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https://www.readbyqxmd.com/read/29790502/inhibition-of-tau-derived-hexapeptide-aggregation-and-toxicity-by-a-self-assembled-cyclic-d-l-%C3%AE-peptide-conformational-inhibitor
#1
A Belostozky, M Richman, E Lisniansky, A Tovchygrechko, J H Chill, S Rahimipour
Aggregation and accumulation of amyloid β and tau proteins to plaques and neurofibrillary tangles are the key pathogenic events in Alzheimer's disease. Here, we studied the capability of the cyclic d,l-α-peptide CP-2 as a conformational inhibitor of different amyloids to cross-interact with tau-derived AcPHF6 peptide and inhibit its aggregation, membrane perturbation and toxicity.
May 23, 2018: Chemical Communications: Chem Comm
https://www.readbyqxmd.com/read/29790198/the-role-of-lysosomes-and-autophagosomes-in-frontotemporal-lobar-degeneration
#2
Hamish Dc Bain, Yvonne S Davidson, Andrew C Robinson, Sarah Ryan, Sara Rollinson, Anna Richardson, Matthew Jones, Julie S Snowden, Stuart Pickering-Brown, David M A Mann
INTRODUCTION: Cell biological and genetic evidence implicates failures in degrading aggregating proteins, such as tau and TDP-43, through autophagy or lysosomal pathways in the pathogenesis of Frontotemporal Lobar degeneration (FTLD). METHODS: We investigated changes in degradative pathways in 60 patients with different pathological or genetic forms of FTLD employing immunohistochemistry for marker proteins such as Lysosomal Associated Membrane Proteins 1 (LAMP-1) and 2 (LAMP-2), Cathepsin D (CTSD) and microtubule-associated protein 1 light chain 3 alpha (LC3A)...
May 23, 2018: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/29790176/tau-filaments-in-neurodegenerative-diseases
#3
Michel Goedert
The ordered assembly of Tau protein into abnormal filamentous inclusions is a defining characteristic of many human neurodegenerative diseases. Thirty years ago, we reported that Tau is an integral component of the intraneuronal filaments of Alzheimer's disease. All six brain Tau isoforms make up those filaments. Twenty years ago, we and others showed that mutations in MAPT, the Tau gene, cause familial forms of frontotemporal dementia, thus proving that dysfunction of Tau protein is sufficient to cause neurodegeneration and dementia...
May 22, 2018: FEBS Letters
https://www.readbyqxmd.com/read/29789140/changes-in-concentrations-of-tau-reactive-antibodies-are-dependent-on-sex-in-alzheimer-s-disease-patients
#4
Michala Krestova, Jan Ricny, Ales Bartos
The presence of pre-existing natural antibodies against Alzheimer's disease (AD) pathological proteins might interfere with immune responses to therapeutic vaccination with these proteins. We aimed to compare levels of antibodies in CSF and serum: We observed higher reactivity of natural tau-reactive antibodies towards phosphorylated bovine tau protein than to human recombinant (non-phosphorylated) tau protein. Males with MCI-AD had higher amounts of these antibodies than corresponding controls. Concentrations of antibodies were lower in females with the MCI-AD than in control females...
May 19, 2018: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/29788790/eeg-differences-in-two-clinically-similar-rapid-dementias-voltage-gated-potassium-channel-complex-associated-autoimmune-encephalitis-and-creutzfeldt-jakob-disease
#5
Brin Freund, John C Probasco, Mackenzie C Cervenka, Raoul Sutter, Peter W Kaplan
Distinguishing treatable causes for rapidly progressive dementia from those that are incurable is vital. Creutzfeldt-Jakob disease (CJD) and voltage-gated potassium channel complex-associated autoimmune encephalitis (VGKC AE) are 2 such conditions with disparate outcomes and response to treatment. To determine the differences in electroencephalography between CJD and VGKC AE, we performed a retrospective review of medical records and examined clinical data, neuroimaging, and electroencephalographs performed in patients admitted for evaluation for rapidly progressive dementia diagnosed with CJD and VGKC AE at the Johns Hopkins Hospital and Bayview Medical Center between January 1, 2007 and December 31, 2015...
