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Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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1

Przybyla, Magdalena, Janet van Eersel, Annika van Hummel, Julia van der Hoven, Miheer Sabale, Anne Harasta, Julius Müller, et al. "Onset of hippocampal network aberration and memory deficits in P301S tau mice are associated with an early gene signature." Brain 143, no. 6 (May 6, 2020): 1889–904. http://dx.doi.org/10.1093/brain/awaa133.

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Abstract Hyperphosphorylation and deposition of tau in the brain characterizes frontotemporal dementia and Alzheimer’s disease. Disease-associated mutations in the tau-encoding MAPT gene have enabled the generation of transgenic mouse models that recapitulate aspects of human neurodegenerative diseases, including tau hyperphosphorylation and neurofibrillary tangle formation. Here, we characterized the effects of transgenic P301S mutant human tau expression on neuronal network function in the murine hippocampus. Onset of progressive spatial learning deficits in P301S tau transgenic TAU58/2 mice were paralleled by long-term potentiation deficits and neuronal network aberrations during electrophysiological and EEG recordings. Gene-expression profiling just prior to onset of apparent deficits in TAU58/2 mice revealed a signature of immediate early genes that is consistent with neuronal network hypersynchronicity. We found that the increased immediate early gene activity was confined to neurons harbouring tau pathology, providing a cellular link between aberrant tau and network dysfunction. Taken together, our data suggest that tau pathology drives neuronal network dysfunction through hyperexcitation of individual, pathology-harbouring neurons, thereby contributing to memory deficits.

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2

Kreilaus, Fabian, Rebecca Masanetz, Georgia Watt, Magdalena Przybyla, Arne Ittner, Lars Ittner, and Tim Karl. "The behavioural phenotype of 14-month-old female TAU58/2 transgenic mice." Behavioural Brain Research 397 (January 2021): 112943. http://dx.doi.org/10.1016/j.bbr.2020.112943.

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3

Van Erum, Jan, Femke Valkenburg, Debby Van Dam, and Peter Paul De Deyn. "Pentylenetetrazole-induced Seizure Susceptibility in the Tau58/4 Transgenic Mouse Model of Tauopathy." Neuroscience 425 (January 2020): 112–22. http://dx.doi.org/10.1016/j.neuroscience.2019.11.007.

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4

Kreilaus, Fabian, Magdalena Przybyla, Lars Ittner, and Tim Karl. "Cannabidiol (CBD) treatment improves spatial memory in 14-month-old female TAU58/2 transgenic mice." Behavioural Brain Research 425 (May 2022): 113812. http://dx.doi.org/10.1016/j.bbr.2022.113812.

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5

Valkenburg, Femke, Debby Van Dam, Yannick Vermeiren, Tony Aerts, and Peter Paul De Deyn. "MONOAMINERGIC CORRELATES OF DISINHIBITED BEHAVIOURS IN THE NOVEL TAU58/4 TRANSGENIC MOUSE MODEL FOR TAUOPATHY." Alzheimer's & Dementia 13, no. 7 (July 2017): P1486. http://dx.doi.org/10.1016/j.jalz.2017.07.565.

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6

Watt, Georgia, Rose Chesworth, Magdalena Przybyla, Arne Ittner, Brett Garner, Lars M. Ittner, and Tim Karl. "Chronic cannabidiol (CBD) treatment did not exhibit beneficial effects in 4-month-old male TAU58/2 transgenic mice." Pharmacology Biochemistry and Behavior 196 (September 2020): 172970. http://dx.doi.org/10.1016/j.pbb.2020.172970.

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7

Heltsley, Brian K. "Experimental summary on hadronic decays: A TAU98 review." Nuclear Physics B - Proceedings Supplements 76, no. 1-3 (April 1999): 391–400. http://dx.doi.org/10.1016/s0920-5632(99)00497-1.

