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Journal articles on the topic 'Transgenic mouse Tg2576'

Author: Grafiati

Published: 4 June 2021

Last updated: 19 February 2022

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1

Dobarro, Marta, Gorka Gerenu, and María J. Ramírez. "Propranolol reduces cognitive deficits, amyloid and tau pathology in Alzheimer's transgenic mice." International Journal of Neuropsychopharmacology 16, no. 10 (November 1, 2013): 2245–57. http://dx.doi.org/10.1017/s1461145713000631.

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Abstract The efficacy of antihypertensive agents in Alzheimer's disease (AD) is controversial. It has been tested here whether some antihypertensive drugs might influence AD through mechanisms independent of blood pressure-lowering activity. The effects of treatment with the antihypertensive propranolol on cognition and AD-related markers have been studied in the Tg2576 mouse model of AD. Propranolol, at a lower dose than that used as antihypertensive (5 mg/kg, 6 wk), attenuated cognitive impairments shown by Tg2576 mice aged 9 months in the novel object recognition and fear conditioning tests. Propranolol was also able to counteract the increases in hippocampal levels of Aβ42 present in Tg2576 mice. This effect was accompanied by an increased expression of insulin degrading enzyme. Changes in markers of synaptic pathology, as shown by decreases in phosphorylation of Akt and in the expression of BDNF in Tg2676 mice, were also counteracted by propranolol treatment. Tau hyperphosphorylation shown by Tg2576 mice was also decreased in the hippocampus of propranolol-treated mice, an effect probably related to an increase of GSK3β phosphorylation (inactive form) and a decreased JNK1 expression. Overall, these data further strengthen the potential of propranolol as a therapeutic agent for AD.

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2

Passos, Giselle F., Kelley Kilday, Daniel L. Gillen, David H. Cribbs, and Vitaly Vasilevko. "Experimental hypertension increases spontaneous intracerebral hemorrhages in a mouse model of cerebral amyloidosis." Journal of Cerebral Blood Flow & Metabolism 36, no. 2 (October 2, 2015): 399–404. http://dx.doi.org/10.1177/0271678x15606720.

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Hypertension and cerebral amyloid angiopathy (CAA) are major risk factors for intracerebral hemorrhage (ICH); however the mechanisms of interplay between the two are not fully understood. We investigated the effect of hypertension in a transgenic mouse model with Alzheimer’s-like pathology (Tg2576) treating them with angiontensin II and L-NG-nitroarginine methyl ester. A similar increase in systolic blood pressure was observed in both Tg2576 and control mice; however Tg2576 mice developed signs of stroke with a markedly shorter latency. Cerebral deposition of amyloid beta promotes the hypertension-induced ICH, thus supporting the notion that hypertension is a risk factor for ICH among patients with CAA.

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3

Toda, Toshihiko, Yoshihiro Noda, Genzo Ito, Masahiro Maeda, and Takahiko Shimizu. "Presenilin-2 Mutation Causes Early Amyloid Accumulation and Memory Impairment in a Transgenic Mouse Model of Alzheimer's Disease." Journal of Biomedicine and Biotechnology 2011 (2011): 1–12. http://dx.doi.org/10.1155/2011/617974.

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In order to clarify the pathophysiological role of presenilin-2 (PS2) carrying the Volga German Kindred mutation (N141I) in a conventional mouse model of Alzheimer's disease (AD) expressing amyloid precursor protein (APP) with the Swedish mutation (Tg2576 line), we generated a double transgenic mouse (PS2Tg2576) by crossbreeding the PS2 mutant with Tg2576 mice. Here, we demonstrate that the PS2 mutation induced the early deposition of amyloid β-protein (Aβ) at 2-3 months of age and progressive accumulation at 4-5 months of age in the brains of the mutant mice. The PS2 mutation also accelerated learning and memory impairment associated with Aβ accumulation at 4-5 months of age in Tg2576 mice. These results suggest that the PS2 mutation causes early cerebral amyloid accumulation and memory dysfunction. PS2Tg2576 mice are a suitable mouse model for studying amyloid-lowering therapies.

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4

Kishimoto, Yasushi, Kai Fukumoto, Mika Nagai, Ayaka Mizuguchi, and Yuiko Kobashi. "Early Contextual Fear Memory Deficits in a Double-Transgenic Amyloid-βPrecursor Protein/Presenilin 2 Mouse Model of Alzheimer’s Disease." International Journal of Alzheimer's Disease 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/8584205.

