• Optimal functioning of neuronal networks is critical to the complex cognitive processes of memory and executive function that deteriorate in Alzheimer's disease (AD). (nature.com)
  • Monocytes emigrate from bone marrow, can infiltrate into brain, differentiate into microglia and clear amyloid β (Aβ) from the brain of mouse models of Alzheimer's disease (AD). (nih.gov)
  • These results suggest that the slow progression and lack of full-fledged Alzheimer's disease pathology in the hippocampal neurons of APP Sw mice result from the genetic reprogramming of neural cells to cope with increased levels of Aβ. (jneurosci.org)
  • Alzheimer's disease (AD) is the most common cause of senile dementia. (jneurosci.org)
  • High choline intake during gestation and early postnatal development in rat and mouse models improves cognitive function in adulthood, prevents age-related memory decline, and protects the brain from the neuropathological changes associated with Alzheimer's disease (AD), and neurological damage associated with epilepsy, fetal alcohol syndrome, and inherited conditions such as Down and Rett syndromes. (mdpi.com)
  • Synaptic loss is intrinsically linked to Alzheimer's disease (AD) neuropathology and symptoms, but its direct impact on clinical symptoms remains elusive. (jneurosci.org)
  • SIGNIFICANCE STATEMENT Although the loss of several synaptic proteins has been described in Alzheimer's disease (AD), it remains unclear whether their reduction contributes to clinical symptoms. (jneurosci.org)
  • Alzheimer's disease (AD) is the most prevalent neurodegenerative disease placing a great burden on people living with it, careers and society. (sdbonline.org)
  • Alzheimer's disease (AD) is a debilitating brain disorder with staggering human and financial costs. (cam.ac.uk)
  • Apolipoprotein E4 (ApoE4) is the strongest known genetic risk variant for sporadic Alzheimer's disease (AD), but a comprehensive understanding of the cell-type-specific effects of APOE4 in the human brain in the presence and absence of AD pathology has yet to be achieved. (cam.ac.uk)
  • In a recent study published in the Journal of the Alzheimer's Association (AA) , researchers examined the effects of a low-carbohydrate-modified Mediterranean ketogenic diet (MMKD) on the gut microbiome and metabolome of patients at risk for Alzheimer's disease (AD). (news-medical.net)
  • Human middle temporal gyrus (MTG) is a vulnerable brain region in early Alzheimer's disease (AD), but little is known about the molecular mechanisms underlying this regional vulnerability. (unboundmedicine.com)
  • PICALM is one of the most significant susceptibility factors for Alzheimer's disease (AD). (qxmd.com)
  • Alzheimer's disease (AD) is the most common neurodegenerative disease, affecting millions of people worldwide and therefore it is fundamental to understand its underlying mechanisms. (alzheimer-europe.org)
  • BACKGROUND: Alzheimer's disease (AD) is a neurodegenerative disorder and the most common cause of dementia worldwide. (aau.dk)
  • This is particularly evident in disorders such as Alzheimer's disease (AD), where the use of metal chaperones (that transport metals), as opposed to chelators (which exclude metals from biological interactions), may prove to be the first truly disease modifying approach for this condition. (frontiersin.org)
  • The existing treatment options for mild to moderate Alzheimer's disease (AD) patients are limited to a small number of FDA-approved pharmaceuticals, including the acetylcholinesterase inhibitors (AChEIs) Tacrine, Donepezil, Galantamine, and Rivastigmine. (frontiersin.org)
  • In the case of Alzheimer's disease (AD), these magnetic nanoparticles have been identified attached to the characteristic brain plaques, which are mainly formed by fibrils of amyloid β peptide (Aβ). (ibecbarcelona.eu)
  • Aberrant modulations in histone post-translational have been suggested to occur in the brain as part of Alzheimer's disease (AD) pathology, consistent with the epigenetic blockade of neurodegeneration. (umd.edu)
  • Previous studies showed that nuclear 82-ChAT levels decrease with advancing age, and this is accelerated in Alzheimer's disease (AD). (uwo.ca)
