ReviewBiological chemistry2008
Alternative pathways for production of beta-amyloid peptides of Alzheimer's disease.
Review in Biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 79 citations in OpenAlex.
- Modulation of Amyloid-β Aggregation by Surface Proteins from Pathogens Associated with Alzheimer's Disease.ACS chemical neuroscience · 2025Article
- Cathepsin B inhibition blocks amyloidogenesis in the mouse models of neurological lysosomal diseases MPS IIIC and sialidosis.Molecular therapy. Methods & clinical development · 2025Article
- A Mouse Model of Sporadic Alzheimer's Disease with Elements of Major Depression.Molecular neurobiology · 2025Article
- Cerebrospinal fluid shotgun proteomics identifies distinct proteomic patterns in cerebral amyloid angiopathy rodent models and human patients.Acta neuropathologica communications · 2024Article
- Varoglutamstat: Inhibiting Glutaminyl Cyclase as a Novel Target of Therapy in Early Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2024Article
- Cathepsin B Deficiency Improves Memory Deficits and Reduces Amyloid-β in hAβPP Mouse Models Representing the Major Sporadic Alzheimer's Disease Condition.Journal of Alzheimer's disease : JAD · 2023Review
- Cathepsin B Gene Knockout Improves Behavioral Deficits and Reduces Pathology in Models of Neurologic Disorders.Pharmacological reviews · 2022Review
- LC-MS Reveals Isomeric Inhibition of Proteolysis by Lysosomal Cathepsins.Analysis & sensing · 2022Article
- Revisiting APP secretases: an overview on the holistic effects of retinoic acid receptor stimulation in APP processing.Cellular and molecular life sciences : CMLS · 2022Review
- Opinion: The Potential Role of Amyloid Beta Peptides as Biomarkers of Subconcussion and Concussion.Frontiers in neurology · 2022Article
- Proteolytic α-Synuclein Cleavage in Health and Disease.International journal of molecular sciences · 2021Review
- Review
- Cathepsin B-associated Activation of Amyloidogenic Pathway in Murine Mucopolysaccharidosis Type I Brain Cortex.International journal of molecular sciences · 2020Article
- On the Role of Platelet-Generated Amyloid Beta Peptides in Certain Amyloidosis Health Complications.Frontiers in immunology · 2020Review
- Accumulation of Amyloid Beta (Aβ) Peptide on Blood Vessel Walls in the Damaged Brain after Transient Middle Cerebral Artery Occlusion.Biomolecules · 2019Article
- Platelet-generated amyloid beta peptides in Alzheimer's disease and glaucoma.Histology and histopathology · 2019Review
- Cysteine-type cathepsins promote the effector phase of acute cutaneous delayed-type hypersensitivity reactions.Theranostics · 2019Article
- Assessing the role ofJournal of oral microbiology · 2019Review
- Chia Seed Does Not Improve Cognitive Impairment in SAMP8 Mice Fed with High Fat Diet.Nutrients · 2018Article
- Ocular indicators of Alzheimer's: exploring disease in the retina.Acta neuropathologica · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 3 countries.
Funding
Abstract
This highlight article describes three Alzheimer's disease (AD) studies presented at the 5th General Meeting of the International Proteolysis Society that address enzymatic mechanisms for producing neurotoxic beta-amyloid (Abeta) peptides. One group described the poor kinetics of BACE 1 for cleaving the wild-type (WT) beta-secretase site of APP found in most AD patients. They showed that cathepsin D displays BACE 1-like specificity and cathepsin D is 280-fold more abundant in human brain than BACE 1. Nevertheless, as BACE 1 and cathepsin D show poor activity towards the WT beta-secretase site, they suggested continuing the search for additional beta-secretase(s). The second group reported cathepsin B as an alternative beta-secretase possessing excellent kinetic efficiency and specificity for the WT beta-secretase site. Significantly, inhibitors of cathepsin B improved memory, with reduced amyloid plaques and decreased Abeta(40/42) in brains of AD animal models expressing amyloid precursor protein containing the WT beta-secretase site. The third group addressed isoaspartate and pyroglutamate (pGlu) posttranslational modifications of Abeta. Results showed that cathepsin B, but not BACE 1, efficiently cleaves the WT beta-secretase isoaspartate site. Furthermore, cyclization of N-terminal Glu by glutaminyl cyclase generates highly amyloidogenic pGluAbeta(3-40/42). These presentations suggest cathepsin B and glutaminyl cyclase as potential new AD therapeutic targets.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.