41,108 results match your criteria amyloid pathology


A study on the interaction of the amyloid fibrils of α-synuclein and hen egg white lysozyme with biological membranes.

Biochim Biophys Acta Biomembr 2021 Sep 18:183776. Epub 2021 Sep 18.

Stanford Genome Technology Center, Stanford University, Palo Alto, CA, USA.

Alpha-synuclein (α-syn) aggregation and mitochondrial dysfunction are considered as two of the main factors associated with Parkinson's disease (PD). In the present investigation, the effectiveness of the amyloid fibrils obtained from α-syn with those of hen egg white lysozyme (HEWL), as disease-related and-unrelated proteins, to damage rat brain and rat liver mitochondria have been investigated. This was extended by looking at SH-SY5Y human neuroblastoma cells and erythrocytes, thereby investigating the significance of structural characteristics of amyloid fibrils related to their interactions with biomembranes obtained from various sources. Read More

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September 2021

Thiophene-Based Dual Modulators of Aβ and Tau Aggregation.

Chembiochem 2021 Sep 21. Epub 2021 Sep 21.

JNCASR: Jawaharlal Nehru Centre for Advanced Scientific Research, New Chemistry Unit, 560064, Bengaluru, INDIA.

Alzheimer's disease is characterized by the accumulation of amyloid beta (Aβ) and Tau aggregates in the brain, which induces various pathological events resulting in neurodegeneration. There have been continuous efforts to develop modulators of the Aβ and tau aggregation process to halt or modify the disease progression. A few small molecule-based inhibitors to target both Aβ and tau pathology are reported. Read More

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September 2021

Head-to-Head Comparison of 8 Plasma Amyloid-β 42/40 Assays in Alzheimer Disease.

JAMA Neurol 2021 Sep 20. Epub 2021 Sep 20.

Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.

Importance: Blood-based tests for brain amyloid-β (Aβ) pathology are needed for widespread implementation of Alzheimer disease (AD) biomarkers in clinical care and to facilitate patient screening and monitoring of treatment responses in clinical trials.

Objective: To compare the performance of plasma Aβ42/40 measured using 8 different Aβ assays when detecting abnormal brain Aβ status in patients with early AD.

Design, Setting, And Participants: This study included 182 cognitively unimpaired participants and 104 patients with mild cognitive impairment from the BioFINDER cohort who were enrolled at 3 different hospitals in Sweden and underwent Aβ positron emission tomography (PET) imaging and cerebrospinal fluid (CSF) and plasma collection from 2010 to 2014. Read More

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September 2021

Stereological Changes in Microvascular Parameters in Hippocampus of a Transgenic Rat Model of Alzheimer's Disease.

J Alzheimers Dis 2021 Sep 10. Epub 2021 Sep 10.

SRC Biosciences, Tampa, FL, USA.

Background: Microcirculatory factors play an important role in amyloid-β (Aβ)-related neuropathology in Alzheimer's disease (AD). Transgenic (Tg) rat models of mutant Aβ deposition can enhance our understanding of this microvascular pathology.

Objective: Here we report stereology-based quantification and comparisons (between- and within-group) of microvessel length and number and associated parameters in hippocampal subregions in Tg model of AD in Fischer 344 rats and non-Tg littermates. Read More

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September 2021

A Novel Approach to the Treatment and Prevention of Alzheimer's Disease Based on the Pathology and Microbiology.

Authors:
Herbert B Allen

J Alzheimers Dis 2021 Sep 14. Epub 2021 Sep 14.

Professor and Chair Emeritus, Drexel University College of Medicine, Department of Dermatology, Philadelphia, PA, USA.

Utilizing the pathology and microbiology found in tissue from patients with documented Alzheimer's disease (AD), the pathogenesis of this fateful disorder has been made clear. Borrelia burgdorferi and Treponema denticola spirochetes enter the brain, mostly via neuronal pathways and the entorhinal circulation. These organisms easily pass through the blood-brain barrier and have an affinity for neural tissue. Read More

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September 2021

Somatostatin-derived amyloidosis: a novel type of amyloidosis associated with well-differentiated somatostatin-producing neuroendocrine tumours.