May 1, 2018: Clinical EEG and Neuroscience: Official Journal of the EEG and Clinical Neuroscience Society (ENCS)
https://www.readbyqxmd.com/read/29788004/juvenile-traumatic-brain-injury-results-in-cognitive-deficits-associated-with-impaired-endoplasmic-reticulum-stress-and-early-tauopathy
#6
Michael J Hylin, Ryan C Holden, Aidan C Smith, Aric F Logsdon, Rabia Qaiser, Brandon P Lucke-Wold
The leading cause of death in the juvenile population is trauma, and in particular neurotrauma. The juvenile brain response to neurotrauma is not completely understood. Endoplasmic reticulum (ER) stress has been shown to contribute to injury expansion and behavioral deficits in adult rodents and furthermore has been seen in adult postmortem human brains diagnosed with chronic traumatic encephalopathy. Whether endoplasmic reticulum stress is increased in juveniles with traumatic brain injury (TBI) is poorly delineated...
May 22, 2018: Developmental Neuroscience
https://www.readbyqxmd.com/read/29782836/dancing-with-the-diva-hsp90-client-interactions
#7
REVIEW
Martina Radli, Stefan G D Rüdiger
The molecular chaperone Hsp90 is involved in the folding, maturation and degradation of a large number structurally and sequentially unrelated clients, often connected to serious diseases. Elucidating the principles of how Hsp90 recognises this large variety of substrates is essential for comprehending the mechanism of this chaperone machinery, as well as it is a prerequisite for the design of client specific drugs targeting Hsp90. Here, we discuss the recent progress in understanding the substrate recognition principles of Hsp90 and its implications for the role of Hsp90 in the lifecycle of (signalling) molecules...
May 18, 2018: Journal of Molecular Biology
https://www.readbyqxmd.com/read/29782833/insights-into-stabilizing-forces-in-amyloid-fibrils-of-differing-sizes-from-polarizable-molecular-dynamics-simulations
#8
Darcy S Davidson, Anne M Brown, Justin A Lemkul
Pathological aggregation of amyloid-forming proteins is a hallmark of a number of human diseases, including Alzheimer's, type 2 diabetes, Parkinson's, and more. Despite having very different primary amino acid sequences, these amyloid proteins form similar supramolecular, fibril structures that are highly resilient to physical and chemical denaturation. To better understand the structural stability of disease-related amyloids and to gain a greater understanding of factors that stabilize functional amyloid assemblies, insights into tertiary and quaternary interactions are needed...
May 18, 2018: Journal of Molecular Biology
https://www.readbyqxmd.com/read/29782794/peptides-peptidomimetics-and-carbohydrate-peptide-conjugates-as-amyloidogenic-aggregation-inhibitors-for-alzheimer-s-disease
#9
Philip Ryan, Bhautikkumar Patel, Vivek Makwana, Hemant Jadhav, Milton John Kiefel, Andrew Davey, Tristan Reekie, Santosh Rudrawar, Michael Kassiou
Alzheimer's disease (AD) is a progressive neurodegenerative disorder accounting for 60-80% of dementia cases. For many years, AD causality was attributed to amyloid-β (Aβ) aggregated species. Recently, multiple therapies that target Aβ aggregation have failed in clinical trials, since Aβ aggregation is found in AD and healthy patients. Attention has therefore shifted towards the aggregation of the peptide tau as a major driver of AD. Numerous inhibitors of tau-based pathology have recently been developed...
May 21, 2018: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/29782323/role-of-blood-brain-barrier-in-alzheimer-s-disease
#10
Zhiyou Cai, Pei-Feng Qiao, Cheng-Qun Wan, Min Cai, Nan-Kai Zhou, Qin Li
The blood-brain barrier (BBB) is involved in the pathogenesis of Alzheimer's disease (AD). BBB is a highly selective semipermeable structural and chemical barrier which ensures a stable internal environment of the brain and prevents foreign objects invading the brain tissue. BBB dysfunction induces the failure of Aβ transport from brain to the peripheral circulation across the BBB. Especially, decreased levels of LRP-1 (low density lipoprotein receptor-related protein 1) and increased levels of RAGE (receptor for advanced glycation endproducts) at the BBB can cause the failure of Aβ transport...