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8

Al-Nakkash, Layla, Daniel Mason, Niamatullah Ismail, Taylor Bowman, John Ahlert, Maxwell Rubin, Emma Smith, Abigail Rosander, and Tom L. Broderick. "Exercise Training Prevents the Loss of Wall Thickness and Lowers Expression of Alzheimer’s Related Proteins in 3xTg Mouse Jejunum." International Journal of Environmental Research and Public Health 19, no. 21 (October 29, 2022): 14164. http://dx.doi.org/10.3390/ijerph192114164.

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Growing evidence has demonstrated the benefits of regular exercise on cardiovascular, neural, and cognitive function in humans with Alzheimer’s disease (AD). However, the consequences of AD on gastrointestinal morphology and the effects of regular exercise, which plays an important role against the development of certain gastrointestinal-related diseases, are still poorly understood. Therefore, to assess the changes in intestinal structure in a mouse model of AD and the impact of exercise, 2-month-old 3xTg-AD male mice were subjected to treadmill running 5 days per week for a period of 5 months. Jejunum from 3xTg-AD mice analyzed by histochemical methods revealed significant alterations in morphology. Compared to age-matched wild-type (WT) mice, villi length and crypt depth were increased, and collagen content of jejunum was elevated in 3xTg-AD mice. Jejunum wall dimensions, expressed as total wall thickness, outer longitudinal thickness, and inner circular thickness were decreased in 3xTg-AD compared to WT. Smooth muscle actin expression in jejunal wall was decreased in 3xTg-AD. Most of these aberrations were improved with exercise. Western blot expression of cyclin dependent kinase 5 (CDK5, involved in neural cell death and hyperphosphorylation of tau), was elevated in 3xTg-AD jejunum. This was associated with a 4-fold increase in tau5 expression. Exercise prevented the increase in expression of CDK5 and tau5. Expression of caspase 3 (an apoptotic marker) was elevated in 3xTg-AD jejunum and exercise prevented this. The results of our study indicate that the abnormalities in jejunum of the 3xTg mouse model of AD were prevented with exercise training.

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9

González, Andrea, Leonardo Guzmán-Martínez, and Ricardo B. Maccioni. "Plasma Tau Variants Detected by a Novel Anti-Tau Monoclonal Antibody: A Potential Biomarker for Alzheimer’s Disease." Journal of Alzheimer's Disease 77, no. 2 (September 15, 2020): 877–83. http://dx.doi.org/10.3233/jad-200386.

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Background: A major drawback in Alzheimer’s disease (AD) is the lack of validated biomarkers for routine clinical diagnostic. We have reported earlier a novel blood biomarker, named Alz-tau®, based on variants of platelet tau. This marker evaluates the ratio of high molecular weight tau (HMWtau) and the low molecular weight (LMWtau) tau. Objective: To analyze a potential novel source of antigen for Alz-tau®, plasma tau, detected by immunoreactivity with the novel monoclonal antibody, tau51. Methods: We evaluated tau variants in plasma precipitated with ammonium sulfate from 36 AD patients and 15 control subjects by western blot with this novel monoclonal antibody. Results: The HMW/LMWtau ratio was statistically different between AD patients and controls. Conclusions: Plasma tau variants are suitable to be considered as a novel antigen source for the Alz-tau® biomarker for AD.

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10

Bohrer, Laura R., Ping Liu, Jian Zhong, Yunqian Pan, James Angstman, Lucas J. Brand, Scott M. Dehm, and Haojie Huang. "FOXO1 binds to the TAU5 motif and inhibits constitutively active androgen receptor splice variants." Prostate 73, no. 10 (February 6, 2013): 1017–27. http://dx.doi.org/10.1002/pros.22649.

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11

Porzig, Robert, David Singer, and Ralf Hoffmann. "Epitope mapping of mAbs AT8 and Tau5 directed against hyperphosphorylated regions of the human tau protein." Biochemical and Biophysical Research Communications 358, no. 2 (June 2007): 644–49. http://dx.doi.org/10.1016/j.bbrc.2007.04.187.