Amyloid 2021 Sep 20:1-6. Epub 2021 Sep 20.

Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.

Objective: To report the clinicopathologic and proteomic characteristics of a novel form of amyloidosis derived from the precursor protein somatostatin.

Materials And Methods: Cases were identified by searching the Mayo Clinic amyloid liquid chromatography and tandem mass spectrometry (LC-MS/MS) typing database from 1 January 2008 to 1 September 2020 for specimens with the amyloid signature proteins and abundant somatostatin, in the absence of other amyloid precursor proteins. All available medical records and pathologic materials were examined. Read More

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September 2021

Amyloid-Beta Influences Memory Functional Connectivity During Memory Retrieval in Alzheimer's Disease.

Front Aging Neurosci 2021 1;13:721171. Epub 2021 Sep 1.

Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Amnesia in Alzheimer's disease (AD) appears early and could be caused by encoding deficiency, consolidation dysfunction, and/or impairment in the retrieval of stored memory information. The relationship between AD pathology biomarker β-amyloid and memory dysfunction is unclear. The memory task functional MRI and amyloid PET were simultaneously performed to investigate the relationship between memory performance, memory phase-related functional connectivity, and cortical β-amyloid deposition. Read More

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September 2021

Staging tau pathology with tau PET in Alzheimer's disease: a longitudinal study.

Transl Psychiatry 2021 Sep 18;11(1):483. Epub 2021 Sep 18.

Department of Neurology and Institute of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.

A biological research framework to define Alzheimer' disease with dichotomized biomarker measurement was proposed by National Institute on Aging-Alzheimer's Association (NIA-AA). However, it cannot characterize the hierarchy spreading pattern of tau pathology. To reflect in vivo tau progression using biomarker, we constructed a refined topographic F-AV-1451 tau PET staging scheme with longitudinal clinical validation. Read More

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September 2021

Associations between air pollution and biomarkers of Alzheimer's disease in cognitively unimpaired individuals.

Environ Int 2021 Sep 16;157:106864. Epub 2021 Sep 16.

Barcelonaβeta Brain Research Center (BBRC), Pasqual Maragall Foundation, Barcelona, Spain. Electronic address:

Background: Air quality contributes to incidence of Alzheimer's disease (AD) although the underlying neurobiological mechanisms are unclear. This study was aimed to examine the association between air pollution and concentrations of cerebrospinal fluid (CSF) AD biomarkers and amyloid-β (Aβ) deposition. Participants and methods The sample included 156 cognitively unimpaired adults aged 57 years (61 at biomarkers assessment) with increased risk of AD from the ALFA + Study. Read More

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September 2021

The effect of beta-amyloid and tau protein aggregations on magnetic susceptibility of anterior hippocampal laminae in Alzheimer's diseases.

Neuroimage 2021 Sep 16:118584. Epub 2021 Sep 16.

Key Laboratory for Biomedical Engineering of Ministry of Education, Department of Biomedical Engineering, College of Biomedical Engineering & Instrument Science, Zhejiang University, Hangzhou, China. Electronic address:

Previous studies have reported the changes of magnetic susceptibility induced by iron deposition in hippocampus of Alzheimer's disease (AD) brains. It is well-known that hippocampus is divided into well-defined laminar architecture, which, however, is difficult to be resolved with in-vivo MRI due to the limited imaging resolution. The present study aims to investigate layer-specific magnetic susceptibility in the hippocampus of AD patients using high-resolution ex-vivo MRI, and elucidate its relationship with beta amyloid (Aβ) and tau protein histology. Read More

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September 2021

Alternative platelet activation pathways and their role in neurodegenerative diseases.

Neurobiol Dis 2021 Sep 16;159:105512. Epub 2021 Sep 16.

