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Home › Research › Topics › autophagy

autophagy

241 studies tagged autophagy, dated 1993-05-01 to 2026-10-30. Bibliography: BibTeX (.bib) · RIS (.ris)

Newest in this topic

  1. Disrupting SORL1-retromer endosomal recycling in mice drives the age-dependent neurodegenerative signature of Alzheimer's disease 2026-10-30
  2. TMEM106B C-Terminal fragment aggregation exacerbates α-synuclein and TDP-43 proteinopathy phenotypes 2026-10-30
  3. 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

241 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.

  1. Autophagy and heat-shock response impair stress granule assembly during cellular senescence

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Mechanisms of ageing and development 2020-10-10 Disease mechanisms

    Stress granules (SGs) are membraneless organelles formed in response to insult.

  2. Endosomal-lysosomal dysfunction in metabolic diseases and Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. International review of neurobiology 2020-07-10 Disease mechanisms

    The endosomal-lysosomal pathways and related autophagic processes are responsible for proteostasis, involving complexes between lysosomes and autophagosomes.

  3. TDP-1/TDP-43 potentiates human α-Synuclein (HASN) neurodegeneration in Caenorhabditis elegans

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Biochimica et biophysica acta. Molecular basis of disease 2020-06-09 Brain tissue and pathology

    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.

  4. Structures of α-synuclein filaments from multiple system atrophy

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Nature 2020-05-27 Brain tissue and pathology

    Synucleinopathies, which include multiple system atrophy (MSA), Parkinson's disease, Parkinson's disease with dementia and dementia with Lewy bodies (DLB), are human neurodegenerative diseases 1 .

  5. The Braak hypothesis in prion disease with a focus on Creutzfeldt-Jakob disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neuropathology : official journal of the Japanese Society of Neuropathology 2020-05-03 Brain tissue and pathology

    This review considers whether the Braak hypothesis on protein propagation could account for prion disease, particularly Creutzfeldt-Jakob disease (CJD).

  6. Proteostasis Failure in Neurodegenerative Diseases: Focus on Oxidative Stress

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Oxidative medicine and cellular longevity 2020-03-27 Disease mechanisms

    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.

  7. Autophagy modulates Aβ accumulation and formation of aggregates in yeast

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Molecular and cellular neurosciences 2020-01-18 Disease mechanisms

    Intracellular accumulation of amyloid-β protein (Aβ) is an early event in Alzheimer's disease (AD).

  8. TDP-43 and Limbic-Predominant Age-Related TDP-43 Encephalopathy

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Frontiers in aging neuroscience 2020-01-14 Brain tissue and pathology

    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).

  9. Parkinson's disease: proteinopathy or lipidopathy?

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. NPJ Parkinson's disease 2020-01-03 Genetics

    Lipids play a more significant role in Parkinson's disease and its related brain disorders than is currently recognized, supporting a "lipid cascade".

  10. Development of LNA Gapmer Oligonucleotide-Based Therapy for ALS/FTD Caused by the C9orf72 Repeat Expansion

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Methods in molecular biology (Clifton, N.J.) 2020 Drug development

    Several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), have a complex genetic background, in addition to cases where the disease appears to manifest sporadically.

  11. The Ubiquitin System in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Advances in experimental medicine and biology 2020 Disease mechanisms

    Alzheimer's disease (AD) is the most common form of dementia, most prevalent in the elderly population and has a significant impact on individuals and their family as well as the health care system and the economy.

  12. Autophagy and synaptic plasticity: epigenetic regulation

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Current opinion in neurobiology 2019-10-18 Disease mechanisms

    In neurons, autophagy is crucial to proper axon guidance, vesicular release, dendritic spine architecture, spine pruning and synaptic plasticity and, when dysregulated, is associated with brain disorders, including autism spectrum disorders, and neurodegenerative diseases such as Parkinson's and Alzheimer's disease.

