Read by QxMD icon Read

Amyloid aging microglia

Elodie Martin, Céline Boucher, Bertrand Fontaine, Cécile Delarasse
Alzheimer's disease (AD) is a neurodegenerative disease characterized by formation of amyloid-β (Aβ) plaques, activated microglia, and neuronal cell death leading to progressive dementia. Recent data indicate that microglia and monocyte-derived macrophages (MDM) are key players in the initiation and progression of AD, yet their respective roles remain to be clarified. As AD occurs mostly in the elderly and aging impairs myeloid functions, we addressed the inflammatory profile of microglia and MDM during aging in TgAPP/PS1 and TgAPP/PS1dE9, two transgenic AD mouse models, compared to WT littermates...
October 8, 2016: Aging Cell
F Guerriero, C Sgarlata, M Francis, N Maurizi, A Faragli, S Perna, M Rondanelli, M Rollone, G Ricevuti
Due to an increasingly aging population, Alzheimer disease (AD) represents a crucial issue for the healthcare system because of its widespread prevalence and the burden of its care needs. Several hypotheses on AD pathogenesis have been proposed and current therapeutical strategies have shown limited effectiveness. In the last decade, more evidence has supported a role for neuroinflammation and immune system dysregulation in AD. It remains unclear whether astrocytes, microglia and immune cells influence disease onset, progression or both...
October 7, 2016: Aging Clinical and Experimental Research
Kathryn E Hopperton, Marc-Olivier Trépanier, Vanessa Giuliano, Richard P Bazinet
BACKGROUND: Neuroinflammation is a proposed mechanism by which Alzheimer's disease (AD) pathology potentiates neuronal death and cognitive decline. Consumption of omega-3 polyunsaturated fatty acids (PUFA) is associated with a decreased risk of AD in human observational studies and exerts protective effects on cognition and pathology in animal models. These fatty acids and molecules derived from them are known to have anti-inflammatory and pro-resolving properties, presenting a potential mechanism for these protective effects...
September 29, 2016: Journal of Neuroinflammation
Michelle Go, Jinghong Kou, Jeong-Eun Lim, Junling Yang, Ken-Ichiro Fukuchi
Microglia-mediated clearance of amyloid beta-protein (Aβ) via Toll-like receptor 4 (TLR4) signaling may play an important role in the pathogenesis of Alzheimer's disease (AD). However, as the disease progresses, activated microglia appear to become incapable of clearing Aβ deposits. Because repeated exposure to a TLR4 ligand leads to a diminished response of monocytes/macrophages to lipopolysaccharide (LPS) and because aggregated Aβ is a TLR4 ligand, we hypothesize that chronic exposure of microglia to Aβ deposits may induce a state of Toll-like receptor (TLR) signaling dysfunction, leading to decreased Aβ clearance and accelerated disease progression...
October 14, 2016: Biochemical and Biophysical Research Communications
Hyunjeong Liew, Yun-Mi Kim, Hee Soon Choi, Ah Ram Jang, David Churchill, Sang Hyung Lee, Yoo-Hun Suh
Neuregulin-1 (NRG-1) is a ligand of the epidermal growth factor receptor (erbB), and its interaction involves activation of the glutamatergic N-methyl-D-aspartate receptor, which increases the expression of the β2 subunit of the γ-aminobutyric acid receptor and subunits of the nicotinic acetylcholine receptor. In the dentate gyrus of 14-month-old Tg2576 mice, NRG-1 was strongly expressed compared with age-matched controls. The supernatant of oligomeric amyloid β peptide (Aβ42)-treated glial cells enhanced the Aβ42-induced cytotoxic effects, but the expression of Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand in microglial cells was not changed upon cytotoxic treatment...
August 15, 2016: CNS & Neurological Disorders Drug Targets
Ling Guo, Aras Rezvanian, Lokesh Kukreja, Ramez Hoveydai, Eileen H Bigio, M-Marsel Mesulam, Joseph El Khoury, Changiz Geula
Microglia are immune cells of the brain that display a range of functions. Most of our knowledge about microglia biology and function is based on cells from the rodent brain. Species variation in the complexity of the brain and differences in microglia response in the primate when compared with the rodent, require use of adult human microglia in studies of microglia biology. While methods exist for isolation of microglia from postmortem human brains, none allow culturing cells to high passage. Thus cells from the same case could not be used in parallel studies and multiple conditions...
October 4, 2016: Journal of Alzheimer's Disease: JAD
Zhen Wei, Xiao-Chun Chen, Yue Song, Xiao-Dong Pan, Xiao-Man Dai, Jing Zhang, Xiao-Li Cui, Xi-Lin Wu, Yuan-Gui Zhu
BACKGROUND: Amyloid β (Aβ) has been established as a key factor for the pathological changes in the brains of patients with Alzheimer's disease (AD), and cellular senescence is closely associated with aging and cognitive impairment. However, it remains blurred whether, in the AD brains, Aβ accelerates the neuronal senescence and whether this senescence, in turn, impairs the cognitive function. This study aimed to explore the expression of senescence-associated genes in the hippocampal tissue from young to aged 5XFAD mice and their age-matched wild type (WT) mice to determine whether senescent neurons are present in the transgenic AD mouse model...
