APPlications of amyloid-β precursor protein metabolites in macrocephaly . . . In this review, we highlight several lines of evidence supporting APP metabolites’ potential contribution to macrocephaly in ASD First, APP appears early in corticogenesis, placing APP in a prime position to accelerate growth in neurons and glia
Intraneuronal accumulation of amyloid-β peptides as the pathomechanism . . . Plasma levels of secreted APP were reported to be two or more times higher in children with severe autism and aggressive behavior than in children without autism and up to four times higher than in children with mild autism (Sokol et al , 2006; Ray et al , 2011)
How proteins interact may hold the key to future autism treatments That’s where looking at proteins comes in We wanted to look at the impact of mutations in around 100 of the genes that are associated with autism First, we wanted to know about the proteins these genes code for and what their activity is in a neurotypical situation
Intraneuronal accumulation of amyloid-β peptides as the . . . - PubMed Enhanced production and altered processing of APP, as well as accumulation of Aβ in the brain are also frequent consequences of traumatic brain injuries which result from self-injurious behaviors, another ASD co-morbidity
Dysfunctional proteins in neuropsychiatric disorders: From . . . Abnormal APP and sAPPα elevation may lead to the frequently observed excessive neuronal growth, connectivity, and seizure risk in ASD (Lahiri et al , 2013; Westmark et al , 2016) In contrast, adults with autism display reduced APP immunoreactivity (120 kDa isoform measured in the cerebellar vermis) (Fatemi et al , 2013)
CNTN4 Protein’s Role in Autism and Alzheimer’s Unveiled Researchers found that CNTN4, linked to autism, interacts with the Alzheimer-related protein APP, affecting neuron growth in the brain’s cortex This discovery highlights a co-dependent relationship essential for healthy brain development
Autism, Alzheimer disease, and fragile X: APP, FMRP, and mGluR5 are . . . The present review highlights an association between autism, Alzheimer disease (AD), and fragile X syndrome (FXS) We propose a conceptual framework involving the amyloid-β peptide (Aβ), Aβ precursor protein (APP), and fragile X mental retardation protein (FMRP) based on experimental evidence