ArticleExperimental neurology2012
Wild type TDP-43 induces neuro-inflammation and alters APP metabolism in lentiviral gene transfer models.
Article in Experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- TDP-43 pathology triggers neuroinflammation and cognitive impairment by inducing microglial necroptosis.EMBO molecular medicine · 2026Article
- TDP-43 overexpression in the hypothalamus drives neuropathology, dysregulates metabolism and impairs behavior in mice.Acta neuropathologica communications · 2025Article
- The Fault in Our Astrocytes - cause or casualties of proteinopathies of ALS/FTD and other neurodegenerative diseases?Frontiers in molecular medicine · 2023Review
- Review
- Glial TDP-43 and TDP-43 induced glial pathology, focus on neurodegenerative proteinopathy syndromes.Glia · 2022Review
- Review
- Sex-dependent effects of amyloid precursor-like protein 2 in the SOD1-G37R transgenic mouse model of MND.Cellular and molecular life sciences : CMLS · 2021Article
- TDP-43 and amyloid precursor protein processing: implications for Alzheimer's disease.Neural regeneration research · 2021Article
- Review
- The Path to Progress Preclinical Studies of Age-Related Neurodegenerative Diseases: A Perspective on Rodent and hiPSC-Derived Models.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Review
- Neurodegenerative Disease and the NLRP3 Inflammasome.Frontiers in pharmacology · 2021Review
- TDP-43 interacts with amyloid-β, inhibits fibrillization, and worsens pathology in a model of Alzheimer's disease.Nature communications · 2020Article
- The cellular expression and proteolytic processing of the amyloid precursor protein is independent of TDP-43.Bioscience reports · 2020Article
- Oligomeric amyloid-β induces early and widespread changes to the proteome in human iPSC-derived neurons.Scientific reports · 2020Article
- TDP-43: From Alzheimer's Disease to Limbic-Predominant Age-Related TDP-43 Encephalopathy.Frontiers in molecular neuroscience · 2020Article
- Notch Signalling in the Hippocampus of Patients With Motor Neuron Disease.Frontiers in neuroscience · 2019Article
- Microglia-mediated recovery from ALS-relevant motor neuron degeneration in a mouse model of TDP-43 proteinopathy.Nature neuroscience · 2018Article
- Role and Therapeutic Potential of Astrocytes in Amyotrophic Lateral Sclerosis.Current pharmaceutical design · 2017Review
- The Role of TDP-43 in Alzheimer's Disease.Molecular neurobiology · 2016Review
- Gene Therapy Models of Alzheimer's Disease and Other Dementias.Methods in molecular biology (Clifton, N.J.) · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The transactivation DNA-binding protein (TDP-43) pathology is associated with fronto-temporal lobar dementia (FTLD) with ubiquitinated inclusions and some cases of Alzheimer's disease (AD). Proteolytic fragments of β-amyloid precursor protein (βAPP) are detected in AD as well as the cerebrospinal fluid (CSF) from FTLD and Amyotrophic Lateral Sclerosis (ALS) patients, suggesting alteration in APP processing. Because of the overlap in TDP-43 pathology between FTLD and AD, we sought to determine whether there is a relationship between TDP-43 and APP metabolism. We generated gene transfer models using lentiviral delivery of human TDP-43 and Aβ(1-42) into the rat primary motor cortex and examined their role 2 weeks post-injection. Expression of TDP-43 and/or Aβ(1-42) increase pro-inflammatory markers, including Interleukin (IL)-6, tumor necrosis factor (TNF-α), glial neurofibrillary proteins (GFAP) and ionized calcium binding adaptor molecule 1 (IBA-1). Lentiviral Aβ(1-42) up-regulates endogenous TDP-43 and promotes its phosphorylation, aggregation and cleavage into 35 kDa fragments. Inversely, lentiviral TDP-43 expression increases the levels and activity of β-secretase (BACE), accelerating production of APP C-terminal fragments (C99) and Aβ(1-40). Here we show that TDP-43 up-regulates APP metabolism and suggest a mechanistic link between TDP-43 and BACE.
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