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Presenilin 1 and presenilin 2 (PS1 and PS2) play a critical role inγ-secretase-mediated cleavage of amyloid-βprecursor protein (APP) and the subsequent generation ofβ-amyloid peptides. The purpose of the present study was to test whether PS2 mutation accelerates the onset of contextual fear memory deficits in a mouse model of AD that expresses a mutation (K670N/M671L) of the human APP with the Swedish mutation (Tg2576 mice). In the present study, an APP/PS2 double-transgenic mouse model (PS2Tg2576) was generated by crossbreeding transgenic mice carrying the human mutant PS2 (N141I) with Tg2576 mice. Contextual fear conditioning was tested in PS2Tg2576 mice aged 3, 4, 6, and 10–12 months. PS2Tg2576 mice showed a tendency of lower freezing behavior as early as 3 months of age, but significant memory impairment was observed from the age of 4 months. The cognitive impairment was more prominent at ages of 6 and 10–12 months. In contrast, Tg2576 mice aged 3 and 4 months exhibited successful acquisition of contextual fear learning, but Tg2576 mice aged 6 months or older showed significantly impaired fear memory. These results show that PS2 mutation significantly accelerates the onset of fear memory deficits in the APP AD model mice.

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Portbury, Stuart D., Dominic J. Hare, Charlotte Sgambelloni, Kali Perronnes, Ashley J. Portbury, David I. Finkelstein, and Paul A. Adlard. "Trehalose Improves Cognition in the Transgenic Tg2576 Mouse Model of Alzheimer’s Disease." Journal of Alzheimer's Disease 60, no. 2 (September 18, 2017): 549–60. http://dx.doi.org/10.3233/jad-170322.

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6

Alexander, Gaukhman, Amanda Hanna, Vanida Serna, Linda Younkin, Steve Younkin, and Christopher Janus. "Increased aggression in males in transgenic Tg2576 mouse model of Alzheimer's disease." Behavioural Brain Research 216, no. 1 (January 2011): 77–83. http://dx.doi.org/10.1016/j.bbr.2010.07.016.

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7

Kim, Ka, Yoo-Hun Suh, and Keun-A. Chang. "Therapeutic Effects of Human Amniotic Epithelial Stem Cells in a Transgenic Mouse Model of Alzheimer’s Disease." International Journal of Molecular Sciences 21, no. 7 (April 10, 2020): 2658. http://dx.doi.org/10.3390/ijms21072658.

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Alzheimer’s disease (AD), a progressive neurodegenerative disorder, is characterized clinically by cognitive decline and pathologically by the development of amyloid plaques. AD is the most common cause of dementia among older people. However, there is currently no cure for AD. In this study, we aimed to elucidate the therapeutic effects of human amniotic epithelial stem cells (hAESCs) in a transgenic mouse model of AD. Tg2576 transgenic (Tg) mice underwent behavioral tests, namely the Morris water maze and Y-maze tests, to assess their cognitive function. In the Morris water maze test, hAESC-treated Tg mice exhibited significantly shorter escape latencies than vehicle-treated Tg mice. In the Y-maze test, hAESC-treated Tg mice exhibited significantly higher rate of spontaneous alteration than vehicle-treated Tg mice, while the total number of arm entries did not differ between the groups. Furthermore, Congo red staining revealed that hAESCs injection reduced the number of amyloid plaques present in the brains of Tg mice. Finally, beta-secretase (BACE) activity was significantly decreased in Tg mice at 60 min after hAESCs injection. In this study, we found that intracerebral injection of hAESCs alleviated cognitive impairment in a Tg2576 mouse model of AD. Our results indicate that hAESCs injection reduced amyloid plaques caused by reduced BACE activity. These results indicate that hAESCs may be a useful therapeutic agent for the treatment of AD-related memory impairment.

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8

O'Hare, Eugene, Tara Ardis, Deaglan Page, David I. C. Scopes, and Eun-Mee Kim. "AβPP-Overexpressing Transgenic Rat Model of Alzheimer's Disease Utilizing the Tg2576 Mouse Protocol." Journal of Alzheimer's Disease 37, no. 1 (August 20, 2013): 77–88. http://dx.doi.org/10.3233/jad-130212.

