The DOI matches its Crossref record; 387 of the 387 references it cites were found in a registry or an index.
Autophagy and apoptosis dysfunction in neurodegenerative disorders
Open accessAbstract
Autophagy and apoptosis are basic physiologic processes contributing to the maintenance of cellular homeostasis. Autophagy encompasses pathways that target long-lived cytosolic proteins and damaged organelles. It involves a sequential set of events including double membrane formation, elongation, vesicle maturation and finally delivery of the targeted materials to the lysosome. Apoptotic cell death is best described through its morphology. It is characterized by cell rounding, membrane blebbing, cytoskeletal collapse, cytoplasmic condensation, and fragmentation, nuclear pyknosis, chromatin condensation/fragmentation, and formation of membrane-enveloped apoptotic bodies, that are rapidly phagocytosed by macrophages or neighboring cells. Neurodegenerative disorders are becoming increasingly prevalent, especially in the Western societies, with larger percentage of members living to an older age. They have to be seen not only as a health problem, but since they are care-intensive, they also carry a significant economic burden. Deregulation of autophagy plays a pivotal role in the etiology and/or progress of many of these diseases. Herein, we briefly review the latest findings that indicate the involvement of autophagy in neurodegenerative diseases. We provide a brief introduction to autophagy and apoptosis pathways focusing on the role of mitochondria and lysosomes. We then briefly highlight pathophysiology of common neurodegenerative disorders like Alzheimer's diseases, Parkinson's disease, Huntington's disease and Amyotrophic lateral sclerosis. Then, we describe functions of autophagy and apoptosis in brain homeostasis, especially in the context of the aforementioned disorders. Finally, we discuss different ways that autophagy and apoptosis modulation may be employed for therapeutic intervention during the maintenance of neurodegenerative disorders.
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“For example, some “neurodevelopmental” disorders can present later in the teens to early adulthood, while early-onset “neurodegenerative” disorders can be seen in the 4th or 5th decade of life.”
From The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases (2025) · cites this paper as [63]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“It can present in adulthood, quite late for a neurodevelopmental disorder.62,63”
From The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases (2025) · cites this paper as [63]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“A striking example of this overlap is Kufor-Rakeb syndrome, an autosomal recessive early-onset form of Parkinson’s disease caused by mutations in the lysosomal ATPase protein, ATP13A2.”
From The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases (2025) · cites this paper as [63]
Experimental — accuracy not yet measuredIn the citing paper
“The data suggest that a disruption of normal autophagy/mitophagy may contribute to mitochondrial malfunction and thereby promote PCD (Ghavami et al., 2014; Hroudova et al., 2014; Nixon and Yang, 2012).”
From Programmed cell death in aging (2015) · cites this paper as Ghavami et al., 2014
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“However, PCD is increasingly implicated in several aging-associated neurodegenerative diseases(Ghavami et al., 2014).”
From Programmed cell death in aging (2015) · cites this paper as Ghavami et al., 2014
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Metadata
- Authors
- Ghavami, S., Shojaei, S., Yeganeh, B., Ande, S. R., Jangamreddy, J. R., Mehrpour, M., Christoffersson, J., Chaabane, W., Moghadam, A. R., Kashani, H. H., Hashemi, M., Owji, A. A., & Łos, M. J.
- Affiliations
- Children's Hospital Research Institute of Manitoba (CA)
- Shiraz University of Medical Sciences (IR)
- University of Toronto (CA)
- University of Manitoba (CA)
- Linköping University (SE)
- Inserm (FR)
- Islamic Azad University Ardabil (IR)
- Zahedan University of Medical Sciences (IR)
- Corresponding author
- Owji, Ali A.
- ORCID
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2014-01
- Volume
- 112
- Pages
- 24-49
- ISSN
- 0301-0082 (ISSN-L)
- OpenAlex
- W2125461230
- Cited by
- 1,039
- References
- 387
- Citations by year
- 2026: 31 · 2025: 56 · 2024: 90 · 2023: 78 · 2022: 87 · 2021: 112 · 2020: 110 · 2019: 102 · 2018: 86 · 2017: 72 · 2016: 93 · 2015: 81 · 2014: 39
- FWCI
- 8.45
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Progress in Neurobiology (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- KTH Publication Database DiVA (KTH Royal Institute of Technology) (submittedVersion, other-oa)
- Funders
- Manitoba Health Research Council
- Cancerfonden
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- autophagy, apoptosis, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, mitochondria, lysosomes, brain homeostasis, autophagy modulation, therapeutic interventions
- MeSH terms
- Animals, Autophagy, Brain, Brain Diseases, Humans, Neurons, Peripheral Nervous System Diseases, Apoptosis, Neurodegenerative Diseases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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