Search
Search Results
-
Microbial infection promotes amyloid pathology in a mouse model of Alzheimer’s disease via modulating γ-secretase
Microbial infection as a type of environmental risk factors is considered to be associated with long-term increased risk of dementia, including...
-
CNTNAP2 intracellular domain (CICD) generated by γ-secretase cleavage improves autism-related behaviors
As the most prevalent neurodevelopmental disorders in children, autism spectrum disorders (ASD) are characterized by deficits in language...
-
Hypoxia Inducible Factor-1α binds and activates γ-secretase for Aβ production under hypoxia and cerebral hypoperfusion
Hypoxic-ischemic injury has been linked with increased risk for developing Alzheimer’s disease (AD). The underlying mechanism of this association is...
-
Molecular pathogenesis of desmoid tumor and the role of γ-secretase inhibition
Desmoid tumor (DT) is a rare, soft tissue neoplasm associated with an unpredictable clinical course. Although lacking metastatic potential, DT is...
-
Nirogacestat: First Approval
Nirogacestat (OGSIVEO™) is an oral, selective, reversible, small molecule γ-secretase inhibitor developed by SpringWorks Therapeutics, Inc....
-
Contactin-associated protein-like 2 (CNTNAP2) mutations impair the essential α-secretase cleavages, leading to autism-like phenotypes
Mutations in the Contactin-associated protein-like 2 ( CNTNAP2 ) gene are associated with autism spectrum disorder (ASD), and ectodomain shedding of...
-
Inhibition of NOTCH4 sensitizes FLT3/ITD acute myeloid leukemia cells to FLT3 tyrosine kinase inhibition
Internal tandem duplication mutations of FLT3 (FLT3/ITD) confer poor prognosis in AML. FLT3 tyrosine kinase inhibitors (TKIs) alone have limited and...
-
ADAMTS4 is involved in the production of the Alzheimer disease amyloid biomarker APP669-711
Amyloid-β (Aβ) deposition in the brain parenchyma is one of the pathological hallmarks of Alzheimer disease (AD). We have previously identified...
-
Switched Aβ43 generation in familial Alzheimer’s disease with presenilin 1 mutation
Presenilin (PS) with a genetic mutation generates abundant β-amyloid protein (Aβ) 43. Senile plaques are formed by Aβ43 in the cerebral parenchyma...
-
The anti-malarial drug chloroquine sensitizes oncogenic NOTCH1 driven human T-ALL to γ-secretase inhibition
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive cancer arising from T-cell progenitors. Although current treatments, including...
-
Inhibition of the m6A reader IGF2BP2 as a strategy against T-cell acute lymphoblastic leukemia
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignant leukemia with extremely limited treatment for relapsed patients....
-
Notch signaling is activated in knee-innervating dorsal root ganglia in experimental models of osteoarthritis joint pain
BackgroundWe aimed to explore activation of the Notch signaling pathway in knee-innervating lumbar dorsal root ganglia (DRG) in the course of...
-
Accumulation of amyloid precursor protein C-terminal fragments triggers mitochondrial structure, function, and mitophagy defects in Alzheimer’s disease models and human brains
Several lines of recent evidence indicate that the amyloid precursor protein-derived C-terminal fragments (APP-CTFs) could correspond to an...
-
Aβ profiles generated by Alzheimer’s disease causing PSEN1 variants determine the pathogenicity of the mutation and predict age at disease onset
Familial Alzheimer’s disease (FAD), caused by mutations in Presenilin (PSEN1/2) and Amyloid Precursor Protein (APP ) genes, is associated with an...
-
Targeting oncogenic Notch signaling with SERCA inhibitors
P-type ATPase inhibitors are among the most successful and widely prescribed therapeutics in modern pharmacology. Clinical transition has been safely...
-
Clarity on the blazing trail: clearing the way for amyloid-removing therapies for Alzheimer’s disease
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder with a complex pathogenesis. Senile plaques composed of the amyloid-β (Aβ)...
-
Amyloid β-based therapy for Alzheimer’s disease: challenges, successes and future
Amyloid β protein (Aβ) is the main component of neuritic plaques in Alzheimer’s disease (AD), and its accumulation has been considered as the...
-
Presenilin 1 phosphorylation regulates amyloid-β degradation by microglia
Amyloid-β peptide (Aβ) accumulation in the brain is a hallmark of Alzheimer’s Disease. An important mechanism of Aβ clearance in the brain is uptake...
-
Desmoid Tumors: Current Perspective and Treatment
Desmoid tumors are rare tumors with a tendency to infiltrate locally. The lack of a standard treatment approach makes choosing the most appropriate...
-
Akt signaling pathway: a potential therapy for Alzheimer’s disease through glycogen synthase kinase 3 beta inhibition
Alzheimer’s disease (AD) is a form of dementia marked by the accumulation of neuritic plaques and neurofibrillary tangles through the action of...