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9

Kohjima, Motoyuki, Yuxiang Sun, and Lawrence Chan. "Increased Food Intake Leads to Obesity and Insulin Resistance in the Tg2576 Alzheimer’s Disease Mouse Model." Endocrinology 151, no. 4 (February 22, 2010): 1532–40. http://dx.doi.org/10.1210/en.2009-1196.

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Recent studies suggest that hyperinsulinemia and insulin resistance are linked to Alzheimer’s disease (AD). In this study, we used Tg2576 transgenic (Tg) mice, a widely used transgenic mouse model for AD, to explore the relationship between increased amyloid β-peptide (Aβ) and insulin resistance. When fed a high-fat diet (HFD), Tg mice developed obesity and insulin resistance at 16 wk of age. Furthermore, HFD-fed Tg mice displayed abnormal feeding behavior and increased caloric intake with time. Although caloric intake of HFD-fed Tg mice was similar to that of normal diet-fed Tg or wild-type mice during 4 to 8 wk of age, it increased sharply at 12 wk, and went up further at 16 wk, which paralleled changes in the level of Aβ40 and Aβ42 in the brain of these mice. Limiting food intake in HFD-fed Tg mice by pair-feeding a caloric intake identical with that of normal diet-fed mice completely prevented the obesity and insulin intolerance of HFD-fed Tg mice. The hypothalamus of HFD-fed Tg mice had a significant decrease in the expression of the anorexigenic neuropeptide, brain-derived neurotrophic factor, at both the mRNA and protein levels. These findings suggest that the increased Aβ in the brain of HFD-fed Tg2576 mice is associated with reduced brain-derived neurotrophic factor expression, which led to abnormal feeding behavior and increased food intake, resulting in obesity and insulin resistance in these animals.

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10

Bigl, M., J. Apelt, E. A. Luschekina, C. Lange-Dohna, S. Roßner, and R. Schliebs. "Expression of β-secretase mRNA in transgenic Tg2576 mouse brain with Alzheimer plaque pathology." Neuroscience Letters 292, no. 2 (October 2000): 107–10. http://dx.doi.org/10.1016/s0304-3940(00)01452-x.

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11

Nojima, Jun, Azusa Maeda, Sho Aoki, Satoshi Suo, Dai Yanagihara, Yuichiro Watanabe, Taiji Yoshida, and Shoichi Ishiura. "Effect of rice-expressed amyloid β in the Tg2576 Alzheimer's disease transgenic mouse model." Vaccine 29, no. 37 (August 2011): 6252–58. http://dx.doi.org/10.1016/j.vaccine.2011.06.073.

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12

Chen, Liming. "P1-152: The changing of distribution and location of neuroglobin in Tg2576 transgenic mouse." Alzheimer's & Dementia 5, no. 4S_Part_7 (July 2009): P222. http://dx.doi.org/10.1016/j.jalz.2009.04.158.

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13

Hoogendoorn, Bastiaan, Darko Turic, Ed Dudley, Julia Grassl, Richard Abraham, Paul Hollingworth, Valentina Moskvina, et al. "P1-073: Protein profiling of the hippocampus of the Tg2576 transgenic AD mouse model." Alzheimer's & Dementia 2 (July 2006): S116. http://dx.doi.org/10.1016/j.jalz.2006.05.448.

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14

Salazar, Jose Gregorio, Judit Marsillach, Ingrid Reverte, Bharti Mackness, Michael Mackness, Jorge Joven, Jordi Camps, and Maria Teresa Colomina. "Paraoxonase-1 and -3 Protein Expression in the Brain of the Tg2576 Mouse Model of Alzheimer’s Disease." Antioxidants 10, no. 3 (February 24, 2021): 339. http://dx.doi.org/10.3390/antiox10030339.