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12

Christiaens, Valerie, Charlotte L. Bevan, Leen Callewaert, Anna Haelens, Guy Verrijdt, Wilfried Rombauts, and Frank Claessens. "Characterization of the Two Coactivator-interacting Surfaces of the Androgen Receptor and Their Relative Role in Transcriptional Control*." Journal of Biological Chemistry 277, no. 51 (October 4, 2002): 49230–37. http://dx.doi.org/10.1074/jbc.m209322200.

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The androgen receptor interacts with the p160 coactivators via two surfaces, one in the ligand binding domain and one in the amino-terminal domain. The ligand binding domain interacts with the nuclear receptor signature motifs, whereas the amino-terminal domain has a high affinity for a specific glutamine-rich region in the p160s. We here describe the implication of two conserved motifs in the latter interaction. The amino-terminal domain of the androgen receptor is a very strong activation domain constituent of Tau5, which is mainly active in the absence of the ligand binding domain, and Tau1, which is only active in the presence of the ligand binding domain. Both domains are, however, implicated in the recruitment of the p160s. Mutation analysis of the p160s has shown that the relative contribution of the two recruitment mechanisms via the signature motifs or via the glutamine-rich region depend on the nature of the enhancers tested. We propose, therefore, that the androgen receptor-coactivator complex has several alternative conformations, depending partially on the context of the enhancer.

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13

Krishnan, Vidya S., Annemieke Aartsma-Rus, Maurice Overzier, Cathleen Lutz, Laurent Bogdanik, and Miranda D. Grounds. "Implications of increased S100β and Tau5 proteins in dystrophic nerves of two mdx mouse models for Duchenne muscular dystrophy." Molecular and Cellular Neuroscience 105 (June 2020): 103484. http://dx.doi.org/10.1016/j.mcn.2020.103484.

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14

Cehlar, Ondrej, Rostislav Skrabana, Andrej Kovac, Branislav Kovacech, and Michal Novak. "Crystallization and preliminary X-ray diffraction analysis of tau protein microtubule-binding motifs in complex with Tau5 and DC25 antibody Fab fragments." Acta Crystallographica Section F Structural Biology and Crystallization Communications 68, no. 10 (September 25, 2012): 1181–85. http://dx.doi.org/10.1107/s1744309112030382.

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15

Li, Ling, Tian Li, Xin Tian, and Ling Zhao. "Ginsenoside Rd Attenuates Tau Phosphorylation in Olfactory Bulb, Spinal Cord, and Telencephalon by Regulating Glycogen Synthase Kinase 3β and Cyclin-Dependent Kinase 5." Evidence-Based Complementary and Alternative Medicine 2021 (December 26, 2021): 1–7. http://dx.doi.org/10.1155/2021/4485957.

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Objective. Ginseng is a plant of the family Acanthopanaceae. It has been used for thousands of years in China. It is known as the king of hundred herbs. It was recorded first in Shennong Baicao Jing. It has been found that ginsenoside Rd is a neuroprotective agent. This article aims to explore the protective roles of ginsenoside Rd in Alzheimer’s disease. Rd, a Chinese herb, may be a promising treatment drug for Alzheimer’s disease (AD) and is also reported to be related to several pathological changes, including the deposition of Aβ and tau hyperphosphorylation in AD as it decreases the deposition of tau hyperphosphorylation in APP transgenic mice. Methods. In this study, APP transgenic mice were pretreated with 10 mg/kg Rd for six months, and the effect of Rd on neuropathological deficits in the olfactory bulb, spinal cord, and telencephalon of APP transgenic mice was investigated. The phosphorylation levels of tau (S199/202, S396, S404, and Tau5) and the activities of the proteins glycogen synthase kinase 3β (Tyr216) and cyclin-dependent kinase 5 (P25/P35) were measured. Results. The pretreatment of Rd effectively decreased the production and deposition of hyperphosphorylated tau (S199/202, S396, and S404) protein by depressing the expression of glycogen synthase kinase 3β (GSK-3β/Tyr216) and cyclin-dependent kinase 5 (CDK5/P25). Conclusion. These findings suggest that ginsenoside Rd could improve the pathological changes of AD in the olfactory bulb, spinal cord, and telencephalon, which further demonstrated the potential therapeutic effect of Rd in early AD.

