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proteostasis
240 studies tagged proteostasis, dated 1993-05-01 to 2026-10-30. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Disrupting SORL1-retromer endosomal recycling in mice drives the age-dependent neurodegenerative signature of Alzheimer's disease 2026-10-30
- TMEM106B C-Terminal fragment aggregation exacerbates α-synuclein and TDP-43 proteinopathy phenotypes 2026-10-30
- The Filamin A Proteomic Switch: Solubility States and Cytoskeletal Dynamics Explain the Inverse Epidemiological Relationship Between Cancer and Alzheimer’s Disease 2026-10-26
Studies
240 studies carry this tag.
Date range
1993 to 2026
Top journals
- Autophagy 9
- bioRxiv 9
- Nature 8
- Nature communications 6
- Acta neuropathologica 5
145 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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41/100
Alzheimer's disease (AD) represents the most frequent type of dementia worldwide, and aging is the most important risk factor for the sporadic form of the pathology.
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Alzheimer's disease (AD) is characterized by the accumulation of misfolded amyloid-beta and tau proteins.
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Intraneuronal dysproteostasis and extraneuronal microenvironmental abnormalities in Alzheimer's disease (AD) collectively culminate in neuronal deterioration.
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We have recently shown that multiple tRNA synthetase inhibitors can greatly increase lifespan in multiple models by acting through the conserved transcription factor ATF4.
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Neurodegenerative diseases (NDDs) like Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) are defined by a myriad of complex aetiologies.
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48/100
There is increasing interest in studying retinal biomarkers for various neurodegenerative diseases.
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45/100
Parkinson disease (PD) is closely linked to the misfolding and accumulation of α-synuclein (α-syn) into Lewy bodies.
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SRC homology 3 (SH3) domains are fundamental modules that enable the assembly of protein complexes through physical interactions with a pool of proline-rich/noncanonical motifs from partner proteins.
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Retromer controls cellular homeostasis through regulating integral membrane protein sorting and transport and by controlling maturation of the endo-lysosomal network.
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CSF was αSyn-SAA positive (αSyn+) in 36/80 AD patients (45%) and in 2/28 controls (7.1%).
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Cellular deposition of protein aggregates, one of the hallmarks of neurodegeneration, disrupts cellular functions and leads to neuronal death.
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The homeostasis of cellular proteins, or proteostasis, is critical for neuronal function and for brain processes, including learning and memory.
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16/100
Haploinsufficiency of progranulin (PGRN) causes frontotemporal dementia (FTD), a devastating neurodegenerative disease with no effective treatment.
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41/100
TTR (transthyretin) strikes a neuroprotective function in the prevention of amyloid-β (Aβ) deposition in Alzheimer disease (AD).
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It is strongly believed that aluminum is one of the insalubrious agents because of its neurotoxicity effects and influences on amyloid β (Aβ) production and tau protein hyperphosphorylation following oxidative stress, as one of the initial events in neurotoxicity.
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41/100
Autophagy degrades phagocytosed damaged organelles, misfolded proteins, and various pathogens through lysosomes as an essential way to maintain cellular homeostasis.
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Amyloid aggregates of specific proteins constitute important pathological hallmarks in many neurodegenerative diseases, defining neuronal degeneration and disease onset.
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The pathogenesis of neurodegenerative diseases involves the accumulation of misfolded protein aggregates.
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Autophagy is markedly impaired in Alzheimer's disease (AD).
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Alzheimer disease (AD) is a devastating condition associated with loss of proteostasis control and autophagy failure, leading to progressive neuronal cell death.
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Presenilin 1 (PSEN1) mutations are a major cause of familial Alzheimer's disease.
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Neurodegenerative diseases (NDs) are often age-related disorders that can cause dementia in people, usually over 65 years old, are still lacking effective therapies.
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α-synuclein (α-syn) is a presynaptic, lipid-binding protein strongly associated with the neuropathology observed in Parkinson's disease (PD), dementia with Lewy bodies (DLB), and Alzheimer's Disease (AD).
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Alzheimer's disease (AD) is one of the biggest human health threats due to increases in aging of the global population.
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41/100
The multi-site ubiquitination of Tau protein found in Alzheimer's disease filaments hints at the failed attempt of neurons to remove early toxic species.
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Neurodegenerative diseases (ND) pose a serious health burden to society and healthcare systems alike, with increasing incidence rates especially within aging populations.