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Background: Brain oxidative lipid damage and inflammation are common in neurodegenerative diseases such as Alzheimer’s disease (AD). Paraoxonase-1 and -3 (PON1 and PON3) protein expression was demonstrated in tissue with no PON1 or PON3 gene expression. In the present study, we examine differences in PON1 and PON3 protein expression in the brain of a mouse model of AD. Methods: we used peroxidase- and fluorescence-based immunohistochemistry in five brain regions (olfactory bulb, forebrain, posterior midbrain, hindbrain and cerebellum) of transgenic (Tg2576) mice with the Swedish mutation (KM670/671NL) responsible for a familial form of AD and corresponding wild-type mice. Results: We found intense PON1 and PON3-positive staining in star-shaped cells surrounding Aβ plaques in all the studied Tg2576 mouse-brain regions. Although we could not colocalize PON1 and PON3 with astrocytes (star-shaped cells in the brain), we found some PON3 colocalization with microglia. Conclusions: These results suggest that (1) PON1 and PON3 cross the blood–brain barrier in discoidal high-density lipoproteins (HDLs) and are transferred to specific brain-cell types; and (2) PON1 and PON3 play an important role in preventing oxidative stress and lipid peroxidation in particular brain-cell types (likely to be glial cells) in AD pathology and potentially in other neurodegenerative diseases as well.

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15

Chen, Zliming. "IC-P-099: The changing of distribution and location of neuroglobin in Tg2576 transgenic mouse." Alzheimer's & Dementia 5, no. 4S_Part_2 (July 2009): P43. http://dx.doi.org/10.1016/j.jalz.2009.05.653.

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16

Horgan, Jennifer, Jose Javier Miguel-Hidalgo, Martha Thrasher, and Garth Bissette. "Longitudinal Brain Corticotropin Releasing Factor and Somatostatin in a Transgenic Mouse (TG2576) Model of Alzheimer's Disease." Journal of Alzheimer's Disease 12, no. 2 (September 25, 2007): 115–27. http://dx.doi.org/10.3233/jad-2007-12201.

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17

Chang, Keun-A., Tae-Young Ha, Jeonga Kim, and Yoo-Hun Suh. "P4-170: The role of S100a9 in the neuroinflammation of Alzheimer's disease transgenic mouse model, Tg2576." Alzheimer's & Dementia 5, no. 4S_Part_16 (July 2009): P481. http://dx.doi.org/10.1016/j.jalz.2009.04.737.

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18

Wong, Ling Rong, Peiyan Wong, and Paul Chi-Lui Ho. "Metabolic Profiling of Female Tg2576 Mouse Brains Provides Novel Evidence Supporting Intranasal Low-Dose Pioglitazone for Long-Term Treatment at an Early Stage of Alzheimer’s Disease." Biomedicines 8, no. 12 (December 9, 2020): 589. http://dx.doi.org/10.3390/biomedicines8120589.

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Accumulating evidence suggests that disruptions in brain energy metabolism may be a key player in the pathogenesis of Alzheimer’s disease (AD). Pioglitazone (PIO) has been found to exert beneficial effects on metabolic dysfunction in many AD preclinical studies. However, limited success in clinical trials remains an obstacle to its development for the treatment of AD. PIO’s poor brain penetration was often cited as a contributing factor to the lack of clinical benefit. In this study, we prepared PIO-loaded poly(lactic-co-glycolic acid) (PLGA) nanoparticles and administered them as suspended nanoparticles via nebulization. Preliminary investigation of drug distribution to the brain revealed comparatively reduced systemic exposure after administering PIO nanoparticles via the intranasal route. In vitro, extracellular flux analysis showed significantly raised spare respiratory capacity when cells were treated with low-dose PIO nanoparticles. Tg2576 transgenic mice treated with low-dose PIO nanoparticles over four months exhibited an overall trend of reduced hyperactivity in open field tests but did not show any visible effect on alternation rates in the Y-maze task. Subsequent 1H NMR-based metabolic profiling of their plasma and different brain regions revealed differences in metabolic profiles in the cerebellum, cortex, and hippocampus of Tg2576 mice after long-term PIO treatment, but not in their midbrain and plasma. In particular, the specificity of PIO’s treatment effects on perturbed amino acid metabolism was observed in the cortex of transgenic mice with increases in alanine and N-acetylaspartate levels, supporting the notion that PIO treatment exerts beneficial effects on impaired energy metabolism associated with AD. In conclusion, inhalation exposure to PIO nanoparticles presents an exciting opportunity that this drug could be administered intranasally at a much lower dose while achieving a sufficient level in the brain to elicit metabolic benefits at an early stage of AD but with reduced systemic exposure.