  13. Pathogenic Mechanisms and Therapy Development for C9orf72 Amyotrophic Lateral Sclerosis/Frontotemporal Dementia

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics 2019-10 Drug development

    In 2011, a hexanucleotide repeat expansion in the first intron of the C9orf72 gene was identified as the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

  14. Modeling α-Synuclein Propagation with Preformed Fibril Injections

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Journal of movement disorders 2019-09-30 Brain tissue and pathology

    The aggregation of α-synuclein (α-syn) has been implicated in the pathogenesis of many neurodegenerative disorders, including Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA).

  15. [Antisense therapies for neurological diseases]

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Der Nervenarzt 2019-08 Drug development

    Despite identification of many genes causing neurodegenerative diseases in the last decades, development of disease-modifying treatments has been slow.

  16. Alpha-synuclein structure and Parkinson's disease - lessons and emerging principles

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Molecular neurodegeneration 2019-07-22 Getting a diagnosis

    Alpha-synuclein (αS) is the major constituent of Lewy bodies and a pathogenic hallmark of all synucleinopathathies, including Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA).

  17. The proteostasis network and its decline in ageing

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Nature reviews. Molecular cell biology 2019-07-01 Disease mechanisms

    Ageing is a major risk factor for the development of many diseases, prominently including neurodegenerative disorders such as Alzheimer disease and Parkinson disease.

  18. Glia-specific autophagy dysfunction in ALS

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Seminars in cell & developmental biology 2019-05-28 Disease mechanisms

    Neuronal cell death is the main pathological feature of chronic neurodegenerative diseases (NDs) such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

  19. Autophagy Dysfunction in Alzheimer's Disease: Mechanistic Insights and New Therapeutic Opportunities

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Biological psychiatry 2019-05-20 Disease mechanisms

    Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive memory loss due to aberrant accumulation of misfolded proteins inside and outside neurons and glial cells, leading to a loss of cellular protein homeostasis.

  20. Loss of proteins associated with amyotrophic lateral sclerosis affects lysosomal acidification via different routes

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Autophagy 2019-04-28 Disease mechanisms

    Abnormal accumulation of proteins is a hallmark of a variety of neurological diseases including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

  21. Protective function of autophagy during VLCFA-induced cytotoxicity in a neurodegenerative cell model

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Free radical biology & medicine 2019-04-17 Disease mechanisms

    In recent years, a particular interest has focused on the accumulation of fatty acids with very long chains (VLCFA) in the occurrence of neurodegenerative diseases such as Alzheimer's disease, multiple sclerosis or dementia.

  22. Antisense oligonucleotides: A primer

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurology. Genetics 2019-04-01 Drug development

    There are few disease-modifying therapeutics for neurodegenerative diseases, but successes on the development of antisense oligonucleotide (ASO) therapeutics for spinal muscular atrophy and Duchenne muscular dystrophy predict a robust future for ASOs in medicine.

  23. Endo-lysosomal pathway and ubiquitin-proteasome system dysfunction in Alzheimer's disease pathogenesis

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neuroscience letters 2019-03-16 Disease mechanisms

    Several lines of evidence have shown that defects in the endo-lysosomal autophagy degradation pathway and the ubiquitin-proteasome system play a role in Alzheimer's Disease (AD) pathogenesis and pathophysiology.

  24. Protein Arginine Deiminases (PADs): Biochemistry and Chemical Biology of Protein Citrullination

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Accounts of Chemical Research 2019-03-07 Genetics

    Hundreds of proteins are known to be citrullinated and hypercitrullination is associated with autoimmune diseases including rheumatoid arthritis (RA), lupus, ulcerative colitis (UC), Alzheimer's disease, multiple sclerosis (MS), and certain cancers.

  25. Presenilins and γ-Secretase in Membrane Proteostasis

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cells 2019-03-01 Disease mechanisms

    The presenilin (PS) proteins exert a crucial role in the pathogenesis of Alzheimer disease (AD) by mediating the intramembranous cleavage of amyloid precursor protein (APP) and the generation of amyloid β-protein (Aβ).