May 16, 2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29782322/inhibition-of-histone-acetylation-by-anp32a-induces-memory-deficits
#11
Gao-Shang Chai, Qiong Feng, Rong-Hong Ma, Xiao-Hang Qian, Dan-Ju Luo, Zhi-Hao Wang, Yu Hu, Dong-Sheng Sun, Jun-Fei Zhang, Xiao Li, Xiao-Guang Li, Dan Ke, Jian-Zhi Wang, Xi-Fei Yang, Gong-Ping Liu
There is accumulating evidence that decreased histone acetylation is involved in normal aging and neurodegenerative diseases. Recently, we found that ANP32A, a key component of INHAT (inhibitor of acetyltransferases) that suppresses histone acetylation, increased in aged and cognitively impaired C57 mice and expressing wild-type human full length tau (htau) transgenic mice. Downregulating ANP32A restored cognitive function and synaptic plasticity through upregulation of the expressions of synaptic-related proteins via increasing histone acetylation...
May 16, 2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29782321/pyk2-is-a-novel-tau-tyrosine-kinase-that-is-regulated-by-the-tyrosine-kinase-fyn
#12
Chuanzhou Li, Jürgen Götz
The protein tyrosine kinase Pyk2 is encoded by PTK2B, a novel Alzheimer's disease (AD) susceptibility variant, with the PTK2B risk allele being associated with increased mRNA levels, suggestive of increased Pyk2 levels. However, the role of Pyk2, a member of the focal adhesion kinase (FAK) family, in AD pathology and its regulation are largely unknown. To address this, we generated mice with neuronal expression of human Pyk2. Because we had previously reported an association of Pyk2 and hyperphosphorylated tau (a hallmark feature of AD) in human tau transgenic pR5 mice, we also generated Pyk2/tau double-transgenic mice, which exhibit increased tyrosine phosphorylation and accumulation of tau...
May 16, 2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29782318/amyloid-accumulation-and-cognitive-decline-in-clinically-normal-older-individuals-implications-for-aging-and-early-alzheimer-s-disease
#13
Elizabeth C Mormino, Kathryn V Papp
 The aberrant accumulation of the amyloid protein is a critical and early event in the Alzheimer's disease (AD) cascade. Given the early involvement of this pathological process, it is not surprising that many clinically normal (CN) older individuals demonstrate evidence of abnormal Aβ at postmortem examination and in vivo using either CSF or PET imaging. Converging evidence across multiple research groups suggests that the presence of abnormal Aβ among CN individuals is associated with elevated risk of future clinical impairment and cognitive decline...
May 16, 2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29781013/design-and-synthesis-of-aza-indolyl-maleimide-based-covalent-inhibitors-of-glycogen-synthase-kinase-3%C3%AE
#14
Zhimin Yang, Hui Liu, Botao Pan, Fengli He, Zhengying Pan
As an important kinase in multiple signal transduction pathways, GSK-3β has been an attractive target for chemical probe discovery and drug development. Compared to numerous reversible inhibitors that have been developed, covalent inhibitors of GSK-3β are noticeably lacking. Here, we report the discovery of a series of covalent GSK-3β inhibitors by optimizing both non-covalent interactions and reactive groups. Among these covalent inhibitors, compound 38b with a mild α-fluoromethyl amide reactive group emerges as a selective and covalent inhibitor against GSK-3β, effectively inhibits the phosphorylation of glycogen synthase and tau protein, and increases β-catenin's levels in living cells...
May 21, 2018: Organic & Biomolecular Chemistry
https://www.readbyqxmd.com/read/29780866/molecular-imaging-what-is-right-and-what-is-an-illusion
#15
William E Klunk
Over the past 40 years, brain molecular imaging has evolved from measuring cerebral metabolism with fluorodeoxyglucose, to neuroreceptor imaging, to imaging pathological protein deposits. In the early going, the characteristics of successful molecular imaging radiotracers were defined, and a detailed "Process" was developed for the collection of basic pharmacodynamic and pharmacokinetic data. These data are essential for the interpretation of in vivo imaging data and for defining the strengths, weaknesses, and limitations of new tracers...
2018: Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring
https://www.readbyqxmd.com/read/29776378/differential-induction-of-mutant-sod1-misfolding-and-aggregation-by-tau-and-%C3%AE-synuclein-pathology
#16
Michael C Pace, Guilian Xu, Susan Fromholt, John Howard, Benoit I Giasson, Jada Lewis, David R Borchelt
BACKGROUND: Prior studies in C. elegans demonstrated that the expression of aggregation-prone polyglutamine proteins in muscle wall cells compromised the folding of co-expressed temperature-sensitive proteins, prompting interest in whether the accumulation of a misfolded protein in pathologic features of human neurodegenerative disease burdens cellular proteostatic machinery in a manner that impairs the folding of other cellular proteins. METHODS: Mice expressing high levels of mutant forms of tau and α-synuclein (αSyn), which develop inclusion pathologies of the mutant protein in brain and spinal cord, were crossed to mice expressing low levels of mutant superoxide dismutase 1 fused to yellow fluorescent protein (G85R-SOD1:YFP) for aging and neuropathological evaluation...