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19

Van Ess, P. J., W. A. Pedersen, C. Culmsee, M. P. Mattson, and R. A. Blouin. "Elevated hepatic and depressed renal cytochrome P450 activity in the Tg2576 transgenic mouse model of Alzheimer's disease." Journal of Neurochemistry 80, no. 4 (February 2002): 571–78. http://dx.doi.org/10.1046/j.0022-3042.2001.00724.x.

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20

Watanabe, Takuya, Norito Yamagata, Kotaro Takasaki, Kazunori Sano, Kazuhide Hayakawa, Shutaro Katsurabayashi, Nobuaki Egashira, Kenichi Mishima, Katsunori Iwasaki, and Michihiro Fujiwara. "Decreased acetylcholine release is correlated to memory impairment in the Tg2576 transgenic mouse model of Alzheimer's disease." Brain Research 1249 (January 2009): 222–28. http://dx.doi.org/10.1016/j.brainres.2008.10.029.

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21

Seo, Hyeon Jeong, Jung Eun Park, Seong-Min Choi, Taekyoung Kim, Soo Hyun Cho, Kyung-Hwa Lee, Woo Keun Song, et al. "Inhibitory Neural Network’s Impairments at Hippocampal CA1 LTP in an Aged Transgenic Mouse Model of Alzheimer’s Disease." International Journal of Molecular Sciences 22, no. 2 (January 12, 2021): 698. http://dx.doi.org/10.3390/ijms22020698.

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Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a rapid accumulation of amyloid β (Aβ) protein in the hippocampus, which impairs synaptic structures and neuronal signal transmission, induces neuronal loss, and diminishes memory and cognitive functions. The present study investigated the impact of neuregulin 1 (NRG1)-ErbB4 signaling on the impairment of neural networks underlying hippocampal long-term potentiation (LTP) in 5xFAD mice, a model of AD with greater symptom severity than that of TG2576 mice. Specifically, we observed parvalbumin (PV)-containing hippocampal interneurons, the effect of NRG1 on hippocampal LTP, and the functioning of learning and memory. We found a significant decrease in the number of PV interneurons in 11-month-old 5xFAD mice. Moreover, synaptic transmission in the 5xFAD mice decreased at 6 months of age. The 11-month-old transgenic AD mice showed fewer inhibitory PV neurons and impaired NRG1-ErbB4 signaling than did wild-type mice, indicating that the former exhibit the impairment of neuronal networks underlying LTP in the hippocampal Schaffer-collateral pathway. In conclusion, this study confirmed the impaired LTP in 5xFAD mice and its association with aberrant NRG1-ErbB signaling in the neuronal network.

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22

Lattanzi, Roberta, Daniela Maftei, Carla Petrella, Massimo Pieri, Giulia Sancesario, Tommaso Schirinzi, Sergio Bernardini, et al. "Involvement of the Chemokine Prokineticin-2 (PROK2) in Alzheimer’s Disease: From Animal Models to the Human Pathology." Cells 8, no. 11 (November 13, 2019): 1430. http://dx.doi.org/10.3390/cells8111430.

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Among mediators of inflammation, chemokines play a pivotal role in the neuroinflammatory process related to Alzheimer’s disease (AD). The chemokine Bv8/prokineticin 2 (PROK2) is a critical player in inflammatory and neuroinflammatory diseases and has been demonstrated to be involved in Aβ toxicity. The aim of the present study was to extend the research to rats chronically intracerebroventricularly (i.c.v.) injected with Aβ, to an AD transgenic mouse model, and subsequently to AD patients, mainly with the aim of detecting a potential biomarker. Real-time PCR and immunofluorescence analysis were used to evaluate Prokineticin-2 (PROK2) mRNA and the corresponding protein levels in both animal and human AD brain extracts, and the ELISA test was used to measure the amount of PROK2 in the serum of AD patients. We demonstrated a significant upregulation of PROK2 levels in brain tissues of Aβ1–42 i.c.v. injected rats, transgenic AD mice (Tg2576), and in the hippocampus of AD patients. Additionally, through a pilot study, an approximate twofold increase of PROK2 levels has been proved in the serum of AD patients, compared to the control subjects, identifying a potential blood-based biomarker of the disease.

