Increased AβPP Processing in Familial Danish Dementia Patients
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Summary
It is found that the levels of several AβPP metabolites, including Aβ, are significantly increased in the brain sample derived from an FDD patient, suggesting that Familial Danish and Alzheimer's dementias share common pathogenic mechanisms.
- Type
- article
- Published
- 2011-11-18
- Cited by
- 40
- References
- 38
- Access
- Open access
- OpenAlex
- https://openalex.org/W1924662664
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:689339
Keywords
Danish, Dementia, Mutation, Amyloid precursor protein, Biology
References
- Generation of an Apoptotic Intracellular Peptide by γ-Secretase Cleavage of Alzheimer's Amyloid ß Protein Precursor
- Familial Danish Dementia: A Novel Form of Cerebral Amyloidosis Associated with Deposition of Both Amyloid‐Dan and Amyloid‐Beta
- When loss is gain: reduced presenilin proteolytic function leads to increased Aβ42/Aβ40
- The familial dementia BRI2 gene binds the Alzheimer gene amyloid-beta precursor protein and inhibits amyloid-beta production.
- Molecular biology and genetics of Alzheimer's disease.
- A transcriptionally [correction of transcriptively] active complex of APP with Fe65 and histone acetyltransferase Tip60.
- Modeling familial Danish dementia in mice supports the concept of the amyloid hypothesis of Alzheimer's disease
- Generation and Initial Characterization of FDD Knock In Mice
- Thirty years of Alzheimer's disease genetics: the implications of systematic meta-analyses
- Molecular biology and genetics of Alzheimer's disease
- Aph-1, Pen-2, and Nicastrin with Presenilin generate an active gamma-Secretase complex.
- Maturation of BRI2 generates a specific inhibitor that reduces APP processing at the plasma membrane and in endocytic vesicles
- Expression of BRI, the normal precursor of the amyloid protein of familial British dementia, in human brain
- N-APP binds DR6 to cause axon pruning and neuron death via distinct caspases
- Memory deficits due to Familial British Dementia BRI2 mutation are caused by loss of BRI2 function rather than amyloidosis
- BRI2 interacts with amyloid precursor protein (APP) and regulates amyloid beta (Abeta) production.
- Cerebral Amyloid Angiopathy and Parenchymal Amyloid Deposition in Transgenic Mice Expressing the Danish Mutant Form of Human BRI2
- Danish dementia mice suggest that loss of function and not the amyloid cascade causes synaptic plasticity and memory deficits
- Processing of beta-amyloid precursor-like protein-1 and -2 by gamma-secretase regulates transcription.
- BRI2 Inhibits Amyloid β-Peptide Precursor Protein Processing by Interfering with the Docking of Secretases to the Substrate
Cited by
- An Intracellular Threonine of Amyloid-β Precursor Protein Mediates Synaptic Plasticity Deficits and Memory Loss
- Molecular mechanisms of amyloid self-regulation
- Role of BRI2 in Dementia
- Lessons from a Rare Familial Dementia: Amyloid and Beyond
- Interaction of ApoE3 and ApoE4 isoforms with an ITM2b/BRI2 mutation linked to the Alzheimer disease-like Danish dementia: Effects on learning and memory
- Memory deficits of British Dementia knock-in mice are prevented by APP haploinsufficiency
- BRI2 ectodomain affects Aβ42 fibrillation and tau truncation in human neuroblastoma cells
- BRI2-BRICHOS is increased in human amyloid plaques in early stages of Alzheimer's disease.
- Proteomic Characterization of a Mouse Model of Familial Danish Dementia
- Accumulation of BRI2-BRICHOS ectodomain correlates with a decreased clearance of Aβ by insulin degrading enzyme (IDE) in Alzheimer's disease.
- The ITM2B (BRI2) gene is a target of BCL6 repression: Implications for lymphomas and neurodegenerative diseases
- Caspase-9 mediates synaptic plasticity and memory deficits of Danish dementia knock-in mice: caspase-9 inhibition provides therapeutic protection
- Inhibition of γ-secretase worsens memory deficits in a genetically congruous mouse model of Danish dementia
- BRI2 Interacts with BACE1 and Regulates Its Cellular Levels by Promoting its Degradation and Reducing Its mRNA Levels
- β- but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia
- The Familial British Dementia Mutation Promotes Formation of Neurotoxic Cystine Cross-linked Amyloid Bri (ABri) Oligomers*
- Deletion of the γ-secretase subunits Aph1B/C impairs memory and worsens the deficits of knock-in mice modeling the Alzheimer-like familial Danish dementia
- Identification of interacting protein partners of TOPORS in the retina
- A Greek Tragedy: The Growing Complexity of Alzheimer Amyloid Precursor Protein Proteolysis *
- BRICHOS interactions with amyloid proteins and implications for Alzheimer disease
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