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autophagy
240 studies tagged autophagy, 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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MRI studies have mapped the atrophic signature that distinguishes Alzheimer's disease (AD), isolating regions differentially vulnerable to its age-dependent neurodegenerative process.
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16/100
Genetic variation in the human gene encoding the lysosomal transmembrane protein 106B (TMEM106B) drives risk of neurodegenerative dementia.
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This structural configuration shields the scaffold from calpain-mediated cleavage, reconfiguring FLNA into an active motility engine driving invasive lamellipodia but stalls proteolytic processing and forces an absolute loss of the nuclear FLNA-90 tumor-suppressor brake, unleashing uninhibited c-Myc oncogenic transcription.
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Lysosomal distribution is critical for numerous biological functions within the cell, including protein degradation in autophagosomes, cholesterol homeostasis, and cell invasion.
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ABCA7-KO iMGs were deficient for proteins involved in lysosome function, measured by down-regulated lysosomal proteomic signatures, as well as reduced DQ-BSA activity and reduced LAMP1+ area.
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The defining neuropathologic feature of Lewy body dementia (LBD) and Parkinson’s disease (PD) is alpha-synuclein (Asyn) fibril accumulation in Lewy bodies (LBs) and Lewy neurites (LNs).
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TAR DNA-binding protein 43 (TDP-43) is an RNA-binding protein whose low-complexity domain (LCD) mediates self-assembly, liquid-liquid phase separation, and pathological aggregation associated with amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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Alzheimer’s disease (AD) is characterized by a decline in neuronal proteostasis that favours the accumulation of misfolded proteins.
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16/100
Neurodegenerative proteinopathies are defined by distinct proteins whose folding, trafficking and clearance depend on shared proteostasis machinery.
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Scrapie, a prion disease, is usually considered a protein-only infection.
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A key pathophysiological hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is loss of nuclear localization and abnormal cytoplasmic aggregation of TAR DNA-binding protein 43 (TDP-43).
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Alzheimer’s Disease (AD) is characterised by two histopathological hallmarks, intracellular tau-containing neurofibrillary tangles and extracellular amyloid plaques containing β-amyloid (Aβ), a specific cleavage product of Amyloid Precursor Protein (APP).
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Compared to CTR, both AD-αSAA- and AD-αSAA+ showed widespread cortical thinning.
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Neurodegenerative research has long hypothesized that aggregated proteins such as amyloid‑β (Aβ), tau, and α‑synuclein (αSyn) are intrinsically toxic and are directly associated with the etiologies of Alzheimer’s disease (AD) and Parkinson’s disease (PD).
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Autophagy preserves neuronal integrity by clearing damaged proteins and organelles, but its efficiency declines with aging and neurodegeneration.
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46/100
Here, we integrated multiple approaches to characterize proteasome function, composition and regulation in post-mortem human AD brain tissue compared with age-matched controls.
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Evidence indicates that chronic proteotoxic stress, arising from aging, oxidative damage, and environmental influences, disrupts the proteostasis network (PN).
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In synucleinopathies, the protein α-synuclein misfolds into Lewy bodies (LBs) in patients with Lewy body disease (LBD) or into glial cytoplasmic inclusions (GCIs) in patients with multiple system atrophy (MSA).
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Neurodegenerative diseases have long been considered distinct proteinopathies: amyloid-β and tau in Alzheimer's disease, α-synuclein in Parkinson's disease, and TDP-43 in amyotrophic lateral sclerosis.
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Though usually described as isolated models, neurodegenerative diseases exist in a significant proportion of cases as mixed pathologies, particularly in older adults.
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Protein misfolding is a fundamental biological process with profound implications for human health and disease.
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Parkinson's disease (PD) pathogenic mutations in leucine-rich repeat kinase 2 (LRRK2) are associated with endolysosomal dysfunction across cell types, and carriers of LRRK2 mutations variably present with phosphorylated tau and α-synuclein deposits in post-mortem analysis.