May 18, 2018: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29774342/the-distinct-structural-preferences-of-tau-protein-repeat-domains
#17
Xuhua Li, Xuewei Dong, Guanghong Wei, Martin Margittai, Ruth Nussinov, Buyong Ma
The tau fibrillar structures from the brain of an Alzheimer's patient have a core with a C-shaped motif of the third and fourth repeat domains (R3-R4). Our simulations indicated that the C-shaped motif is only stable for R3-R4, while R1-R2 tends to be linear in shape. These two structural motifs appear in the most stable K18 protofilament. Heparin can further stabilize the C-shaped R3-R4 motif, but not other repeats.
May 18, 2018: Chemical Communications: Chem Comm
https://www.readbyqxmd.com/read/29774334/a-comparative-study-of-epa-enriched-ethanolamine-plasmalogen-and-epa-enriched-phosphatidylethanolamine-on-a%C3%AE-42-induced-cognitive-deficiency-in-a-rat-model-of-alzheimer-s-disease
#18
Hongxia Che, Qian Li, Tiantian Zhang, Lin Ding, Lingyu Zhang, Haohao Shi, Teruyoshi Yanagita, Changhu Xue, Yaoguang Chang, Yuming Wang
Ethanolamine plasmalogen (pPE), a major phospholipid in neuronal membranes, is specifically reduced in postmortem brains from patients with Alzheimer's disease (AD). The purpose of the present study was to compare the effects of EPA-enriched ethanolamine plasmalogen (EPA-pPE) and EPA-enriched phosphatidylethanolamine (EPA-PE) on cognitive deficiency and illustrate the possible underlying mechanisms. SD rats were divided into four groups including the sham group injected with 0.9% saline and three amyloid-β (Aβ) infusion groups, Aβ42 group, EPA-pPE group and EPA-PE group...
May 18, 2018: Food & Function
https://www.readbyqxmd.com/read/29774215/importance-of-functional-loss-of-fus-in-ftld-als
#19
REVIEW
Shinsuke Ishigaki, Gen Sobue
Fused in sarcoma (FUS) is an RNA binding protein that regulates RNA metabolism including alternative splicing, transcription, and RNA transportation. FUS is genetically and pathologically involved in frontotemporal lobar degeneration (FTLD)/amyotrophic lateral sclerosis (ALS). Multiple lines of evidence across diverse models suggest that functional loss of FUS can lead to neuronal dysfunction and/or neuronal cell death. Loss of FUS in the nucleus can impair alternative splicing and/or transcription, whereas dysfunction of FUS in the cytoplasm, especially in the dendritic spines of neurons, can cause mRNA destabilization...
2018: Frontiers in Molecular Biosciences
https://www.readbyqxmd.com/read/29772805/ethyl-acetate-fraction-from-persimmon-diospyros-kaki-ameliorates-cerebral-neuronal-loss-and-cognitive-deficit-via-the-jnk-akt-pathway-in-tmt-induced-mice
#20
Jong Min Kim, Seon Kyeong Park, Jin Yong Kang, Su Bin Park, Seul Ki Yoo, Hye Ju Han, Chul-Woo Kim, Uk Lee, Sea-Hyun Kim, Ho Jin Heo
This study was conducted to assess the antioxidant capacity and protective effect of the ethyl acetate fraction from persimmon ( Diospyros kaki ) (EFDK) on H₂O₂-induced hippocampal HT22 cells and trimethyltin chloride (TMT)-induced Institute of Cancer Research (ICR) mice. EFDK had high antioxidant activities and neuroprotective effects in HT22 cells. EFDK ameliorated behavioral and memory deficits in Y-maze, passive avoidance and Morris water maze tests. Also, EFDK restored the antioxidant system by regulating malondialdehyde (MDA), superoxide dismutase (SOD) and reduced gluthathione (GSH), and the cholinergic system by controlling the acetylcholine (ACh) level and acetylcholinesterase (AChE) activity and expression...
May 17, 2018: International Journal of Molecular Sciences
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