Department of Pathology, Germans Trias i Pujol Research Institute (IGTP), Universitat Autònoma de Barcelona (UAB), 08916 Badalona, Barcelona, Spain. Electronic address:

Purpose Of The Review: The study of platelets in the context of neurodegenerative diseases is intensifying, and increasing evidence suggests that platelets may play an important role in the pathogenesis of neurodegenerative disorders. Therefore, we aim to provide a comprehensive overview of the role of platelets and their diverse activation pathways in the development of these diseases.

Recent Findings: Platelets participate in synaptic plasticity, learning, memory, and platelets activated by exercise promote neuronal differentiation in several brain regions. Read More

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September 2021

Differential involvement of insulin receptor substrate (IRS)-1 and IRS-2 in brain insulin signaling is associated with the effects on amyloid pathology in a mouse model of Alzheimer's disease.

Neurobiol Dis 2021 Sep 16:105510. Epub 2021 Sep 16.

Department of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. Electronic address:

Insulin signaling has been implicated in the metabolism as well as aging and longevity. Type 2 diabetes mellitus and its core pathology, insulin resistance, has also been implicated in the development of Alzheimer's disease (AD) and amyloid-β deposition in humans. By contrast, genetic ablation of the insulin/IGF-1 signaling (IIS) pathway components, e. Read More

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September 2021

Reversing pathology in a preclinical model of Alzheimer's disease by hacking cerebrovascular neoangiogenesis with advanced cancer therapeutics.

EBioMedicine 2021 Sep 14;71:103503. Epub 2021 Sep 14.

Department of Medical Genetics, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC V6T 1Z4, Canada; Michael Smith Laboratories, University of British Columbia, 2185 East Mall, Vancouver, BC V6T 1Z4, Canada; Centre for Blood Research, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC V6T 1Z4, Canada; The Djavad Mowafaghian Centre for Brain Health, University of British Columbia, 2215 Wesbrook Mall, Vancouver, BC V6T 1Z4, Canada; Department of Microbiology and Immunology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC V6T 1Z4, Canada; Department of Zoology, University of British Columbia, 6270 University Blvd., Vancouver, BC V6T 1Z4, Canada; The Vancouver Prostate Centre, Vancouver General Hospital, 2660 Oak Street, Vancouver, BC V6T 1Z4, Canada; Department of Urologic Sciences, University of British Columbia, Gordon & Leslie Diamond Health Care Centre, Level 6, 2775 Laurel Street, Vancouver, BC V5Z 1M9, Canada. Electronic address:

Background: Cognitive decline leading to dementia, accompanied by the accumulation of amyloid-beta (Aβ) in neuritic plaques together with the appearance of neurofibrillary tangles (NFT) composed of hyperphosphorylated tau protein (tau), are previously noted hallmarks of Alzheimer's disease (AD). We previously discovered hypervascularity in brain specimens from AD patients and consistent with this observation, we demonstrated that overexpression of Aβ drives cerebrovascular neoangiogenesis leading to hypervascularity and coincident tight-junction disruption and blood-brain barrier (BBB) leakiness in animal models of AD. We subsequently demonstrated that amyloid plaque burden and cerebrovascular pathogenesis subside when pro-angiogenic Aβ levels are reduced. Read More

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September 2021

Changes in the language system as amyloid-β accumulates.

Brain 2021 Sep 17. Epub 2021 Sep 17.

Laboratory for Cognitive Neurology, Department of Neurosciences, Leuven Brain Institute, KU Leuven, 3000 Leuven, Belgium.

Language dysfunction is common in Alzheimer's disease. There is increasing interest in the preclinical or asymptomatic phase of Alzheimer's disease. Here we examined in 35 cognitively intact older adults (age range 52-78 years at baseline, 17 male) in a longitudinal study design the association between accumulation of amyloid over a five to six year period, measured using PET, and functional changes in the language network measured over the same time period using task-related functional MRI. Read More

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September 2021

A critical appraisal of tau-targeting therapies for primary and secondary tauopathies.

Alzheimers Dement 2021 Sep 17. Epub 2021 Sep 17.