  • He is particularly interested in studying the underlying mechanisms and pathways behind disease progression of neurological and cerebrovascular disorders that involve disruption of neural circuits, including Alzheimer's disease (AD) and stroke. (utoronto.ca)
  • Yesterday, the 7th International Conference on Alzheimer's and Parkinson's disease-AD/PD 2005 for short-drew to a close in beautiful Sorrento, Italy. (alzforum.org)
  • The Alzheimer's work has focused on the critical role played by Tau hyperphosphorylation in Alzheimer's disease pathology where it has become clear that a small number of kinases are responsible for the majority of the phosphorylation sites on tau in AD brain. (kcl.ac.uk)
  • The latest results from the Rush Memory and Aging Project, an ongoing community-based cohort study of chronic conditions of aging, showed that in part, the link between ELCE and better late-life cognitive health was tied to fewer pathologic changes related to Alzheimer's disease (AD), including deposition of beta amyloid and tau proteins. (medscape.com)
  • The association," he said, "is partly through upregulation of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B pathway that results in downregulation of glycogen synthase kinase-3-beta, which is implicated in the formation of neurofibrillary tangles, a hallmark of Alzheimer's disease pathology. (medscape.com)
  • BACKGROUND: Inducing brain ATP-binding cassette 1 (ABCA1) activity in Alzheimer's disease (AD) mouse models is associated with improvement in AD pathology. (cdc.gov)
  • We propose the hypothesis that small high-density lipoprotein (HDL) particles reduce the risk of Alzheimer's disease (AD) by virtue of their capacity to exchange lipids, affecting neuronal membrane composition and vascular and synaptic functions. (cdc.gov)
  • We provided the first evidence that age-related pathology in Alzheimer's disease initiates with aberrant accumulation and aggregation of β-amyloid peptides within vulnerable neurons, in particular their neurite terminals (Takahashi RH et al. (lu.se)
  • Our group focuses on the pathophysiological mechanisms by which synapses are sites of early dysfunction and damage in the most common neurodegenerative disease causing dementia, Alzheimer's disease (AD). (lu.se)
  • Our research focuses on identifying new early mechanisms and biomarkers associated with Alzheimer's disease (AD) and thereby improve the development of new treatments and diagnostic tools. (lu.se)
  • It is well-established that innate immunity plays a significant role in responding to and influencing the progression of Alzheimer's disease (AD) (Heneka et al. (lu.se)
  • In a study of 744 autopsies from older adults without a clinical diagnosis of PD, nearly a third showed evidence of post-mortem Lewy bodies and/or substantia nigra neurodegeneration, the defining pathologies of PD, and these changes were associated with parkinsonian motor signs proximate to death (Buchman et al. (bcm.edu)
  • This study makes increasingly clear that there is a critical need for more studies of this kind to understand how perturbations in tau expression levels or tau pathologies are linked to axonal transport failure and tau-mediated neurodegeneration in Alzheimer disease (AD) and related tauopathies. (alzforum.org)
  • At the same time, a substantial amount of data has come more recently from studies of non-AD tauopathies, and it has shown that tau pathology is the critical underlying abnormality that links AD and these disorders to a shared mechanism of neurodegeneration. (alzforum.org)
  • Most elements of this tau-mediated neurodegeneration hypothesis in AD and related tauopathies were demonstrated to occur in experimental animals, when Ishihara et al. (alzforum.org)
  • Our work supports previous findings, suggesting that the KL-VSHET+ on an APOE ε4 genotype background may modulate Aβ and tau pathology, thereby lowering the intensity of neurodegeneration and incidence of cognitive decline in older controls susceptible to AD. (lu.se)
  • Here we use cellular and animal models as well as human biospecimens to show that AD-related stressors mediate global disturbances in dynamic intra- and inter-neuronal networks through pathologic rewiring of the chaperome system into epichaperomes. (nature.com)
