AA amyloidosis is characterized by amyloid deposition in systemic organs, but amyloid deposition in the central nervous system (CNS) or peripheral nervous system (PNS) is rare. In this study, AA amyloidosis was observed in 31 of 48 flamingos that died at a Japanese zoo. Almost all cases developed AA amyloidosis secondary to inflammatory diseases such as enteritis. Affected flamingos had AA amyloid deposition around blood vessels in periventricular white matter of the brain and in peripheral nerves. In addition, cerebral Aβ amyloidosis was observed in one of the 31 cases with AA amyloidosis. In conclusion, flamingos in the zoo commonly developed systemic amyloidosis with frequent amyloid deposition in the CNS and PNS, which seems to be a unique distribution in this avian species. Comparative pathological analyses in flamingos may help elucidate the pathogenesis of amyloid neuropathy.
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http://dx.doi.org/10.1177/0300985820939976 | DOI Listing |
Expert Opin Drug Saf
December 2024
Zhejiang Academy of Traditional Chinese Medicine, Tongde hospital of Zhejiang Province, Hangzhou, Zhejiang, China.
Background: Aducanumab, a monoclonal antibody, received approval for the treatment of Alzheimer's disease in 2021. However, it remains controversial over the security of this drug. In this study, aducanumab-related adverse events (AEs) were evaluated through data mining based on the FDA Adverse Event Reporting System (FAERS) database.
View Article and Find Full Text PDFJ Neurochem
January 2025
Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.
The triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane protein found in microglia within the brain, and its soluble form (sTREM2) has been shown to reduce amyloid deposition. Whether elevated TREM2-mediated microglial activity decreases the risk of Alzheimer's disease (AD) is unclear. The aim of this study was to assess whether high cerebrospinal fluid (CSF) levels of sTREM2 attenuate the risk of APOE ε4-associated amyloid pathology.
View Article and Find Full Text PDFBrain Res
December 2024
Federal University of São Paulo, Paulista School of Medicine, Department of Physiology, Laboratory of Neurophysiology, São Paulo, Brazil.
Alzheimer's disease is a progressive neurodegenerative disease affecting memory, language, and thinking with no curative treatment. Symptoms appear gradually, and pathological brain changes may occur twenty years before the physical and psychological signs, pointing to the urgent development of preventive interventions. Physical activity has been investigated as a preventive tool to defeat the main biological features of AD: pathological amyloid protein plaques, tau tangles, myelin degeneration, and iron deposits in the brain.
View Article and Find Full Text PDFImmunol Cell Biol
December 2024
Cellular and Molecular Medicine Research Institute, Cellular and Molecular Research Center, Urmia University of Medical Sciences, Urmia, Iran.
Neurodegeneration and neuroinflammation disorders are mainly the result of the deposition of various proteins, such as α-synuclein, amyloid-β and prions, which lead to the initiation and activation of inflammatory responses. Different chemokines are involved in the infiltration and movement of inflammatory leukocytes into the central nervous system (CNS) that express chemokine receptors. Dysregulation of several members of chemokines has been shown in the CNS, cerebrospinal fluid and peripheral blood of patients who have neurodegenerative disorders.
View Article and Find Full Text PDFBrain Commun
December 2024
Barcelonaβeta Brain Research Center (BBRC), Pasqual Maragall Foundation, Barcelona 08005, Spain.
CSF concentrations of β-amyloid 42 (Aβ42) and phosphorylated tau (p-tau) are well-established biomarkers of Alzheimer's disease and have been studied in relation to several neuropathological features both in patients and in cognitively unimpaired individuals. The CSF p-tau/Aβ42 ratio, a biomarker combining information from both pathophysiological processes, has emerged as a promising tool for monitoring disease progression, even at pre-clinical stages. Here, we studied the association between the CSF p-tau/Aβ42 ratio with downstream markers of pre-clinical Alzheimer's disease progression including brain structure, glucose metabolism, fibrillary Aβ deposition and cognitive performance in 234 cognitively unimpaired individuals, who underwent cognitive testing, a lumbar puncture, MRI, 18F-fluorodeoxyglucose and 18F-flutemetamol PET scanning.
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