scholarly journals Up-Regulated Production and Activation of the Complement System in Alzheimer's Disease Brain

1999 ◽  
Vol 154 (3) ◽  
pp. 927-936 ◽  
Author(s):  
Koji Yasojima ◽  
Claudia Schwab ◽  
Edith G. McGeer ◽  
Patrick L. McGeer
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Complement System ◽  
The Complement System

Hunting for biomarkers: The complement system in Alzheimer's disease

Immunobiology ◽  
2012 ◽  
Vol 217 (11) ◽  
pp. 1175
Author(s):  
Svetlana Hakobyan ◽  
Mohammed Aiyaz ◽  
Alexandra Stretton ◽  
Martina Sattlecker ◽  
Richard Dobson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Complement System ◽  
The Complement System

scholarly journals Complement System in Alzheimer’s Disease

2021 ◽  
Vol 22 (24) ◽  
pp. 13647
Author(s):  
Akash Shah ◽  
Uday Kishore ◽  
Abhishek Shastri
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Complement System ◽  
Short Term Memory ◽  
Neurodegenerative Disorder ◽  
Membrane Attack Complex ◽  
Future Research ◽  
Chronic Neuroinflammation ◽  
The Central Nervous System ◽  
The Complement System

Alzheimer’s disease is a type of dementia characterized by problems with short-term memory, cognition, and difficulties with activities of daily living. It is a progressive, neurodegenerative disorder. The complement system is an ancient part of the innate immune system and comprises of more than thirty serum and membrane-bound proteins. This system has three different activating pathways and culminates into the formation of a membrane attack complex that ultimately causes target cell lysis (usually pathogens) The complement system is involved in several important functions in the central nervous system (CNS) that include neurogenesis, synaptic pruning, apoptosis, and neuronal plasticity. Here, we discuss how the complement system is involved in the effective functioning of CNS, while also contributing to chronic neuroinflammation leading to neurodegenerative disorders such as Alzheimer’s disease. We also discuss potential targets in the complement system for stopping its harmful effects via neuroinflammation and provide perspective for the direction of future research in this field.

scholarly journals Gamma subunit of complement component 8 is a neuroinflammation inhibitor

Brain ◽  
2020 ◽  
Author(s):  
Jong-Heon Kim ◽  
Ruqayya Afridi ◽  
Jin Han ◽  
Hyun-Gug Jung ◽  
Seung-Chan Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurological Diseases ◽  
Complement Component ◽  
Complement Components ◽  
Gamma Subunit ◽  
Small Proteins ◽  
Sphingosine 1 Phosphate ◽  
The Complement System

Abstract The complement system is part of the innate immune system that comprises several small proteins activated by sequential cleavages. The majority of these complement components, such as components 3a (C3a) and C5a, are chemotactic and pro-inflammatory. However, in this study, we revealed an inhibitory role of complement component 8 gamma (C8G) in neuroinflammation. In patients with Alzheimer's disease, who exhibit strong neuroinflammation, we found higher C8G levels in brain tissue, CSF, and plasma. Our novel findings also showed that the expression level of C8G increases in the inflamed mouse brain, and that C8G is mainly localized to brain astrocytes. Experiments using recombinant C8G protein and shRNA-mediated knockdown showed that C8G inhibits glial hyperactivation, neuroinflammation, and cognitive decline in acute and chronic animal models of Alzheimer’s disease. Additionally, we identified sphingosine-1-phosphate receptor 2 (S1PR2) as a novel interaction protein of C8G and demonstrated that astrocyte-derived C8G interacts with S1PR2 to antagonize the pro-inflammatory action of S1P in microglia. Taken together, our results reveal the previously unrecognized role of C8G as a neuroinflammation inhibitor. Our findings pave the way towards therapeutic containment of neuroinflammation in Alzheimer’s disease and related neurological diseases.

The interaction of complement system with abeta-binding liposomes: towards engineering of safer vesicles for the management of alzheimer's disease

2010 ◽  
Vol 150 ◽  
pp. 97-98 ◽  
Author(s):  
A.J. Andersen ◽  
S.H. Hashemi ◽  
G. Galimberti ◽  
F. Re ◽  
M. Masserini ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Complement System

scholarly journals Complement-dependent Proinflammatory Properties of the Alzheimer's Disease β-Peptide

1998 ◽  
Vol 188 (3) ◽  
pp. 431-438 ◽  
Author(s):  
Bonnie M. Bradt ◽  
William P. Kolb ◽  
Neil R. Cooper
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Complement System ◽  
Active Form ◽  
Membrane Attack Complex ◽  
Amyloid Peptide ◽  
Complement Pathway ◽  
Complement Components ◽  
Classical Complement Pathway ◽  
Neuronal Precursor Cells

Large numbers of neuritic plaques (NP), largely composed of a fibrillar insoluble form of the β-amyloid peptide (Aβ), are found in the hippocampus and neocortex of Alzheimer's disease (AD) patients in association with damaged neuronal processes, increased numbers of activated astrocytes and microglia, and several proteins including the components of the proinflammatory complement system. These studies address the hypothesis that the activated complement system mediates the cellular changes that surround fibrillar Aβ deposits in NP. We report that Aβ peptides directly and independently activate the alternative complement pathway as well as the classical complement pathway; trigger the formation of covalent, ester-linked complexes of Aβ with activation products of the third complement component (C3); generate the cytokine-like C5a complement-activation fragment; and mediate formation of the proinflammatory C5b-9 membrane attack complex, in functionally active form able to insert into and permeabilize the membrane of neuronal precursor cells. These findings provide inflammation-based mechanisms to account for the presence of complement components in NP in association with damaged neurons and increased numbers of activated glial cells, and they have potential implications for the therapy of AD.

Cognitive control constrains memory attributions

2019 ◽  
Vol 42 ◽  
Author(s):  
Colleen M. Kelley ◽  
Larry L. Jacoby
Keyword(s):  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Control

Abstract Cognitive control constrains retrieval processing and so restricts what comes to mind as input to the attribution system. We review evidence that older adults, patients with Alzheimer's disease, and people with traumatic brain injury exert less cognitive control during retrieval, and so are susceptible to memory misattributions in the form of dramatic levels of false remembering.

Formation of paired helical filaments in Alzheimer's disease

1984 ◽  
Vol 42 ◽  
pp. 302-303
Author(s):  
J. Metuzals ◽  
D. F. Clapin ◽  
V. Montpetit
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontal Lobe ◽  
Giant Axon ◽  
Paired Helical Filaments ◽  
Normal Brain ◽  
Protein Assemblies ◽  
Electron Microscopic ◽  
Helical Symmetry ◽  
Structural Levels

Information on the conformation of paired helical filaments (PHF) and the neurofilamentous (NF) network is essential for an understanding of the mechanisms involved in the formation of the primary lesions of Alzheimer's disease (AD): tangles and plaques. The structural and chemical relationships between the NF and the PHF have to be clarified in order to discover the etiological factors of this disease. We are investigating by stereo electron microscopic and biochemical techniques frontal lobe biopsies from patients with AD and squid giant axon preparations. The helical nature of the lesion in AD is related to pathological alterations of basic properties of the nervous system due to the helical symmetry that exists at all hierarchic structural levels in the normal brain. Because of this helical symmetry of NF protein assemblies and PHF, the employment of structure reconstruction techniques to determine the conformation, particularly the handedness of these structures, is most promising. Figs. 1-3 are frontal lobe biopsies.

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