  • These result in imbalances in the connectivity of neuronal circuitry, and also negatively impact the intracellular connectivity of neuronal proteins and protein pathways, contributing to cognitive decline associated with AD 6 . (nature.com)
  • AD is associated with β-amyloid (Aβ) plaques, neurofibrillary tangles, and large-scale neuronal cell loss. (jneurosci.org)
  • Our results may contribute to the understanding of the complex architecture and neuronal and glial response to AD pathology of this vulnerable brain region. (unboundmedicine.com)
  • Although the neuropathologies involved in AD are well-described, the effect of those pathologies on neuronal function are poorly understood. (alzheimer-europe.org)
  • Levels of enzymes involved in processing of APP were examined in human SH-SY5Y neuroblastoma cells and in primary neuronal cultures prepared from cerebral cortex of embryonic APP/PS1 double transgenic mice that serve as a model of AD. (uwo.ca)
  • The overall goal for the three years of our grant support has been to develop viable candidate drugs to reduce the known pathologies of Alzheimer Disease (AD). (ca.gov)
  • Two genetic variants in strong linkage disequilibrium (rs9536314 and rs9527025) in the Klotho (KL) gene, encoding a transmembrane protein, implicated in longevity and associated with brain resilience during normal aging, were recently shown to be associated with Alzheimer disease (AD) risk in cognitively normal participants who are APOE ε4 carriers. (lu.se)
  • Using a transgenic mouse model of AD that overexpresses human amyloid-beta (a-beta), we will study the effects of a-beta accumulation on neocortical synaptic function and receptive field organization using in vivo intracellular recording and in vivo 2-photon laser-scanning microscopy (2PLSM). (alzheimer-europe.org)
  • 10 Department of Paediatrics, Department of Pathology (Neuropathology) and Department of Clinical Neurosciences, University of Calgary Faculty of Medicine, Alberta Children's Hospital Research Institute, Calgary, Alberta, Canada. (nih.gov)
  • The presence of these cells in the brain of non-irradiated APP(Swe)/PS1/CCR2⁻/⁻ mice supports the concept that they can be used as gene vehicles for AD. (nih.gov)
  • Tg2576 mice overexpress a mutant form of human amyloid precursor protein with the Swedish mutation (APP Sw ), resulting in high β-amyloid (Aβ) levels in the brain. (jneurosci.org)
  • These mice, therefore, may not be a good model of the complete pathologic process of AD but rather may be an excellent model for understanding how the brain can adapt to and survive high levels of Aβ. (jneurosci.org)
  • The results of this study in human brain samples and in transgenic mice are consistent with the hypothesis that Shank3 deficiency makes a key contribution to cognitive impairment in AD. (jneurosci.org)
  • The results of this study in human samples show lower levels of SHANK3a in AD brain, correlating with cognitive decline. (jneurosci.org)
  • Therefore, treatment aiming at preserving Shank3 in the aging brain may be beneficial to prevent AD. (jneurosci.org)
  • My lab uses a multi-pronged approach to delineating how cellular, molecular and brain circuit dysfunctions contribute to AD. (cam.ac.uk)
  • Strikingly, the discovery of the gut-brain axis (GBA) has led to the exploration of an altered gut microbiome in AD. (news-medical.net)
  • Bile acids are responsible for cholesterol elimination in the brain, accumulation of which could lead to hepatic encephalopathy, a liver disease that increases the risk of developing AD. (news-medical.net)
  • Anti-malaria drug artesunate prevents development of amyloid-β pathology in mice by upregulating PICALM at the blood-brain barrier. (qxmd.com)
  • In humans and mice, PICALM is highly expressed in brain endothelium. (qxmd.com)
  • Its loss from brain endothelium in mice diminishes Aβ clearance at the BBB, which worsens Aβ pathology, but is reversible by endothelial PICALM re-expression. (qxmd.com)
  • We studied PICALM expression at the BBB, Aβ pathology and clearance from brain to blood, cerebral blood flow (CBF) responses, BBB integrity and behavior. (qxmd.com)
  • Biogenic magnetite (Fe3O4) has been identified in human brain tissue. (ibecbarcelona.eu)