  26. The Autophagy-Lysosomal Pathways and Their Emerging Roles in Modulating Proteostasis in Tumors

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cells 2018-12-20 Disease mechanisms

    In normal physiological condition, the maintenance of cellular proteostasis is a prerequisite for cell growth, functioning, adapting to changing micro-environments, and responding to extracellular stress.

  27. Proteomic analysis of protein homeostasis and aggregation

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Journal of proteomics 2018-12-06 Disease mechanisms

    Protein homeostasis (proteostasis) refers to the ability of cells to preserve the correct balance between protein synthesis, folding and degradation.

  28. Dysregulation of autophagy and stress granule-related proteins in stress-driven Tau pathology

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cell death and differentiation 2018-11-15 Disease mechanisms

    Imbalance of neuronal proteostasis associated with misfolding and aggregation of Tau protein is a common neurodegenerative feature in Alzheimer's disease (AD) and other Tauopathies.

  29. Distinct proteostasis circuits cooperate in nuclear and cytoplasmic protein quality control

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature 2018-10-31 Disease mechanisms

    Protein misfolding is linked to a wide array of human disorders, including Alzheimer's disease, Parkinson's disease and type II diabetes1,2.

  30. Fighting the Cause of Alzheimer's and GNE Myopathy

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Frontiers in neuroscience 2018-10-15 Disease mechanisms

    Age is the common risk factor for both neurodegenerative and neuromuscular diseases.

  31. Cellular Proteostasis in Neurodegeneration

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Molecular neurobiology 2018-09-04 Disease mechanisms

    The term proteostasis reflects the fine-tuned balance of cellular protein levels, mediated through a vast network of biochemical pathways.

  32. Proteolytic ectodomain shedding of membrane proteins in mammals-hardware, concepts, and recent developments

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. The EMBO journal 2018-07-05 Genetics

    Proteolytic removal of membrane protein ectodomains (ectodomain shedding) is a post-translational modification that controls levels and function of hundreds of membrane proteins.

  33. SMPD3 deficiency perturbs neuronal proteostasis and causes progressive cognitive impairment

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cell death & disease 2018-05-01 Disease mechanisms

    Neutral sphingomyelinase smpd3 is most abundantly expressed in neurons of brain.

  34. Neuronal Cell Death

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Physiological reviews 2018-04-01 Inflammation and the immune system

    Neuronal cell death occurs extensively during development and pathology, where it is especially important because of the limited capacity of adult neurons to proliferate or be replaced.

  35. Protein aggregates and proteostasis in aging: Amylin and β-cell function

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Mechanisms of ageing and development 2018-03-23 Disease mechanisms

    The ubiquitin-proteasomal-system (UPS) and the autophagy-lysosomal-system (ALS) are both highly susceptible for disturbances leading to the accumulation of cellular damage.

  36. Murine knockin model for progranulin-deficient frontotemporal dementia with nonsense-mediated mRNA decay

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2018-03-06 Drug development

    Frontotemporal dementia (FTD) is the most common neurodegenerative disorder in individuals under age 60 and has no treatment or cure.

  37. Differential α-synuclein expression contributes to selective vulnerability of hippocampal neuron subpopulations to fibril-induced toxicity

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Acta neuropathologica 2018-03-03 Drug development

    The accumulation of misfolded α-synuclein (aSyn) and neuron loss define several neurodegenerative disorders including Parkinson's disease (PD) and dementia with Lewy bodies (DLB).

  38. TDP-43 Prions

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cold Spring Harbor perspectives in medicine 2018-03-01 Brain tissue and pathology

    The most common neurodegenerative diseases, such as Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis, are all protein-misfolding diseases and are characterized by the presence of disease-specific protein aggregates in affected neuronal cells.