August 5, 2016: Chinese Medical Journal
Risa Takamura, Naoto Watamura, Miyu Nikkuni, Toshio Ohshima
Alzheimer's disease (AD) is the most common neurodegenerative disorder characterized by cognitive impairment with neuronal loss. The number of patients suffering from AD has increased, but none of the present therapies stops the progressive symptoms in patients with AD. It has been reported that the activation of microglial cells induces harmful chronic inflammation, leading to neuronal death. Furthermore, the impairment of adult neurogenesis in the hippocampus has been observed earlier than amyloid plaque formation...
July 22, 2016: Journal of Neuroscience Research
Zhiping Mi, Willi Halfter, Eric E Abrahamson, William E Klunk, Chester A Mathis, Elliott J Mufson, Milos D Ikonomovic
Tenascin-C (TN-C) is an extracellular matrix glycoprotein linked to inflammatory processes in pathological conditions including Alzheimer disease (AD). We examined the distribution of TN-C immunoreactivity (ir) in relation to amyloid-β (Aβ) plaques and vascular Aβ deposits in autopsy brain tissues from 14 patients with clinical and neuropathological AD and 10 aged-matched controls with no cognitive impairment; 5 of the controls had Aβ plaques and 5 did not. TN-C ir was abundant in cortical white matter and subpial cerebral gray matter in all cases, whereas TN-C ir was weak in blood vessels...
September 2016: Journal of Neuropathology and Experimental Neurology
Thomas Liebmann, Nicolas Renier, Karima Bettayeb, Paul Greengard, Marc Tessier-Lavigne, Marc Flajolet
Amyloidosis is a major problem in over one hundred diseases, including Alzheimer's disease (AD). Using the iDISCO visualization method involving targeted molecular labeling, tissue clearing, and light-sheet microscopy, we studied plaque formation in the intact AD mouse brain at up to 27 months of age. We visualized amyloid plaques in 3D together with tau, microglia, and vasculature. Volume imaging coupled to automated detection and mapping enables precise and fast quantification of plaques within the entire intact mouse brain...
July 26, 2016: Cell Reports
Willem Kamphuis, Lieneke Kooijman, Sjoerd Schetters, Marie Orre, Elly M Hol
Amyloid plaques in Alzheimer's disease (AD) mice are surrounded by activated microglia. The functional role of microglia activation in AD is not well understood; both detrimental and beneficial effects on AD progression have been reported. Here we show that the population of activated microglia in the cortex of the APPswe/PS1dE9 mouse AD model is divided into a CD11c-positive and a CD11c-negative subpopulation. Cd11c transcript levels and number of CD11c-positive microglia increase sharply when plaques start to occur and both parameters continue to rise in parallel with the age-related increasing plaque load...
October 2016: Biochimica et Biophysica Acta
Santiago Solé-Domènech, Dana L Cruz, Estibaliz Capetillo-Zarate, Frederick R Maxfield
Microglia, the main phagocytes of the central nervous system (CNS), are involved in the surveillance and maintenance of nervous tissue. During normal tissue homeostasis, microglia migrates within the CNS, phagocytose dead cells and tissue debris, and modulate synapse pruning and spine formation via controlled phagocytosis. In the event of an invasion by a foreign body, microglia are able to phagocytose the invading pathogen and process it proteolytically for antigen presentation. Internalized substrates are incorporated and sorted within the endocytic pathway and thereafter transported via complex vesicular routes...
July 12, 2016: Ageing Research Reviews
Jong Kil Lee, Kai Wang, Min Hee Park, Namoh Kim, Ju Youn Lee, Hee Kyung Jin, In-San Kim, Byung-Heon Lee, Jae-Sung Bae
With the increasing worldwide incidence of Alzheimer's disease (AD), there is a critical need for the discovery of more effective diagnostic methods. However, development of diagnostic tools in AD has been hindered by obstacles such as the absence of exact biomarkers. Apoptosis caused by amyloid-β (Aβ) plays an important role in AD pathology; therefore, provides an attractive biological target for the diagnosis of AD. The present study aimed to evaluate the potential of small peptide, named ApoPep-1 (Apoptosis-targeting peptide-1) as a new apoptosis imaging agent in AD...
September 1, 2016: Brain Research
Wesley Chen, Edsel A Abud, Stephen T Yeung, Anita Lakatos, Trevor Nassi, Jane Wang, David Blum, Luc Buée, Wayne W Poon, Mathew Blurton-Jones
Alzheimer disease is characterized by the accumulation of β-amyloid (Aβ) plaques and tau-laden neurofibrillary tangles. Emerging studies suggest that in neurodegenerative diseases, aggregation of one protein species can promote other proteinopathies and that inflammation plays an important role in this process. To study the interplay between Aβ deposition, tau pathology, and microgliosis, we established a new AD transgenic mouse model by crossing 5xfAD mice with Thy-Tau22 transgenic mice. The resulting 'T5x' mice exhibit a greater than three-fold increase in misfolded and hyperphosphorylated tau and further substantiates the hypothesis that Aβ accelerates tau pathology...