  • However, abnormal concentration of magnetite nanoparticles in the brain has been observed in different neurodegenerative pathologies. (ibecbarcelona.eu)
  • This dissertation details the development and optimization of unique protein standards for quantification, called quantification concatamers, for the absolute quantification of histone deacetylase isoforms in human frontal cortex with AD, human neural retina with AD and age-related macular degeneration, and whole brain hemisphere of a 5XFAD mouse model of AD. (umd.edu)
  • In addition to measuring isoforms of histone-modifying enzymes, measurements of post-translational modifications on histones were also obtained for whole hemispheres of brain from 5XFAD mice and frontal cortex from human donors affected with AD. (umd.edu)
  • He aims to develop novel computational, machine learning and imaging tools for interrogating brain circuits across resolution scales and modelling brain pathology. (utoronto.ca)
  • 2000). Following this work, we were the 1st group to report on the physical association between altered AD-linked Aβ peptides and synapses in the brain, showing that Aβ preferentially accumulates and associates with subcellular pathology within synapses in AD (Takahashi et al. (lu.se)
  • 2009). Remarkably, reduced synaptic activity in vivo in the brain (using either the whisker - barrel cortex system or treatment with benzodiazepine) reduced amyloid plaques but elevated intraneuronal Aβ and damaged synapses, providing experimental evidence for a disconnect between amyloid plaques and Aβ-mediated synapse damage in AD (Tampellini et al. (lu.se)
  • Our strategy is to investigate the effect of AD risk factors like stress, inflammation, metabolic changes, and amyloidogenesis, on different types of brain cells including pericytes, astrocytes, neurons, and NG2 cells. (lu.se)
  • Understand the role of amyloid peptides (including amyloid-beta, IAPP, TDP-43) in blood-brain barrier (BBB) alterations and how it affects the progression of AD. (lu.se)
  • We aim to fulfil Multiparks goals by exploring novel AD mechanisms and investigating how aggregated amyloid peptides affect brain function and cell integrity. (lu.se)
  • Our work also spans from human brain tissue and cohort studies to in vitro and animal studies which is line with Multiparks translational initiative. (lu.se)
  • Dr. Goubran's research focus includes multi-parametric and morphological analysis of the hippocampus and its subregions in AD. (utoronto.ca)
  • report elegant studies of axonal transport in vivo using tau transgenic and tau knockout mice that overexpress human tau isoforms or completely lack tau expression, respectively. (alzforum.org)
  • He is interested in studying human hippocampal circuit remodelling and developing imaging approaches to help predict hippocampal subregion pathology from in vivo imaging. (utoronto.ca)
  • Artesunate increases PICALM levels and Aβ clearance at the BBB which prevents development of Aβ pathology and functional deficits in mice and holds potential for translation to human AD. (qxmd.com)
  • The impact of these biomarkers in early-onset AD (EOAD) is unclear and the novel plasma biomarker, p-tau231, has not been studied in this population. (indianactsi.org)
  • This study highlights the importance of plasma biomarkers for AD diagnosis and disease monitoring. (indianactsi.org)
  • Besides estrogen receptor, progesterone receptor and human epidermal growth factor receptor 2, novel biomarkers have shown their prognostic and predictive values, complicating our understanding towards to the heterogeneity of such cancers. (jcancer.org)
  • This approach has revealed several new mechanisms and biomarkers associated with AD, including alteration of glycogen metabolism, the toxicity of various amyloid peptides aggregation forms, and secretion of a variety of pathology-specific molecules. (lu.se)
  • The major human G types are G1, G2, G3, and P type for 8 RAV isolates, even though their VP7 and G4, and G9, which, when combined with the P types P[8], VP4 genes were successfully amplifi ed by RT-PCR. (cdc.gov)