Department of Neuroscience, Istituto di Ricerche Farmacologiche "Mario Negri" IRCCS, Milan, Italy.

Introduction: Primary tauopathies are neurological disorders in which tau protein deposition is the predominant pathological feature. Alzheimer's disease is a secondary tauopathy with tau forming hyperphosphorylated insoluble aggregates. Tau pathology can propagate from region to region in the brain, while alterations in tau processing may impair tau physiological functions. Read More

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September 2021

A Novel Selective PKR Inhibitor Restores Cognitive Deficits and Neurodegeneration in Alzheimer Disease Experimental Models.

J Pharmacol Exp Ther 2021 Sep 16;378(3):262-275. Epub 2021 Jun 16.

Neurodegeneration Cluster, Rare and Neurologic Disease Research TA (M.L.-G., N.M., E.G., C.V., V.R., D.I., L.P., V.T.), Integrated Drug Discovery (P.B., J.-F.S., D.M.), and DMPK (A.K.), Sanofi R&D, Chilly-Mazarin, France

In Alzheimer disease (AD), the double-strand RNA-dependent kinase protein kinase R (PKR )/EIF2AK2 is activated in brain with increased phosphorylation of its substrate eukaryotic initiation factor 2 (eIF2). AD risk-promoting factors, such as ApoE4 allele or the accumulation of neurotoxic amyloid- oligomers (AOs), have been associated with activation of PKR-dependent signaling. Here, we report the discovery of a novel potent and selective PKR inhibitor (SAR439883) and demonstrate its neuroprotective pharmacological activity in AD experimental models. Read More

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September 2021

MFG-E8 (LACTADHERIN): a novel marker associated with cerebral amyloid angiopathy.

Acta Neuropathol Commun 2021 09 16;9(1):154. Epub 2021 Sep 16.

Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Hospital Universitari Vall d´Hebron, Universitat Autónoma de Barcelona, Pg. Vall d´Hebron, 119-129, 08035, Barcelona, Spain.

Brain accumulation of amyloid-beta (Aβ) is a crucial feature in Alzheimer´s disease (AD) and cerebral amyloid angiopathy (CAA), although the pathophysiological relationship between these diseases remains unclear. Numerous proteins are associated with Aβ deposited in parenchymal plaques and/or cerebral vessels. We hypothesized that the study of these proteins would increase our understanding of the overlap and biological differences between these two pathologies and may yield new diagnostic tools and specific therapeutic targets. Read More

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September 2021

Neuroinflammation in Alzheimer's disease: focus on NLRP1 and NLRP3 inflammasomes.

Curr Protein Pept Sci 2021 Sep 16. Epub 2021 Sep 16.

Instituto de Ensino e Pesquisa, Santa Casa BH, Belo Horizonte. Brazil.

Background: Alzheimer's disease (AD) is the main cause of dementia worldwide. The definitive diagnosis of AD is clinicopathological and based on the identification of cerebral deposition of amyloid β (Aβ) plaques and neurofibrillary tangles. However, the link between amyloid cascade and depositions of phosphorylated tau (p-tau) is still missing. Read More

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September 2021

Hypoxia/ischemia impairs CD33 (Siglec-3)/TREM2 signaling: Potential role in Alzheimer's pathogenesis.

Neurochem Int 2021 Sep 13;150:105186. Epub 2021 Sep 13.

School of Pharmacy, Faculty of Health Sciences, University of Eastern Finland, P.O. Box 1627, FI-70211, Kuopio, Finland.

Recent genetic and molecular studies have indicated that the innate immune system, especially microglia, have a crucial role in the accumulation of β-amyloid plaques in Alzheimer's disease (AD). In particular, the CD33 receptor, also called Siglec-3, inhibits the TREM2 receptor-induced phagocytic activity of microglia. CD33 receptors recognize the α2,3 and α2,6-linked sialic groups in tissue glycocalyx, especially sialylated gangliosides in human brain. Read More

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September 2021

Clinical and prognostic implications of capillary density in patients with cardiac light chain amyloidosis.

