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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N-methyl-D-aspartate receptors (NMDARs) play a pivotal role in the synaptic transmission and synaptic plasticity thought to underlie learning and memory.
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β-Amyloid (Aβ) oligomers may play an important role in the early pathogenesis of Alzheimer's disease: cognitive impairment caused by synaptic dysfunction.
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Alzheimer's disease (AD) is an irreversible brain disorder characterized by progressive cognitive decline and neurodegeneration of brain regions that are crucial for learning and memory.
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38/100
Small molecular weight compounds able to inhibit formation of tau oligomers and fibrils have already been tested for Alzheimer's disease (AD) treatment.
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Proteostasis are integrated biological pathways within cells that control synthesis, folding, trafficking and degradation of proteins.
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38/100
In recent years, tau immunotherapy has advanced from proof-of-concept studies [Sigurdsson EM, NIH R01AG020197, 2001; Asuni AA, et al: J Neurosci 2007;27:9115-9129], which have now been confirmed and extended by us and others.
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In Alzheimer's disease (AD), the deposition of β-amyloid (Aβ) is hypothesized to result in a series of secondary neurodegenerative processes, leading ultimately to synaptic dysfunction and neuronal loss.
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Amyotrophic lateral sclerosis is a devastating disease characterized by rapidly progressive paresis.
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In mature neurons, the number of synapses is determined by a neuronal activity-dependent dynamic equilibrium between positive and negative regulatory factors.
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Cognitive decline and disease progression in different neurodegenerative diseases typically involves synaptic dysfunction preceding the neuronal loss.
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Aberrant cleavage of amyloid precursor protein (APP) by γ-secretase contributes to the development of Alzheimer's disease.
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Alzheimer's disease (AD) is a chronic neurodegenerative disorder and the most common cause of dementia among the elderly population.
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One of the shared hallmarks of neurodegenerative diseases is the accumulation of misfolded proteins.
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The extracellular aggregation of proteins into proteotoxic oligomers and amyloid fibrils is implicated in the onset and pathology of numerous diseases referred to as amyloid diseases.
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The autophagic process is the only known mechanism for mitochondrial turnover and it has been speculated that dysfunction of autophagy may result in mitochondrial error and cellular stress.
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Dose-dependent decrease of Aβ40 levels in vivo confirmed suppression of BACE1 activity by both inhibitors.
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All synapses are not the same. They differ in their morphology, molecular constituents, and malleability.
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Accumulation of misfolded α-synuclein (α-syn) protein in Lewy bodies and neurites is the cardinal pathologic feature of Parkinson disease (PD), but abnormal deposition of other proteins may also play a role.
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Cerium oxide nanoparticles (CeONPs) have attracted much attention because they possess multi-enzyme mimetic properties and have been used in bioanalysis, biomedicine, drug delivery, bioscaffold and so on.
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Impairment of the ubiquitin-proteasome system (UPS) has been implicated in the pathogenesis of a wide variety of neurodegenerative disorders, including Alzheimer's, Parkinson's, and Huntington's diseases.
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Early-onset FAD (familial Alzheimer's disease) is caused by mutations of PS1 (presenilin 1), PS2 (presenilin 2) and APP (amyloid precursor protein).
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Disappointing findings from recent phase III trials on amyloid-β (Aβ) immunotherapy for Alzheimer's disease (AD) have shifted the focus of such treatments to the tau protein.
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The choroid plexus (CP) is present on the ventricular walls of the brain, produces cerebrospinal fluid (CSF), contains many blood vessels, and is a major functional component of the blood-CSF barrier.
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38/100
Neuronal calcium sensors (NCS) readily bind calcium and undergo conformational changes enabling them to interact and regulate specific target molecules.
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38/100
Dementias are a varied group of disorders typically associated with memory loss, impaired judgment and/or language and by symptoms affecting other cognitive and social abilities to a degree that interferes with daily functioning.
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.
- Cell biology of protein misfolding: the examples of Alzheimer's and Parkinson's diseases
- Development of tau aggregation inhibitors for Alzheimer's disease
- Fragile X-associated tremor/ataxia syndrome: clinical features, genetics, and testing guidelines
- Cerebral amyloid angiopathy: pathogenetic mechanisms and link to dense amyloid plaques
- Identification of amyloid plaques in retinas from Alzheimer's patients and noninvasive in vivo optical imaging of retinal plaques in a mouse model
- Trafficking of cell surface beta-amyloid precursor protein: retrograde and transcytotic transport in cultured neurons
- The cell biology of beta-amyloid precursor protein and presenilin in Alzheimer's disease
- Superoxide dismutase activity in Alzheimer's disease: possible mechanism for paired helical filament formation
- Recent advances in the design, synthesis, and biological evaluation of selective DYRK1A inhibitors: a new avenue for a disease modifying treatment of Alzheimer's?
- Impacts of Cd(II) on the conformation and self-aggregation of Alzheimer's tau fragment corresponding to the third repeat of microtubule-binding domain