  • In addition to the potential for fundamental biological insights, functional dissection of susceptibility genes will be essential to realize the full promise of human genetics for clinical applications. (bcm.edu)
  • To better understand the molecular changes associated with AD, genome-wide association studies (GWAS) have identified hundreds of candidate genes linked to the disease, like the receptor tyrosine kinase EphA1. (sdbonline.org)
  • However, demonstration of whether and how these genes cause pathology is largely lacking. (sdbonline.org)
  • This presents a starting point for studies into the underlying mechanisms of AD including interactions with other AD-associated genes, like Rho1, Ankyrin, Tau and APP with the potential to identify new targets for treatment. (sdbonline.org)
  • We identify unique marker genes for cortical layers and the white matter, and layer-specific differentially expressed genes (DEGs) in human AD compared to CT. (unboundmedicine.com)
  • The co-expression patterns of hub genes and enriched pathways in the presence of AD pathology indicate an important role of cell-cell-communications among microglia, oligodendrocytes, astrocytes, and neurons, which may contribute to the cellular and regional vulnerability in early AD. (unboundmedicine.com)
  • As a result of the rapid advances in genetics technology and the Human Genome Project, most of the estimated 100,000 genes in humans will be identified by the year 2005 (1). (cdc.gov)
  • From the cover: Manganese and rotenone-induced oxidative stress signatures differ in iPSC-derived human dopamine neurons. (purdue.edu)
  • Via interaction network mapping, significant proteins could be annotated to specific pathways of mitochondrial function (oxidative phosphorylation and TCA cycle), metabolic pathways, AD pathway and synaptic functions (long term potentiation). (aau.dk)
  • the majority of which target one or both of the primary aggregating proteins implicated in the pathogenesis of AD. (frontiersin.org)
  • These studies have important implications for AD pathology and broaden our understanding of the function of 82-ChAT proteins. (uwo.ca)
  • We recently reported the first single-nucleus transcriptomic analysis of the prefrontal cortex to accurately map the cell types and molecular pathways impacted by AD. (cam.ac.uk)
  • The purpose of this mini-review is to highlight the emerging notion that metal chaperones, such as PBT2 (Prana Biotechnology), modulate a variety of critical pathways affecting key aspects of the AD cascade to provide a more "holistic" approach to the treatment of this disease. (frontiersin.org)
  • Proteome analysis of human primary monocytes was used to determine the immunological pathways activated by these adjuvants. (bvsalud.org)
  • We aim to distinguish and understand different pathways that fuel AD progression in humans. (lu.se)
  • We thus sought to determine whether a SHANK3 deficiency could contribute to the emergence or worsening of AD symptoms and neuropathology. (jneurosci.org)
  • We observed synergistic deleterious effects of Shank3a deficiency and AD neuropathology on object recognition memory at 9, 12, and 18 months of age and on anxious behavior at 9 and 12 months of age in hemizygous Shank3 Δex4-9 -3xTg-AD mice. (jneurosci.org)
  • Data gathered in a novel transgenic mouse suggest that Shank3a deficiency synergizes with AD neuropathology to induce cognitive impairment, consistent with a causal role in AD. (jneurosci.org)
  • Our work took a different direction from the mainstream of AD research that focused on extracellular β-amyloid (Aβ) peptides with our discovery of the accumulation of Aβ within AD vulnerable neurons of human brains (Gouras et al. (lu.se)
  • 2010). We were also the first group to use primary neurons from AD transgenic mice to model Aβ accumulation in culture (Takahashi et al. (lu.se)
  • This adds preliminary human data to an emerging body of animal data suggesting that tau pathogenesis occurs downstream of amyloid pathology and that amyloid removal can hold its early stages at bay. (alzforum.org)
  • To further probe the role of SHANK3 in AD, we crossed male and female 3xTg-AD mice modelling Aβ and tau pathologies with Shank3a -deficient mice (Shank3 Δex4-9 ). (jneurosci.org)