ESC Heart Fail 2021 Sep 16. Epub 2021 Sep 16.

Division of Cardiology, Department of Medicine, Heart Vascular Stroke Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro Gangnam-gu, Seoul, 06351, Republic of Korea.

Aims: Cardiac involvement is crucial factor determining outcomes of light chain (AL) amyloidosis. This study evaluated whether capillary density (CD) quantified from endomyocardial biopsy is associated with structural and functional parameters of amyloid heart. Also, we investigated whether capillary density improves the prognostic value of the current staging system in AL amyloidosis patients with cardiac involvement. Read More

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September 2021

Analysis of genes (TMEM106B, GRN, ABCC9, KCNMB2, and APOE) implicated in risk for LATE-NC and hippocampal sclerosis provides pathogenetic insights: a retrospective genetic association study.

Acta Neuropathol Commun 2021 09 15;9(1):152. Epub 2021 Sep 15.

Department of Biostatistics, College of Public Health, University of Kentucky, 201 Multidisciplinary Science Building, 725 Rose Street, Lexington, KY, 40536-0082, USA.

Limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) is the most prevalent subtype of TDP-43 proteinopathy, affecting up to 1/3rd of aged persons. LATE-NC often co-occurs with hippocampal sclerosis (HS) pathology. It is currently unknown why some individuals with LATE-NC develop HS while others do not, but genetics may play a role. Read More

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September 2021

Adult-onset CNS myelin sulfatide deficiency is sufficient to cause Alzheimer's disease-like neuroinflammation and cognitive impairment.

Mol Neurodegener 2021 09 15;16(1):64. Epub 2021 Sep 15.

Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, 4939 Charles Katz Drive, San Antonio, TX, 78229, USA.

Background: Human genetic association studies point to immune response and lipid metabolism, in addition to amyloid-beta (Aβ) and tau, as major pathways in Alzheimer's disease (AD) etiology. Accumulating evidence suggests that chronic neuroinflammation, mainly mediated by microglia and astrocytes, plays a causative role in neurodegeneration in AD. Our group and others have reported early and dramatic losses of brain sulfatide in AD cases and animal models that are mediated by ApoE in an isoform-dependent manner and accelerated by Aβ accumulation. Read More

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September 2021

Amyloid beta emerges from below the neck to disable the brain.

PLoS Biol 2021 Sep 15;19(9):e3001388. Epub 2021 Sep 15.

Buck Institute for Research on Aging, Novato, California, United States of America.

Accumulation of amyloid beta (Aβ) in the brain in Alzheimer disease drives pathophysiology. A study in this issue of PLOS Biology revealed that Aβ from the liver can promote brain pathology, supporting that peripheral Aβ can contribute to neurodegeneration. Read More

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September 2021

Implication of exosomes derived from cholesterol-accumulated astrocytes in Alzheimer's disease pathology.

Dis Model Mech 2021 Sep 15. Epub 2021 Sep 15.

Department of Medicine (Neurology), Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada.

Amyloid β (Aβ) peptides generated from the amyloid precursor protein (APP) play a critical role in the development of Alzheimer's disease (AD) pathology. Aβ-containing neuronal exosomes, which represent a novel form of intercellular communication, have been shown to influence function/vulnerability of neurons in AD. Unlike neurons, the significance of exosomes derived from astrocytes remains unclear. Read More

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September 2021

Adiponectin improves amyloid-β 31-35-induced circadian rhythm disorder in mice.

J Cell Mol Med 2021 Sep 15. Epub 2021 Sep 15.

Basic Medical Sciences Center, Shanxi Medical University, Taiyuan, China.

Adiponectin is an adipocyte-derived hormone, which is closely associated with the development of Alzheimer's disease (AD) and has potential preventive and therapeutic significance. In the present study, we explored the relationship between adiponectin and circadian rhythm disorder in AD, the effect of adiponectin on the abnormal expression of Bmal1 mRNA/protein induced by amyloid-β protein 31-35 (Aβ31-35), and the underlying mechanism of action. We found that adiponectin-knockout mice exhibited amyloid-β deposition, circadian rhythm disorders and abnormal expression of Bmal1. Read More

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September 2021

Suppression of a core metabolic enzyme dihydrolipoamide dehydrogenase () protects against amyloid beta toxicity in model of Alzheimer's disease.

