ArticleBrain pathology (Zurich, Switzerland)2019
Lysosomal cathepsin D is upregulated in Alzheimer's disease neocortex and may be a marker for neurofibrillary degeneration.
Article in Brain pathology (Zurich, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 69 citations in OpenAlex.
- Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer's disease.Neural regeneration research · 2026Article
- The Central Role of Neuronal Cell Death in Alzheimer's Disease Pathobiology.Biomedicines · 2026Review
- Early microglial priming in Alzheimer's disease revealed by ME-seq.bioRxiv : the preprint server for biology · 2026Article
- Coordinated regional association of cathepsins and dipeptidyl peptidases with N-truncated Abeta42, Abeta40, and tau in Alzheimer's brain.Acta neuropathologica communications · 2025Article
- Capsaicin Alleviates Autophagy-Lysosomal Dysfunction via PPARA-Mediated V-ATPase Subunit ATP6V0E1 Signaling in 3xTg-AD Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cathepsins in Neurological Diseases.International journal of molecular sciences · 2025Review
- A Quantitative Systems Pharmacology Model That Describes Neurofilament Light Dynamics During Alzheimer's Disease Progression.CPT: pharmacometrics & systems pharmacology · 2025Article
- Multi-Omics Analysis of Hippocampus in Rats Administered Trimethyltin Chloride.Neurotoxicity research · 2025Article
- Targeted demethylation of cathepsin D via epigenome editing rescues pathology in Alzheimer's disease mouse model.Theranostics · 2025Article
- New preclinical biomarkers for prion diseases in the cerebrospinal fluid proteome revealed by mass spectrometry.The veterinary quarterly · 2024Article
- Broadening Horizons: Exploring the Cathepsin Family as Therapeutic Targets for Alzheimer's Disease.Aging and disease · 2024Review
- Multi-cohort cerebrospinal fluid proteomics identifies robust molecular signatures for asymptomatic and symptomatic Alzheimer's disease.Research square · 2024Article
- Spatial proteomics of hippocampal subfield-specific pathology in Alzheimer's disease and primary age-related tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Decreased DHA-containing phospholipids in the neocortex of dementia with Lewy bodies are associated with soluble AβBrain pathology (Zurich, Switzerland) · 2023Article
- Functional genomics identify causal variant underlying the protective CTSH locus for Alzheimer's disease.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Article
- Cathepsin B abundance, activity and microglial localisation in Alzheimer's disease-Down syndrome and early onset Alzheimer's disease; the role of elevated cystatin B.Acta neuropathologica communications · 2023Article
- Defective lysosomal acidification: a new prognostic marker and therapeutic target for neurodegenerative diseases.Translational neurodegeneration · 2023Review
- Progress in pH-Sensitive sensors: essential tools for organelle pH detection, spotlighting mitochondrion and diverse applications.Frontiers in pharmacology · 2023Review
- Age-related changes in tau and autophagy in human brain in the absence of neurodegeneration.PloS one · 2023Article
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Authors and funding
11 authors at 4 institutions in 3 countries.
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Abstract
Alzheimer's disease (AD) is characterized by accumulation of β-amyloid plaques (AP) and neurofibrillary tangles (NFT) in the cortex, together with synaptic loss and amyloid angiopathy. Perturbations in the brain lysosomal system, including the cathepsin family of proteases, have been implicated in AD where they may be involved in proteolytic clearance of misfolded and abnormally aggregated peptides. However, the status of cathepsin D (catD) is unclear in Lewy body dementia, the second most common form of neurodegenerative dementia after AD, and characterized by Lewy bodies (LB) containing aggregated α-synuclein. Furthermore, earlier reports of catD changes in AD have not been entirely consistent. We measured CatD immunoreactivities in the temporal (Brodmann area BA21) and parietal (BA40) cortices of well characterized AD brains as well as two clinical subtypes of Lewy body dementia, namely Parkinson disease dementia (PDD) and dementia with Lewy bodies (DLB), known to show varying degrees of concomitant AD pathology. Increased catD immunoreactivities in AD were found for both neocortical regions measured, where they also correlated with neuropathological NFT scores and phosphorylated pSer396 tau burden, and appeared to co-localize at least partly to NFT-containing neurons. In contrast, catD was increased only in BA40 in DLB and not at all in PDD, did not correlate with LB scores, and did not appreciably co-localize with α-synuclein inclusions. Our study suggests that catD upregulation may be an adaptive response to AD-related processes leading to neurofibrillary degeneration, but may not be directly associated with formation of α-synuclein inclusions in Lewy body dementia.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.