  • However, Shank3a deficiency increased the levels of soluble Aβ 42 and human tau at 18 months of age compared with 3xTg-AD mice with normal Shank3 expression. (jneurosci.org)
  • While genomic studies increasingly identify genetic risk alleles that correlate with AD, there is still no clear picture of the underlying molecular and cellular mechanisms involved. (cam.ac.uk)
  • Despite decades of investigation, the etiology of AD is not fully understood, although emerging evidence suggest that chronic environmental and psychological stress plays a role in the mechanisms and contributes to the risk of developing AD. (aau.dk)
  • Measurements and structural mechanisms were consistent with the global decrease in gene expression observed in AD, which supports the data. (umd.edu)
  • He also noted that the mechanisms underlying the association between ELCE and cognitive decline have not been studied in humans before. (medscape.com)
  • 2006). Moreover, we carried out studies on the cellular mechanisms whereby β-amyloid antibodies can reduce Aβ peptides and protect synapses in cell models of AD, providing a biological mechanism for a leading therapeutic direction for AD: Aβ immunotherapy (Tampellini et al. (lu.se)
  • Most significantly, the 8c mice overexpress human tau isoforms but do not develop neurofibrillary tau pathology, as do our T44 transgenic mice (4,5,14). (alzforum.org)
  • The purpose of this study was to investigate the effects of the ABCA1 agonist peptide CS-6253 on amyloid- peptides (A) and lipoproteins in plasma and cerebrospinal fluid (CSF) of cynomolgus monkeys, a species with amyloid and lipoprotein metabolism similar to humans. (cdc.gov)
  • However, it is not forthright to identify metabolites associated with AD because its metabolic signatures vary with gender and apolipoprotein E (APOE) genotype. (news-medical.net)
  • Finally, gene therapy using a lentivirus-expressing CCR2 transgene in BMCs prevented cognitive decline in this mouse model of AD. (nih.gov)
  • We first found a 30%-50% postmortem loss of SHANK3a associated with cognitive decline in the parietal cortex of individuals with AD. (jneurosci.org)
  • Additionally, triglycerides are implicated with mild cognitive impairment (MCI) and the onset of AD. (news-medical.net)
  • Pathologic change related to AD attenuated the association between ELCE and cognitive decline, suggesting that part of the association was independent of AD pathologic changes. (medscape.com)
  • The investigators found that 80% of the association between ELCE and cognitive decline was direct and 20% indirect as indicated by AD pathology scores. (medscape.com)
  • Through a better knowledge of how neural development normally occurs and how neurodegenerative pathologies develop we hope to provide information to aid neural regrowth and combat neural disease and injury. (kcl.ac.uk)
  • Auditory neuropathy/auditory dyssynchrony (AN/AD) is a condition that affects the neural processing of auditory stimuli. (medscape.com)
  • The CNT/F represent a good model as they are known to induce cytotoxicity, inflammation, pathology, and genotoxicity. (cdc.gov)
  • Humans understand that both these views are real, even if in order to be communicated they need different methods. (cia.gov)
  • PICALM endothelial levels are reduced in AD brains. (qxmd.com)
  • To identify a drug that could increase PICALM expression, we screened a library of 2007 FDA-approved drugs in HEK293t cells expressing luciferase driven by a human PICALM promoter, followed by a secondary mRNA screen in human Eahy926 endothelial cell line. (qxmd.com)
  • 2017. Fourth national report on human exposure to environmental chemicals. (cdc.gov)
  • 2010). In addition, we provided novel evidence indicating that Aβ secretion is reduced with AD (Tampellini et al. (lu.se)
  • This first installment of our hot-off-the-podium dispatches summarizes the status of AD immunotherapy research. (alzforum.org)
  • A particular emphasis in our group then turned to better understanding how synaptic activity modulates the pathophysiology of synapse damage in models of AD. (lu.se)
  • Acute toxicity, inflammation, inflammasome signaling, and phagocytic activity were evaluated in the differentiated human monocyte cell line, THP-1, at 0-60 microg/ml. (cdc.gov)