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16

Krishnan, Vidya S., Lakshana P. Thanigaiarasu, Robert White, Rachael Crew, Thibaut Larcher, Caroline Le Guiner, and Miranda D. Grounds. "Dystrophic Dmd rats show early neuronal changes (increased S100β and Tau5) at 8 months, supporting severe dystropathology in this rodent model of Duchenne muscular dystrophy." Molecular and Cellular Neuroscience 108 (October 2020): 103549. http://dx.doi.org/10.1016/j.mcn.2020.103549.

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17

Haroun, Medhat A., José A. Pires, and Adrian Y. J. Won. "Suppression of Environmentally-Induced Vibrations in Tall Buildings by Hybrid Liquid Column Dampers." Structural Design of Tall Buildings 5, no. 1 (March 1996): 45–54. http://dx.doi.org/10.1002/(sici)1099-1794(199603)5:1<45::aid-tal58>3.0.co;2-f.

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18

Hong, Nan Hyung, Berenger Biannic, Peter Virsik, Han-Jie Zhou, and Ronan Le Moigne. "Abstract 429: Androgen receptor (AR) N-terminal domain degraders can degrade AR full length and AR splice variants in CRPC preclinical models." Cancer Research 82, no. 12_Supplement (June 15, 2022): 429. http://dx.doi.org/10.1158/1538-7445.am2022-429.

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Abstract Introduction: Androgen receptor (AR) signaling is a main driver of prostate cancer progression and remains a crucial target for therapeutic intervention even in late stages of the disease. Current antiandrogen therapies directly or indirectly target the AR ligand binding domain (LBD) and are initially effective in prostate cancer patients. However, resistance ultimately develops, and new methods of inhibiting the AR pathway are needed. The selective targeting of the N-terminal domain (NTD) of the AR by small molecule anitens represents a novel method of blocking AR signaling that can bypass LBD-related resistance mechanisms. AR NTD is an intrinsically disordered region (IDR) which has no stable ordered structure and is generally regarded as an undruggable target due to the lack of a well-defined small-molecule binding pocket. However, we recently demonstrated that EPI-7386, an AR NTD small molecule inhibitor, inhibits AR activity by binding to Tau5 region of the NTD. By developing an aniten based bifunctional degrader (ANITAC for ANITen bAsed Chimera), our goal is to eliminate any forms of AR protein found in castration-resistant prostate cancer (CRPC), that can potentially drive disease progression, including LBD mutants and AR truncated variants. Methods: AR degradation was monitored by Western Blot or by using the HiBit assay. AR transcriptional activity was measured using different reporter assays following AR full length (FL) or truncated AR activity in in vitro models. Results: Here we report the first series of AR degraders targeting the NTD of AR, which lead to degradation of all forms of AR, including AR-V7 and AR-v567es. ANITACs eliminate AR in all cell lines tested through an E3 ligase dependent mechanism, with an observed 50% degradation concentration (DC50) < 20 nM in 22Rv1 cells for the most potent compounds. AR degradation mediated by ANITACs suppresses the expression of AR target genes and decreases the viability of prostate cancer cells. ANITACs also degrade clinically relevant AR mutants and AR splice variants and show inhibition of AR transcriptional activity in multiple cell lines expressing different forms of AR including AR FL (LNCaP, CWR-AD1), AR-V7 (22Rv1), AR-V567es (CWR-D567). In vitro and in vivo PK studies show the compounds are metabolically stable and exhibit excellent oral bioavailability in mice. Conclusion: In summary, we report preclinical data on the first generation of ANITAC molecules, that can be orally bioavailable and show activity against forms of AR expressed in late stage CRPC patients. Citation Format: Nan Hyung Hong, Berenger Biannic, Peter Virsik, Han-Jie Zhou, Ronan Le Moigne. Androgen receptor (AR) N-terminal domain degraders can degrade AR full length and AR splice variants in CRPC preclinical models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 429.

