Relevant bibliographies by topics / Autism; Amyloid-beta protein

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Academic literature on the topic 'Autism; Amyloid-beta protein'

Author: Grafiati
Published: 2 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "Autism; Amyloid-beta protein"

1

Westmark, C. J., D. K. Sokol, B. Maloney, and D. K. Lahiri. "Novel roles of amyloid-beta precursor protein metabolites in fragile X syndrome and autism." Molecular Psychiatry 21, no. 10 (2016): 1333–41. http://dx.doi.org/10.1038/mp.2016.134.

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2

Bagyinszky, Eva, and Seong Soo A. An. "Haploinsufficiency and Alzheimer’s Disease: The Possible Pathogenic and Protective Genetic Factors." International Journal of Molecular Sciences 25, no. 22 (2024): 11959. http://dx.doi.org/10.3390/ijms252211959.

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Alzheimer’s disease (AD) is a complex neurodegenerative disorder influenced by various genetic factors. In addition to the well-established amyloid precursor protein (APP), Presenilin-1 (PSEN1), Presenilin-2 (PSEN2), and apolipoprotein E (APOE), several other genes such as Sortilin-related receptor 1 (SORL1), Phospholipid-transporting ATPase ABCA7 (ABCA7), Triggering Receptor Expressed on Myeloid Cells 2 (TREM2), Phosphatidylinositol-binding clathrin assembly protein (PICALM), and clusterin (CLU) were implicated. These genes contribute to neurodegeneration through both gain-of-function and los
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3

Fatemi, S., Timothy D. Folsom, Rachel E. Kneeland, Mahtab K. Yousefi, Stephanie B. Liesch, and Paul D. Thuras. "Impairment of fragile X mental retardation protein-metabotropic glutamate receptor 5 signaling and its downstream cognates ras-related C3 botulinum toxin substrate 1, amyloid beta A4 precursor protein, striatal-enriched protein tyrosine phosphatase, and homer 1, in autism: a postmortem study in cerebellar vermis and superior frontal cortex." Molecular Autism 4, no. 1 (2013): 21. http://dx.doi.org/10.1186/2040-2392-4-21.

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4

"Amyloid Plaque and Autism: Exploring the Potential Link and Implications for Treatment." Advances in Neurology and Neuroscience 6, no. 1 (2023). http://dx.doi.org/10.33140/an.06.01.05.

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Amyloid plaque, a protein aggregate typically associated with Alzheimer's disease, has also been observed in the brains of individuals with autism spectrum disorder (ASD). This has raised questions about a potential connection between amyloid plaque and ASD development. While the significance of this finding is not fully understood, several theories propose mechanisms by which amyloid plaque could contribute to the development of ASD. One theory suggests that amyloid-beta protein, the main component of amyloid plaque, could disrupt normal brain development and function by impairing synaptic fo
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5

SINGH, Vijendra K. "SERUM ANALYSIS OF AMYLOID BETA-PROTEIN 1-40 IN HEALTHY SUBJECTS, AUTISTIC CHILDREN AND ALZHEIMER’S PATIENTS." August 20, 2015. https://doi.org/10.5281/zenodo.28632.

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6

Sokol, Deborah K., та Debomoy K. Lahiri. "Neurodevelopmental disorders and microcephaly: how apoptosis, the cell cycle, tau and amyloid-β precursor protein APPly". Frontiers in Molecular Neuroscience 16 (22 вересня 2023). http://dx.doi.org/10.3389/fnmol.2023.1201723.

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Recent studies promote new interest in the intersectionality between autism spectrum disorder (ASD) and Alzheimer’s Disease. We have reported high levels of Amyloid-β Precursor Protein (APP) and secreted APP-alpha (sAPPa) and low levels of amyloid-beta (Aβ) peptides 1–40 and 1–42 (Aβ40, Aβ42) in plasma and brain tissue from children with ASD. A higher incidence of microcephaly (head circumference less than the 3rd percentile) associates with ASD compared to head size in individuals with typical development. The role of Aβ peptides as contributors to acquired microcephaly in ASD is proposed. Aβ
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7

Sah, Saroj, Ryan Keable, Grant Pfundstein, et al. "Deficiency in the neural cell adhesion molecule 2 (NCAM2) reduces axonal levels of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), affects axonal organization in the hippocampus, and leads to behavioral deficits." Cerebral Cortex, July 29, 2023. http://dx.doi.org/10.1093/cercor/bhad264.

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Abstract The neural cell adhesion molecule 2 (NCAM2) regulates axonal organization in the central nervous system via mechanisms that have remained poorly understood. We now show that NCAM2 increases axonal levels of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), a protease that regulates axonal guidance. In brains of NCAM2-deficient mice, BACE1 levels are reduced in hippocampal mossy fiber projections, and the infrapyramidal bundle of these projections is shortened. This abnormal axonal organization correlates with impaired short-term spatial memory and cognitive flexibility in
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8

Martínez‐Cañada, Pablo, Eduardo Perez‐Valero, Jesus Minguillon, Francisco Pelayo, Miguel A. López‐Gordo, and Christian Morillas. "Combining aperiodic 1/f slopes and brain simulation: An EEG/MEG proxy marker of excitation/inhibition imbalance in Alzheimer's disease." Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring 15, no. 3 (2023). http://dx.doi.org/10.1002/dad2.12477.

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AbstractINTRODUCTIONAccumulation and interaction of amyloid‐beta (Aβ) and tau proteins during progression of Alzheimer's disease (AD) are shown to tilt neuronal circuits away from balanced excitation/inhibition (E/I). Current available techniques for noninvasive interrogation of E/I in the intact human brain, for example, magnetic resonance spectroscopy (MRS), are highly restrictive (i.e., limited spatial extent), have low temporal and spatial resolution and suffer from the limited ability to distinguish accurately between different neurotransmitters complicating its interpretation. As such, t
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