological disease associated with behavioral abnormalities, memory loss, and cognitive impairment that cause major causes of dementia in the elderly.
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43/100
Alzheimer's disease (AD) is a complex neurodegenerative disease that affects elderly individuals, characterized by senile plaques formed by extracellular amyloid beta (Aβ).
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Mutations in the PSEN genes are the major cause of familial Alzheimer's disease, and presenilin (PS) is the catalytic subunit of γ-secretase, which cleaves type I transmembrane proteins, including the amyloid precursor protein (APP) to release Aβ peptides.
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Alzheimer's disease (AD) is the most prevalent dementia, pathologically featuring abnormal accumulation of amyloid-β (Aβ) and hyperphosphorylated tau, while sleep, divided into rapid eye movement sleep (REM) and nonrapid eye movement sleep (NREM), plays a key role in consolidating social and spatial memory.
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The misfolding and aggregation of beta-amyloid (Aβ) peptides have been implicated as key pathogenic events in the early stages of Alzheimer's disease (AD).
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The brain contains the highest concentration of cholesterol in the human body, which emphasizes the importance of cholesterol in brain physiology.
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Protein aggregation caused by the disruption of proteostasis will lead to cellular cytotoxicity and even cell death, which is implicated in multiple neurodegenerative diseases.
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Pathological tau disrupts protein homeostasis (proteostasis) within neurons in Alzheimer's disease (AD) and related disorders.
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Pathological tau aggregates cause cognitive decline in neurodegenerative tauopathies, including Alzheimer's disease (AD).
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Anti-ac-tauK174 treatment mitigates neurobehavioral impairment and reduces tau pathology in PS19 mice.
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the loss of neural connections and decreased brain tissue volume.
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The accumulation of protein aggregates is a hallmark of many diseases, including Alzheimer's disease.
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Alzheimer's disease (AD) involves reduced glutathione levels, causing oxidative stress and contributing to neuronal cell death.
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A new class of compounds, namely highly substituted diaminocyclopentane-l-lysine adducts, have been discovered as potent inhibitors of O-GlcNAcase, an enzyme crucial for protein de-O-glycosylation.
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Alzheimer's disease is a progressive neurodegenerative disorder characterized by impairments in synaptic plasticity and cognitive performance.
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Proteostasis is essential for normal function of proteins and vital for cellular health and survival.
From across this topic
10 of the 1,352 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Oxidative modifications and down-regulation of ubiquitin carboxyl-terminal hydrolase L1 associated with idiopathic Parkinson's and Alzheimer's diseases
- Defective proteostasis in Alzheimer's disease
- TDP-43: From Alzheimer's Disease to Limbic-Predominant Age-Related TDP-43 Encephalopathy
- Neurotoxicity of HIV-1 proteins gp120 and Tat in the rat striatum
- Modeling Alzheimer's disease with iPSCs reveals stress phenotypes associated with intracellular Aβ and differential drug responsiveness
- Synaptic plasticity modulation by circulating peptides and metaplasticity: Involvement in Alzheimer's disease
- Pharmacological inhibition of BACE1 impairs synaptic plasticity and cognitive functions
- Decreased nuclear beta-catenin, tau hyperphosphorylation and neurodegeneration in GSK-3beta conditional transgenic mice
- Integrative Multiomics Analysis Reveals a Coordinated Molecular Signature of Neuroresilience in human MAPT-knockout hiPSC-derived Neurons with relevance for Alzheimer’s and Neurodegenerative Disease
- The autophagy of stress granules