Local deposition of amyloid without systemic involvement is rather uncommon and has been found in many organs. A 67-year- old man was admitted to our hospital presenting with weight loss, fatigue and poor appetite. Blood work and bone marrow examination revealed megaloblastic anemia. Upper gastrointestinal endoscopy reveeled e purple polypoid wass lesion of 5mm eliameter in the paracardiac region. Histopathologic examination of the gastric biopsy showed the deposition of amyloid materials in the mucosa. The patient had no evidence suggesting systemic amyloidosis. We report a rare case of localized amyloidosis of the stomach. The clinical and pathological features of this rare condition and association with megaloblastic anemia are discussed.
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Apolipoprotein E4 (APOE4) is the strongest genetic risk factor for sporadic Alzheimer's disease (AD). Individuals with one copy of APOE4 exhibit greater amyloid-beta (Aβ) deposition compared to noncarriers, an effect that is even more pronounced in APOE4 homozygotes. Interestingly, APOE4 carriers not only show more AD pathology but also experience more rapid cognitive decline, particularly in episodic memory.
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January 2025
Normandie Univ, UNICAEN, INSERM, U1237, PhIND 'Physiopathology and Imaging of Neurological Disorders', Institut Blood and Brain @ Caen-Normandie, Cyceron, 14000 Caen, France.
Four important imaging biomarkers of Alzheimer's disease, namely grey matter atrophy, glucose hypometabolism and amyloid-β and tau deposition, follow stereotypical spatial distributions shaped by the brain network of structural and functional connections. In this case-control study, we combined several predictors reflecting various possible mechanisms of spreading through structural and functional pathways to predict the topography of the four biomarkers in amyloid-positive patients while controlling for the effect of spatial distance along the cortex. For each biomarker, we quantified the relative contribution of each predictor to the variance explained by the model.
View Article and Find Full Text PDFBiochemistry
January 2025
George and Anne Ryan Institute for Neuroscience, Department of Biomedical and Pharmacological Sciences, University of Rhode Island, Kingston, Rhode Island 02881, United States.
Cerebral vascular deposition of the amyloid-β (Aβ) peptide, a condition known as cerebral amyloid angiopathy (CAA), is associated with intracerebral hemorrhaging and contributes to disease progression in Alzheimer's disease (AD) and vascular cognitive impairment and dementia (VCID). Familial mutations at positions 22 and 23 within the Aβ peptide lead to early onset and severe CAA pathology. Here, we evaluate the effects of fibrillar Aβ peptides on the viability of primary-cultured human cerebral smooth muscle (HCSM) cells, which are the major site of amyloid deposition in cerebral blood vessel walls.
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January 2025
Department of Pharmaceutical Sciences, Maharshi Dayanand University, Rohtak, 124001, Haryana, India.
Insulin resistance is a condition characterized by the attenuated biological response in the presence of normal or elevated insulin level and therefore is characterized by the impaired sensitivity to insulin and impaired glucose disposal and utilization. Insulin resistance in brain/Brain insulin resistance (BIR) is accompanied by the various manifestations including alteration in glucose sensing by hypothalamic neurons, impaired sympathetic outflow in response to hypoglycemia, increased ROS production, impaired mitochondrial oxygen consumption in the brain, cognitive deficits and neuronal cell damage. It has been reported that the disrupted insulin signaling is accompanied by the reduced expression of insulin receptor (IR)/insulin receptor substrate 1 (IRS1)/PI3K/AKT and IGF-1 receptor (IGF-1R)/IRS2/PI3K pathways.
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January 2025
Department of Physiology, School of Medicine, Urmia University of Medical Sciences, Urmia, Iran; Neurophysiology Research Center, Cellular and Molecular Medicine Research Institute, Urmia University of Medical Sciences, Urmia, Iran. Electronic address:
Within the aging cortex, amyloid beta peptide (Aβ) is a crucial element of the senile plaques, a hallmark feature often observed in cases of Alzheimer's disease (AD). The UPR (unfolded protein response), a cellular mechanism for protein folding, is switched on by Aβ accumulation. Endoplasmic reticulum (ER) stress has been identified as playing a role in aging and the development of neurodegenerative diseases.
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