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Alzheimer's disease (AD) is the most common type of dementia associated with age-related neurodegeneration.
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Neurodegenerative diseases (NDs) are characteristic with progression of neuron degeneration, resulting in dysfunction of cognition and mobility.
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We identified a novel mutation c.401_406delinsTCTAT; p.(Asp134Valfs*55) in exon 3 of TREM2 in an Alzheimer's disease patient also carrying the p.Arg62His TREM2 variant.
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45/100
Expansions of a G 4 C 2 repeat in the C9ORF72 gene are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two devastating adult-onset neurodegenerative disorders.
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41/100
Dementia with Lewy bodies (DLB) is epitomized by the pathognomonic manifestation of α-synuclein-laden Lewy bodies within selectively vulnerable neurons in the brain.
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Protein homeostasis, or proteostasis, is essential for cell function and viability.
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Immunohistochemical analysis of M20/L85 mice revealed that pre-existing Aβ plaques exacerbate the spread and deposition of induced α-synuclein pathology.
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One evident hallmark of Alzheimer's disease (AD) is the irregular accumulation of proteins due to changes in proteostasis involving endoplasmic reticulum (ER) stress.
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Chaperone-mediated autophagy (CMA) is a lysosome-dependent selective degradation pathway implicated in the pathogenesis of cancer and neurodegenerative diseases.
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Neurodegenerative disorders like Alzheimer's disease and Parkinson's disease are characterized by progressive degeneration of synapses and neurons.
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Neurodegenerative diseases, including Alzheimer's disease, Huntington's disease, and Parkinson's disease, are a class of diseases that lead to dysfunction of cognition and mobility.
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Different types of autophagy co-exist in all mammalian cells, however, the specific contribution of each of these autophagic pathways to the maintenance of cellular proteostasis and cellular function remains unknown.
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Tightly orchestrated programmed cell death (PCD) signalling events occur during normal neuronal development in a spatially and temporally restricted manner to establish the neural architecture and shaping the CNS.
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Dysfunction of the endolysosomal-autophagy network is emerging as an important pathogenic process in Alzheimer's disease.
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Mechanisms of protein homeostasis are crucial for overseeing the clearance of misfolded and toxic proteins over the lifetime of an organism, thereby ensuring the health of neurons and other cells of the central nervous system.
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In Parkinson's disease, aggregates of α-synuclein within Lewy bodies and Lewy neurites represent neuropathological hallmarks.
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Precursor messenger RNA (pre-mRNA) splicing is a fundamental step in eukaryotic gene expression that systematically removes non-coding regions (introns) and ligates coding regions (exons) into a continuous message (mature mRNA).
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41/100
Autophagy, a main degradation pathway for maintaining cellular homeostasis, and redox homeostasis have recently been considered to play protective roles in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis.
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Dementia with Lewy bodies (DLB) is characterized by the toxic accumulation of α-synuclein protein inside neural cells; this results in neurodegeneration which is clinically accompanied by behavioral and psychological changes.
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Components of the proteostasis network malfunction in aging, and reduced protein quality control in neurons has been proposed to promote neurodegeneration.
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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are two clinically distinct classes of neurodegenerative disorders.
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Protein homeostasis, or proteostasis, is crucial for the functioning of a cell, as proteins that are mislocalized, present in excessive amounts, or aberrant due to misfolding or other type of damage can be harmful.
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Hereditary diseases are caused by mutations in genes, and more than 7,000 rare diseases affect over 30 million Americans.
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Stress granules (SGs) are membraneless organelles formed in response to insult.
From across this tag
8 of the 240 studies in this tag, 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 8. The same 8 appear here every time.
- Cellular Proteostasis in Neurodegeneration
- The proteostasis network and its decline in ageing
- α-Synuclein strains cause distinct synucleinopathies after local and systemic administration
- Efficient introduction of specific homozygous and heterozygous mutations using CRISPR/Cas9
- Widespread transneuronal propagation of α-synucleinopathy triggered in olfactory bulb mimics prodromal Parkinson’s disease
- Glia-specific autophagy dysfunction in ALS
- Intersectin scaffold proteins and their role in cell signaling and endocytosis
- NEURODEGENERATION. Alzheimer's and Parkinson's diseases: The prion concept in relation to assembled Aβ, tau, and α-synuclein