  39. Presynaptic endocytic factors in autophagy and neurodegeneration

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Current opinion in neurobiology 2018-01-06 Disease mechanisms

    Neuronal signaling depends on the exocytic fusion and subsequent endocytic retrieval and reformation of neurotransmitter-containing synaptic vesicles at synapses.

  40. A refined concept: α-synuclein dysregulation disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neurochemistry international 2018-01-02 Brain tissue and pathology

    α-synuclein (αSyn) still remains a mysterious protein even two decades after SNCA encoding it was identified as the first causative gene of familial Parkinson's disease (PD).

  41. Pathways of cellular proteostasis in aging and disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of cell biology 2017-11-10 Disease mechanisms

    Ensuring cellular protein homeostasis, or proteostasis, requires precise control of protein synthesis, folding, conformational maintenance, and degradation.

  42. Neurodegeneration and the ordered assembly of α-synuclein

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cell and tissue research 2017-11-08 Brain tissue and pathology

    In 2017, it was 200 years since James Parkinson published 'An Essay on the Shaking Palsy' and 20 years since α-synuclein aggregation came to the fore.

  43. Brains with sporadic Creutzfeldt-Jakob disease and copathology showed a prolonged end-stage of disease

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of clinical pathology 2017-11-02 Brain tissue and pathology

    Copathology was significantly associated with survival in brains with CJD (4.2±1.2 vs 9.2±1.9; P=0.019) and in brains with MM1/MV1 CJD (2.1±1.0 vs 6.7±2.8; P=0.012).

  44. β-Amyloid and the Pathomechanisms of Alzheimer's Disease: A Comprehensive View

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Molecules (Basel, Switzerland) 2017-10-10 Disease mechanisms

    Protein dyshomeostasis is the common mechanism of neurodegenerative diseases such as Alzheimer's disease (AD).

  45. Receptors make the pathway choice for protein degradation

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Autophagy 2017-08-10 Disease mechanisms

    Damaged or aggregated proteins and organelles accumulate with age and contribute to various age-related pathologies including Alzheimer, Parkinson or Huntington diseases.

  46. Mitophagy in neurodegenerative diseases

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neurochemistry international 2017-08-08 Disease mechanisms

    Neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), and Amyotrophic Lateral Sclerosis (ALS), are a complex "family" of pathologies, characterised by the progressive loss of neurons and/or neuronal functions, leading to severe physical and cognitive inabilities in affected patients.

  47. Protein Quality Control and the Amyotrophic Lateral Sclerosis/Frontotemporal Dementia Continuum

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Frontiers in molecular neuroscience 2017-05-10 Disease mechanisms

    Protein homeostasis, or proteostasis, has an important regulatory role in cellular function.

  48. Control of mitochondrial biogenesis and function by the ubiquitin-proteasome system

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Open biology 2017-04 Disease mechanisms

    Mitochondria are pivotal organelles in eukaryotic cells.

  49. Individuals with progranulin haploinsufficiency exhibit features of neuronal ceroid lipofuscinosis

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Science translational medicine 2017-04-01 Brain scans and imaging

    Heterozygous mutations in the GRN gene lead to progranulin (PGRN) haploinsufficiency and cause frontotemporal dementia (FTD), a neurodegenerative syndrome of older adults.

  50. Loss-of-function mutations in the ATP13A2/PARK9 gene cause complicated hereditary spastic paraplegia (SPG78)

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Brain : a journal of neurology 2017-02-01 Genetics

    Molecular defects in this gene have been causally associated with Kufor-Rakeb syndrome (#606693), an autosomal recessive form of juvenile-onset parkinsonism, and neuronal ceroid lipofuscinosis (#606693), a neurodegenerative disorder characterized by the intracellular accumulation of autofluorescent lipopigments.

From across this tag

5 of the 241 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 5. The same 5 appear here every time.

All topic tags with their study counts