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The autophagy-lysosome pathway (ALP) and the ubiquitin-proteasome system (UPS) are the primary protein degradative mechanisms maintaining proteostasis in neurons.
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Age-related proteinopathies, including Alzheimer's and Parkinson's disease, are driven by toxic accumulation of misfolded and intrinsically disordered proteins (IDPs) that overwhelm cellular proteostasis.
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Optineurin (OPTN) is an autophagy adaptor protein involved in selective autophagy, including aggrephagy and mitophagy.
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DLB brains show PINK1 deficiency alongside α-syn and Aβ co-pathology.
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Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by neuronal loss, cognitive decline, and pathological hallmarks such as amyloid-beta (Aβ) plaques and tau neurofibrillary tangles.
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Alzheimer's disease (AD) is the primary cause of dementia in older individuals, exhibiting an increasing incidence worldwide.
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In the present study, we found senescent aVICs exhibited impaired macroautophagy/autophagy as evidenced by compromised autophagy flux and immature autophagosomes.
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Aging leads to progressive decline in organ and tissue integrity and function, partly due to loss of proteostasis and autophagy malfunctioning.
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Neurodegenerative diseases, including Alzheimer disease, frontotemporal dementia, Parkinson disease, Huntington disease, and amyotrophic lateral sclerosis, are often casually linked to protein aggregation and inclusion.
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Chaperone-mediated autophagy (CMA) is the lysosomal degradation of individually selected proteins, independent of vesicle fusion.
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Rare mutations in the gene encoding presenilin2 (PSEN2) are known to cause familial Alzheimer's disease (FAD).
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Neurodegenerative diseases represent the most common cause of dementia.
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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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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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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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46/100
TAR DNA-binding protein 43 (TDP-43) is an RNA binding protein found within ribonucleoprotein granules tethered to lysosomes via annexin A11.
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The accumulation of protein aggregates is a hallmark of many diseases, including Alzheimer's disease.
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Proteostasis is essential for normal function of proteins and vital for cellular health and survival.
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Cognitive dysfunction and dementia are critical symptoms of Lewy Body dementias (LBD).
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Neurodegenerative disorders are devastating disorders characterized by gradual loss of neurons and cognition or mobility impairment.
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Spinocerebellar ataxia type 3 (SCA3) is the most common dominantly inherited ataxia.
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Intersectin (ITSN) is a multi-domain scaffold protein with a diverse array of functions including regulation of endocytosis, vesicle transport, and activation of various signal transduction pathways.
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Highly penetrant autosomal dominant Alzheimer's disease (ADAD) comprises a distinct disease entity as compared to the far more prevalent form of AD in which common variants collectively contribute to risk.
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Although loss of TAR DNA-binding protein 43 kDa (TDP-43) splicing repression is well documented in postmortem tissues of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), whether this abnormality occurs during early-stage disease remains unresolved.
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Our understanding of stress granule (SG) biology has deepened considerably in recent years, and with this, increased understanding of links has been made between SGs and numerous neurodegenerative diseases.
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Neurodegenerative disorders, such as Alzheimer's disease (AD) or Huntington's disease (HD), are linked to protein aggregate neurotoxicity.
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The spectrum of neurodegenerative diseases known today is quite extensive.
From across this tag
9 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 9. The same 9 appear here every time.
- Supramolecular organizing centers at the interface of inflammation and neurodegeneration
- Autophagy and synaptic plasticity: epigenetic regulation
- Receptors make the pathway choice for protein degradation
- The Braak hypothesis in prion disease with a focus on Creutzfeldt-Jakob disease
- Direct transfer of alpha-synuclein from neuron to astroglia causes inflammatory responses in synucleinopathies
- Synucleins are developmentally expressed, and alpha-synuclein regulates the size of the presynaptic vesicular pool in primary hippocampal neurons
- Chaperone-mediated autophagy: a gatekeeper of neuronal proteostasis
- Autophagy and heat-shock response impair stress granule assembly during cellular senescence
- The endoplasmic reticulum stress response in aging and age-related diseases