2016: Acta Neuropathologica Communications
Hongxia Xing, Shuangxi Guo, Yi Zhang, Zhiyong Zheng, Haoliang Wang
Activated microglia are capable of facilitating amyloid-β (Aβ) accumulation via the release of inflammatory factors, thus resulting in the exacerbation of Alzheimer's disease (AD). MicroRNAs (miRs) participate in the activation of microglia, which is associated with AD. Insulin-like growth factor 1 (IGF1) is a neuroprotective, anti-inflammatory factor, which is able to accelerate clearance of Aβ peptides. The present study aimed to investigate the precise role of miR‑206 and IGF1 in lipopolysaccharide (LPS)‑induced microglial inflammation...
August 2016: Molecular Medicine Reports
Jacqueline Hofrichter, Markus Krohn, Toni Schumacher, Cathleen Lange, Bjöorn Feistel, Bernd Walbroel, Jens Pahnke
Nowadays, Alzheimer's disease is the most prevalent epiphenomenon of the aging population. Although soluble amyloid-β (Aβ) species (monomers, oligomers) are recognized triggers of the disease, no therapeutic approach is able to stop it. Herbal medicines are used to treat different diseases in many regions of the world. On the Balkan Peninsula, at the eastern Mediterranean Sea, and adjacent regions, Sideritis species are used as traditional medicine to prevent age-related problems in elderly. To evaluate this traditional knowledge in controlled experiments, we tested extracts of two commonly used Sideritis species, Sideritis euboea and Sideritis scardica, with regard to their effects on cognition in APP-transgenic and aged, non-transgenic C57Bl/6 mice...
May 31, 2016: Journal of Alzheimer's Disease: JAD
Anna Chiarini, Ubaldo Armato, Daisong Liu, Ilaria Dal Prà
In aged subjects, late-onset Alzheimer's disease (LOAD) starts in the lateral entorhinal allocortex where a failure of clearance mechanisms triggers an accumulation of neurotoxic amyloid-β42 oligomers (Aβ42-os). In neurons and astrocytes, Aβ42-os enhance the transcription of Aβ precursor protein (APP) and β-secretase/BACE1 genes. Thus, by acting together with γ-secretase, the surpluses of APP and BACE1 amplify the endogenous production of Aβ42-os which pile up, damage mitochondria, and are oversecreted...
2016: Frontiers in Physiology
Renata Novotny, Franziska Langer, Jasmin Mahler, Angelos Skodras, Andreas Vlachos, Bettina M Wegenast-Braun, Stephan A Kaeser, Jonas J Neher, Yvonne S Eisele, Marie J Pietrowski, K Peter R Nilsson, Thomas Deller, Matthias Staufenbiel, Bernd Heimrich, Mathias Jucker
UNLABELLED: The aggregation of amyloid-β peptide (Aβ) in brain is an early event and hallmark of Alzheimer's disease (AD). We combined the advantages of in vitro and in vivo approaches to study cerebral β-amyloidosis by establishing a long-term hippocampal slice culture (HSC) model. While no Aβ deposition was noted in untreated HSCs of postnatal Aβ precursor protein transgenic (APP tg) mice, Aβ deposition emerged in HSCs when cultures were treated once with brain extract from aged APP tg mice and the culture medium was continuously supplemented with synthetic Aβ...
May 4, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Miguel Ángel Ontiveros-Torres, María Luisa Labra-Barrios, Sofía Díaz-Cintra, Azucena Ruth Aguilar-Vázquez, Samadhi Moreno-Campuzano, Paola Flores-Rodríguez, Claudia Luna-Herrera, Raúl Mena, George Perry, Benjamín Florán-Garduño, José Luna-Muñoz, Juan Pedro Luna-Arias
Alzheimer's disease (AD) is a degenerative and irreversible disorder whose progressiveness is dependent on age. It is histopathologically characterized by the massive accumulation of insoluble forms of tau and amyloid-β (Aβ) asneurofibrillary tangles and neuritic plaques, respectively. Many studies have documented that these two polypeptides suffer several posttranslational modifications employing postmortem tissue sections from brains of patients with AD. In order to elucidate the molecular mechanisms underlying the posttranslational modifications of key players in this disease, including Aβ and tau, several transgenic mouse models have been developed...
March 22, 2016: Journal of Alzheimer's Disease: JAD
Makiko Ozawa, James K Chambers, Kazuyuki Uchida, Hiroyuki Nakayama
Canine cognitive dysfunction (CCD) is a syndrome that manifests itself in abnormal behaviors, such as disorientation and wandering. β-amyloid deposition in the brain, including the senile plaque (SP) and cerebral amyloid angiopathy (CAA), has been suggested as a major cause of the syndrome. However, the pathological significance of β-amyloid deposition in CCD dogs remains unclear. The present study was conducted using 16 dogs aged 10 years or older to clarify the relationship between the age-related histopathological lesions, such as β-amyloid deposition, in the brain and the clinical symptoms of CCD as evaluated in a questionnaire previously established in a large survey...
July 1, 2016: Journal of Veterinary Medical Science
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"