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19

Parr, E., R. D. Page, D. T. Joss, F. A. Ali, K. Auranen, L. Capponi, T. Grahn, et al. "Fine structure in the α decay of Lu156 and Ta158." Physical Review C 99, no. 5 (May 9, 2019). http://dx.doi.org/10.1103/physrevc.99.054307.

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20

Ba, Li, Lifang Huang, Ziyu He, Saiyue Deng, Yi Xie, Min Zhang, Cornelius Jacob, et al. "Does Chronic Sleep Fragmentation Lead to Alzheimer's Disease in Young Wild-Type Mice?" Frontiers in Aging Neuroscience 13 (December 21, 2021). http://dx.doi.org/10.3389/fnagi.2021.759983.

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Chronic sleep insufficiency is becoming a common issue in the young population nowadays, mostly due to life habits and work stress. Studies in animal models of neurological diseases reported that it would accelerate neurodegeneration progression and exacerbate interstitial metabolic waste accumulation in the brain. In this paper, we study whether chronic sleep insufficiency leads to neurodegenerative diseases in young wild-type animals without a genetic pre-disposition. To this aim, we modeled chronic sleep fragmentation (SF) in young wild-type mice. We detected pathological hyperphosphorylated-tau (Ser396/Tau5) and gliosis in the SF hippocampus. 18F-labeled fluorodeoxyglucose positron emission tomography scan (18F-FDG-PET) further revealed a significant increase in brain glucose metabolism, especially in the hypothalamus, hippocampus and amygdala. Hippocampal RNAseq indicated that immunological and inflammatory pathways were significantly altered in 1.5-month SF mice. More interestingly, differential expression gene lists from stress mouse models showed differential expression patterns between 1.5-month SF and control mice, while Alzheimer's disease, normal aging, and APOEε4 mutation mouse models did not exhibit any significant pattern. In summary, 1.5-month sleep fragmentation could generate AD-like pathological changes including tauopathy and gliosis, mainly linked to stress, as the incremented glucose metabolism observed with PET imaging suggested. Further investigation will show whether SF could eventually lead to chronic neurodegeneration if the stress condition is prolonged in time.

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21

Kanaan, Nicholas M., and Tessa Grabinski. "Neuronal and Glial Distribution of Tau Protein in the Adult Rat and Monkey." Frontiers in Molecular Neuroscience 14 (April 27, 2021). http://dx.doi.org/10.3389/fnmol.2021.607303.

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Tau is a microtubule-associated protein for which the physiological functions remain a topic of vigorous investigation. Additionally, tau is a central player in the pathogenesis of several diseases such as Alzheimer’s disease and several frontotemporal dementias. A critical variable to understanding tau in physiological and disease contexts is its normal localization within cells of the adult CNS. Tau is often described as an axon-specific (or enriched) and neuron-specific protein with little to no expression in glial cells, all of which are untrue. Understanding normal tau distribution also impacts interpretation of experimental results and hypotheses regarding its role in disease. Thus, we set out to help clarify the normal localization of tau in the adult CNS of middle-aged rats and rhesus macaque using the hippocampus as a representative brain structure. The physiological concentration of tau in the rat hippocampus was 6.6 μM and in white matter was 3.6 μM as determined by quantitative sandwich ELISAs. We evaluated the cellular localization of tau using multiple tau-specific antibodies with epitopes to different regions, including Tau1, Tau5, Tau7, R1, and two novel primate-specific antibodies NT9 and NT15. In the rat and monkey, tau was localized within the somatodendritic and axonal compartments, as well as a subset of neuronal nuclei. Semi-quantitative fluorescence intensity measurements revealed that depending on the specific reagent used the somatodendritic tau is relatively equal to, higher than, or lower than axonal tau, highlighting differential labeling of tau with various antibodies despite its distribution throughout the neuron. Tau was strongly expressed in mature oligodendrocytes and displayed little to no expression in oligodendrocyte precursor cells, astrocytes or microglia. Collectively, the data indicate tau is ∼3 – 7 μM under physiological conditions, is not specifically enriched in axons, and is normally found in both neurons and mature oligodendrocytes in the adult CNS. The full landscape of tau distribution is not revealed by all antibodies suggesting availability of the epitopes is different within specific neuronal compartments. These findings set the stage for better understanding normal tau distributions and interpreting data regarding the presence of tau in different compartments or cell types within disease conditions.

