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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We found a beginning synaptic impairment (LTP deficit) at 3-4 months in the prefrontal cortex of AppNL-G-F mice that is further aggravated and extended to the hippocampus at 6-8 months.
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Zinc is the second abundant trace element in the human central nervous system (CNS).
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The endosomal-lysosomal pathways and related autophagic processes are responsible for proteostasis, involving complexes between lysosomes and autophagosomes.
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39/100
Synaptic plasticity is the neural basis of physiological processes involved in learning and memory.
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39/100
TAR DNA binding protein (TDP-43) is a DNA/RNA binding protein whose pathological role in amyotrophic lateral sclerosis (ALS) and frontal temporal lobe dementia (FTLD) via formation of protein aggregates is well established.
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The rising prevalence of Alzheimer's disease (AD), together with the lack of effective treatments, portray it as one of the major health challenges of our times.
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Dendrites and dendritic spines are dynamic structures with pivotal roles in brain connectivity and have been recognized as the locus of long-term synaptic plasticity related to cognitive processes such as learning and memory.
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This review considers whether the Braak hypothesis on protein propagation could account for prion disease, particularly Creutzfeldt-Jakob disease (CJD).
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The strength and efficiency of synaptic connections are affected by the environment or the experience of the individual.
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Alzheimer's disease (AD) is a progressive brain disorder characterized by memory loss and the accumulation of two insoluble protein aggregates, tau neurofibrillary tangles and beta-amyloid plaques.
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Like several neurodegenerative disorders, such as Prion and Parkinson diseases, Alzheimer's disease (AD) is characterized by spreading mechanism of aggregated proteins in the brain in a typical "prion-like" manner.
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39/100
We found that tau phosphorylation undergoes sleep-driven circadian variations as it is hyperphosphorylated during sleep but not during acute sleep deprivation.
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Protein homeostasis or proteostasis is an essential balance of cellular protein levels mediated through an extensive network of biochemical pathways that regulate different steps of the protein quality control, from the synthesis to the degradation.
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Innovations in cryogenic electron microscopy (Cryo-EM) have led to high-quality structures of important proteins such as the ribosome and γ-secretase, the membrane protease that produces Aβ involved in Alzheimer's disease.
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Hippocampal synaptic dysfunction is a hallmark of Alzheimer's disease (AD).
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Since the discovery of TAR DNA-binding protein 43 (TDP-43) in 1995, our understanding of its role continues to expand as research progresses.
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Synaptic dysfunction has been implicated as an early cause of cognitive decline in neurodegenerative diseases (NDDs) such as Alzheimer's disease (AD).
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39/100
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by Aβ-driven synaptic dysfunction in the early phases of pathogenesis.
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Although the basis of Alzheimer's disease (AD) etiology remains unknown, oxidative stress (OS) has been recognized as a prodromal factor associated to its progression.
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Alzheimer's disease (AD) is the most common form of dementia.
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Intracellular accumulation of amyloid-β protein (Aβ) is an early event in Alzheimer's disease (AD).
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39/100
Apolipoprotein E (ApoE) has become a primary focus of research after the discovery of its strong linkage to Alzheimer's disease (AD), where the ApoE4 variant is the highest genetic risk factor for this disease.
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Programmed cell death protein 1 (PD-1) checkpoint blockade with an antibody has been shown to reduce amyloid-β plaques, associated pathologies and cognitive impairment in mouse models.
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Through a number of an extensive autopsy, biomarker, and genomics studies, researchers have recently defined a novel type of dementia known as limbic-predominant age-related TDP-43 encephalopathy (LATE).
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39/100
Mutations in the PSEN1 gene, encoding presenilin 1 (PS1), are the most common cause of familial Alzheimer's disease (fAD).
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.
- Specific targeting of tau oligomers in Htau mice prevents cognitive impairment and tau toxicity following injection with brain-derived tau oligomeric seeds
- Disturbed mitochondrial dynamics and neurodegenerative disorders
- Tau passive immunization blocks seeding and spread of Alzheimer hyperphosphorylated Tau-induced pathology in 3 × Tg-AD mice
- Electron transport chain defects in Alzheimer's disease brain
- PINK1/PARKIN signalling in neurodegeneration and neuroinflammation
- Effects of secreted oligomers of amyloid beta-protein on hippocampal synaptic plasticity: a potent role for trimers
- Presenilin mutations and their impact on neuronal differentiation in Alzheimer's disease
- GSK3 and tau: two convergence points in Alzheimer's disease
- The endoplasmic reticulum stress response in aging and age-related diseases
- Hereditary parkinsonism with dementia is caused by mutations in ATP13A2, encoding a lysosomal type 5 P-type ATPase