Genes Dis 2021 Nov 20;8(6):849-866. Epub 2020 Aug 20.

School of Biological Sciences, The University of Queensland, Brisbane, QLD 4072, Australia.

A decrease in energy metabolism is associated with Alzheimer's disease (AD), but it is not known whether the observed decrease exacerbates or protects against the disease. The importance of energy metabolism in AD is reinforced by the observation that variants of dihydrolipoamide dehydrogenase (DLD), is genetically linked to late-onset AD. To determine whether DLD is a suitable therapeutic target, we suppressed the gene in that express human Aβ peptide in either muscles or neurons. Read More

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November 2021

Changes in cortical gene expression in the muscarinic M1 receptor knockout mouse: potential relevance to schizophrenia, Alzheimer's disease and cognition.

NPJ Schizophr 2021 Sep 14;7(1):44. Epub 2021 Sep 14.

Melbourne Veterinary School, Faculty of Veterinary and Agricultural Sciences, The University of Melbourne, Parkville, VIC, Australia.

Postmortem and neuroimaging studies show low levels of cortical muscarinic M1 receptors (CHRM1) in patients with schizophrenia which is significant because CHRM signalling has been shown to change levels of gene expression and cortical gene expression is altered in schizophrenia. We decided to identify CHRM1-mediated changes in cortical gene expression by measuring levels of RNA in the cortex of the Chrm1 mouse (n = 10), where there would be no signalling by that receptor, and in wild type mouse (n = 10) using the Affymetrix Mouse Exon 1.0 ST Array. Read More

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September 2021

Curcumin Complex Analogues as Near-Infrared Fluorescent Probes for Monitoring all Aβ Species in the Early Alzheimer's Disease Model.

ACS Chem Neurosci 2021 Sep 14. Epub 2021 Sep 14.

Shanghai Engineering Research Center of Organ Repair, School of Medicine School of Medicine, Shanghai University, Shanghai 200444, PR China.

Aggregation of amyloid β-peptide (Aβ) is closely related to the pathology of Alzheimer's disease (AD). In this pathology, the beginning stage is characterized by excessive accumulation of Aβ monomers due to imbalanced Aβ in the process of clearance. The Aβ peptide exists in many forms such as soluble and insoluble Aβ species, both of which coexist during the progression of AD and contribute to AD pathology. Read More

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September 2021

Citrullination of Amyloid-β Peptides in Alzheimer's Disease.

ACS Chem Neurosci 2021 Sep 14. Epub 2021 Sep 14.

Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Victoria 3010, Australia.

Protein citrullination (deimination of arginine residue) is a well-known biomarker of inflammation. Elevated protein citrullination has been shown to colocalize with extracellular amyloid plaques in AD patient brains. Amyloid-β (Aβ) peptides which aggregate and accumulate in the plaques of Alzheimer's disease (AD) have sequential N-terminal truncations and multiple post-translational modifications (PTM) such as isomerization, pyroglutamate formation, phosphorylation, nitration, and dityrosine cross-linking. Read More

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September 2021

Positron emission tomography imaging of serotonin degeneration and beta-amyloid deposition in late-life depression evaluated with multi-modal partial least squares.

Transl Psychiatry 2021 Sep 13;11(1):473. Epub 2021 Sep 13.

Banner Alzheimer's Institute, Phoenix, AZ, USA.

Depression in late-life is associated with increased risk of cognitive decline and development of all-cause dementia. The neurobiology of late-life depression (LLD) may involve both neurochemical and neurodegenerative mechanisms that are common to depression and dementia. Transgenic amyloid mouse models show evidence of early degeneration of monoamine systems. Read More

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September 2021