  • Disease progression was exacerbated in APP(Swe)/PS1 mice (transgenic mice expressing a chimeric amyloid precursor protein [APPSwe] and human presenilin 1 [PS1]) harboring CCR2-deficient BMCs. (nih.gov)
  • Utilising fly genetics, this study generated the first Drosophila model of human wild-type and P460L mutant EphA1 and tested the effects of Eph /ephrin signalling on AD-relevant behaviour and neurophysiology. (sdbonline.org)
  • For instance, familial AD is linked to mutations in the amyloid precursor protein (APP), presenilin 1, and presenilin 2, all of which lead to increased levels of Aβ. (jneurosci.org)
  • American Cancer Society, American Society for Colposcopy and Cervical Pathology, and American Society for Clinical Pathology screening guidelines for the prevention and early detection of cervical cancer. (aafp.org)
  • however, this approach is potentially limited by etiologic heterogeneity amongst patients and the presence of substantial but sub-clinical pathology in controls. (bcm.edu)
  • We have participated in studies to better understand the clinical impact of this pathology, and its potential as an endophenotype for genetic analyses. (bcm.edu)
  • The team used the National Institute on Aging (NIA)-AA guidelines for the clinical detection of MCI patients and AD Neuroimaging Initiative (ADNI) criteria to identify CN patients. (news-medical.net)
  • To address this, there are numerous compounds currently in various phases of clinical trial, and even more in preclinical development, which are believed may offer some hope for a tangible clinical benefit in AD. (frontiersin.org)
  • on the state of AD clinical trials and therapeutics, and will not be discussed here. (frontiersin.org)
  • Human biospecimens constitute a valu- cal care, while blood samples and other that identifiers such as names, hospital able resource for different types of basic biological specimens are disposed of numbers or national identity numbers and clinical research (1) , and surplus once the requested test is completed. (who.int)
  • This body of work aims to better elucidate the epigenetic pathology of AD and to aid in identification of histone-modifying enzymes involved in AD pathology for drug targets and treatment options. (umd.edu)
  • Although two percent of the population over age 65 are clinically diagnosed with PD, the defining pathology of disease (alpha-synuclein Lewy bodies) is discovered in 20 percent of brains from population-based autopsy studies. (bcm.edu)
  • point out that there is no unequivocal evidence that tau is overexpressed in AD or any other known human tauopathy. (alzforum.org)
  • Taken together, our collected body of work illustrates how ApoE4 causes widespread molecular and cellular alterations in multiple cell types to facilitate the development of AD phenotypes. (cam.ac.uk)
  • Currently, there are no treatments that prevent, delay, or ameliorate AD, stressing the crucial importance of AD pathology research and the promise of epigenetics as the solution. (umd.edu)
  • We also identified multiple processes that are perturbed in AD pathology exclusively in the context of ApoE4. (cam.ac.uk)
  • Pertinent to AD pathophysiology, heat shock protein 90 (HSP90)/co-chaperone complex folds tau or hyperphosphorylated tau, whereas heat shock protein 70-carboxyl-terminus of HSP70 Interacting protein (HSP70-CHIP) complex mediates degradation 13 , 14 . (nature.com)
  • Until recently, our understanding of the genetic causes for human diseases were largely limited to the study of extreme phenotypes produced by Mendelian disorders. (bcm.edu)
  • This study and subsequent studies by our group indicated that the T44 line recapitulates features of AD tau pathology. (alzforum.org)
  • It is understood that human milk provides benefits to babies as they develop, particularly in its ability to help protect babies from a variety of infections. (nyas.org)
  • In parallel, we conducted lipidomic analyses in ApoE4-iPSC-induced astrocytes derived from human ApoE4 carriers. (cam.ac.uk)
  • HIV Nef and Antiretroviral Therapy Have an Inhibitory Effect on Autophagy in Human Astrocytes that May Contribute to HIV-Associated Neurocognitive Disorders. (academictree.org)