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22

Liu, Sen, Min Fan, Jing-Xian Xu, Long-Jun Yang, Cong-Cong Qi, Qing-Rong Xia, and Jin-Fang Ge. "Exosomes derived from bone-marrow mesenchymal stem cells alleviate cognitive decline in AD-like mice by improving BDNF-related neuropathology." Journal of Neuroinflammation 19, no. 1 (February 7, 2022). http://dx.doi.org/10.1186/s12974-022-02393-2.

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Abstract Background Alzheimer's disease (AD) is a neurodegenerative disease characterized by a progressive decline in cognitive ability. Exosomes derived from bone-marrow mesenchymal stem cells (BMSC-exos) are extracellular vesicles that can execute the function of bone-marrow mesenchymal stem cells (BMSCs). Given the versatile therapeutic potential of BMSC and BMSC-exos, especially their neuroprotective effect, the aim of this study was to investigate the potential effect of BMSC-exos on AD-like behavioral dysfunction in mice and explore the possible molecular mechanism. Methods BMSC-exos were extracted from the supernatant of cultured mouse BMSCs, which were isolated from the femur and tibia of adult C57BL/6 mice, purified and sorted via flow cytometry, and cultured in vitro. BMSC-exos were identified via transmission electron microscopy, and typical marker proteins of exosomes were also detected via Western blot. A sporadic AD mouse model was established by intracerebroventricular injection of streptozotocin (STZ). Six weeks later, BMSC-exos were administered via lateral ventricle injection or caudal vein injection lasting five consecutive days, and the control mice were intracerebroventricularly administered an equal volume of solvent. Behavioral performance was observed via the open field test (OFT), elevated plus maze test (EPM), novel object recognition test (NOR), Y maze test (Y-maze), and tail suspension test (TST). The mRNA and protein expression levels of IL-1β, IL-6, and TNF-α in the hippocampus were measured via quantitative polymerase chain reaction (qPCR) and Western blot, respectively. Moreover, the protein expression of Aβ1-42, BACE, IL-1β, IL-6, TNF-α, GFAP, p-Tau (Ser396), Tau5, synaptotagmin-1 (Syt-1), synapsin-1, and brain-derived neurotrophic factor (BDNF) in the hippocampus was detected using Western blot, and the expression of GFAP, IBA1, Aβ1−42 and DCX in the hippocampus was measured via immunofluorescence staining. Results Lateral ventricle administration, but not caudal vein injection of BMSC-exos improved AD-like behaviors in the STZ-injected mouse model, as indicated by the increased number of rearing, increased frequency to the central area, and increased duration and distance traveled in the central area in the OFT, and improved preference index of the novel object in the NOR. Moreover, the hyperactivation of microglia and astrocytes in the hippocampus of the model mice was inhibited after treatment with BMSC-exos via lateral ventricle administration, accompanied by the reduced expression of IL-1β, IL-6, TNF-α, Aβ1-42, and p-Tau and upregulated protein expression of synapse-related proteins and BDNF. Furthermore, the results of the Pearson test showed that the preference index of the novel object in the NOR was positively correlated with the hippocampal expression of BDNF, but negatively correlated with the expression of GFAP, IBA1, and IL-1β. Apart from a positive correlation between the hippocampal expression of BDNF and Syt-1, BDNF abundance was found to be negatively correlated with markers of glial activation and the expression of the inflammatory cytokines, Aβ1-42, and p-Tau, which are characteristic neuropathological features of AD. Conclusions Lateral ventricle administration, but not caudal vein injection of BMSC-exos, can improve AD-like behavioral performance in STZ-injected mice, the mechanism of which might be involved in the regulation of glial activation and its associated neuroinflammation and BDNF-related neuropathological changes in the hippocampus.

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