ReviewTranslational neurodegeneration2022
The use of fibroblasts as a valuable strategy for studying mitochondrial impairment in neurological disorders.
Review in Translational neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 60 citations in OpenAlex.
- Mitochondrial Quality Control Impairment Is a Hallmark of TDP-43Antioxidants (Basel, Switzerland) · 2026Article
- Loss of Function of AFG3L2 Leading to Developmental and Epileptic Encephalopathy.CNS neuroscience & therapeutics · 2026Article
- The ITM2B-associated retinal dystrophy mutation modifies BRI23 peptide interactions in the human retina.Scientific reports · 2026Article
- Mitochondrial Dysfunction as a Driver of Neurodegeneration in Parkinson's and Huntington's Disease: Molecular Insights and Emerging Interventions.Molecular neurobiology · 2026Review
- Cellular Senescence of Patient-derived Fibroblasts Reveals the Mid-old Stage as a Critical Window for Transcriptomic Signatures Linked to Alzheimer's Disease Biomarkers and Classification.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026Article
- Identifying and targeting abnormal mitochondrial localization associated with psychosis.bioRxiv : the preprint server for biology · 2026Article
- Cell Cycle Dysfunction and Metabolic Alterations Consistent With Pathological Tau in Progressive Supranuclear Palsy Derived Fibroblasts.Molecular neurobiology · 2026Article
- Wdfy3-dependent autophagy impairment recapitulates presymptomatic neurodegenerative signatures in mice.Scientific reports · 2026Article
- Molecular genotype-phenotype correlation in ACTB- and ACTG1-related non-muscle actinopathies.American journal of human genetics · 2026Article
- Mitochondrial morphology and mtDNA content in fibroblasts from patients with different types of mucopolysaccharidosis.Acta biochimica Polonica · 2026Article
- Dodecanedioic Acid: Alternative Carbon Substrate or Toxic Metabolite?Biomolecules · 2025Article
- Exploring the skin as an open window onto neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Comparing loss of individual fragile X proteins suggests strong links to cellular senescence and aging.Cellular and molecular life sciences : CMLS · 2025Article
- Article
- Investigating the ageing-Parkinson's disease nexus: standardisation of in vitro models and techniques by the PD-AGE network.NPJ Parkinson's disease · 2025Review
- Elevated hexosylceramides in Parkinson's disease cause gene upregulations in neurons mimicking responses to pathogens.NPJ Parkinson's disease · 2025Article
- Interconnections of insulin/IGF-1 signaling and autophagy abnormalities in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- From Gene to Pathways: Understanding Novel Vps51 Variant and Its Cellular Consequences.International journal of molecular sciences · 2025Article
- Neurodegeneration models in Parkinson's disease: cellular and molecular paths to neuron death.Behavioral and brain functions : BBF · 2025Review
- Skin pathology in ALS: Diagnostic implications and biomarker potential.Biomolecules & biomedicine · 2025Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurological disorders (NDs) are characterized by progressive neuronal dysfunction leading to synaptic failure, cognitive impairment, and motor injury. Among these diseases, Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS) have raised a significant research interest. These disorders present common neuropathological signs, including neuronal dysfunction, protein accumulation, oxidative damage, and mitochondrial abnormalities. In this context, mitochondrial impairment is characterized by a deficiency in ATP production, excessive production of reactive oxygen species, calcium dysregulation, mitochondrial transport failure, and mitochondrial dynamics deficiencies. These defects in mitochondrial health could compromise the synaptic process, leading to early cognitive dysfunction observed in these NDs. Interestingly, skin fibroblasts from AD, PD, HD, and ALS patients have been suggested as a useful strategy to investigate and detect early mitochondrial abnormalities in these NDs. In this context, fibroblasts are considered a viable model for studying neurodegenerative changes due to their metabolic and biochemical relationships with neurons. Also, studies of our group and others have shown impairment of mitochondrial bioenergetics in fibroblasts from patients diagnosed with sporadic and genetic forms of AD, PD, HD, and ALS. Interestingly, these mitochondrial abnormalities have been observed in the brain tissues of patients suffering from the same pathologies. Therefore, fibroblasts represent a novel strategy to study the genesis and progression of mitochondrial dysfunction in AD, PD, HD, and ALS. This review discusses recent evidence that proposes fibroblasts as a potential target to study mitochondrial bioenergetics impairment in neurological disorders and consequently to search for new biomarkers of neurodegeneration.
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