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23

Zhang, Zui, Yoshiko Takeda-Uchimura, Tahmina Foyez, Shiori Ohtake-Niimi, Narentuya, Hiroyasu Akatsu, Kazuchika Nishitsuji, et al. "Deficiency of a sulfotransferase for sialic acid-modified glycans mitigates Alzheimer’s pathology." Proceedings of the National Academy of Sciences 114, no. 14 (March 20, 2017): E2947—E2954. http://dx.doi.org/10.1073/pnas.1615036114.

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We previously showed that microglial keratan sulfate (KS) was induced in amyotrophic lateral sclerosis. However, the functional roles of the glycan and its synthetic enzyme in neurodegenerative diseases, such as Alzheimer’s disease (AD), a progressive disorder, are unclear. In our study, KS modified with sialic acids having a molecular mass of 125–220 kDa and the carbohydrate sulfotransferase GlcNAc6ST1 were up-regulated in the brains of two transgenic mouse models (J20 and Tg2576) and the brains of patients with AD. GlcNAc6ST1-deficient J20 (J20/GlcNAc6ST1−/−) mice demonstrated a complete absence of the microglial sialylated KS. J20/GlcNAc6ST1−/− primary microglia showed an increased level of amyloid-β phagocytosis and were hyperresponsive to interleukin 4, a potent antiinflammatory cytokine. Moreover, J20/GlcNAc6ST1−/− mice manifested reduced cerebral amyloid-β deposition. GlcNAc6ST1-synthesizing sialylated KS thus modulates AD pathology. Inhibition of KS synthesis by targeting GlcNAc6ST1 may therefore be beneficial for controlling AD pathogenesis.

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24

Subash, Selvaraju, Musthafa Mohamed Essa, Abdullah Al-Asmi, Samir Al-Adawi, and Ragini Vaishnav. "Chronic Dietary Supplementation of 4% Figs on the Modification of Oxidative Stress in Alzheimer’s Disease Transgenic Mouse Model." BioMed Research International 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/546357.

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We assessed the changes in the plasma Aβ, oxidative stress/antioxidants, and membrane bound enzymes in the cerebral cortex and hippocampus of Alzheimer’s disease (AD) transgenic mice (Tg2576) after dietary supplementation of Omani figs fruits for 15 months along with spatial memory and learning test. AD Tg mice on control diet without figs showed significant impairment in spatial learning ability compared to the wild-type mice on same diet and figs fed Tg mice as well. Significant increase in oxidative stress and reduced antioxidant status were observed in AD Tg mice. 4% figs treated AD Tg mice significantly attenuated oxidative damage, as evident by decreased lipid peroxidation and protein carbonyls and restoration of antioxidant status. Altered activities of membrane bound enzymes (Na+K+ATPase and acetylcholinesterase (AChE)) in AD Tg mice brain regions and was restored by figs treatment. Further, figs supplementation might be able to decrease the plasma levels of Aβ(1–40, 1–42) significantly in Tg mice suggesting a putative delay in the formation of plaques, which might be due to the presence of high natural antioxidants in figs. But this study warrants further extensive investigation to find a novel lead for a therapeutic target for AD from figs.

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Kent, Brianne A., Stephen M. Strittmatter, and Haakon B. Nygaard. "Sleep and EEG Power Spectral Analysis in Three Transgenic Mouse Models of Alzheimer’s Disease: APP/PS1, 3xTgAD, and Tg2576." Journal of Alzheimer's Disease 64, no. 4 (July 24, 2018): 1325–36. http://dx.doi.org/10.3233/jad-180260.

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26

Klingner, Margrit, Jenny Apelt, Ashok Kumar, Dietlind Sorger, Osama Sabri, Jörg Steinbach, Matthias Scheunemann, and Reinhard Schliebs. "Alterations in cholinergic and non-cholinergic neurotransmitter receptor densities in transgenic Tg2576 mouse brain with β-amyloid plaque pathology." International Journal of Developmental Neuroscience 21, no. 7 (October 21, 2003): 357–69. http://dx.doi.org/10.1016/j.ijdevneu.2003.08.001.

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Paul, Justin, Sidney Strickland, and Jerry P. Melchor. "Fibrin deposition accelerates neurovascular damage and neuroinflammation in mouse models of Alzheimer's disease." Journal of Experimental Medicine 204, no. 8 (July 30, 2007): 1999–2008. http://dx.doi.org/10.1084/jem.20070304.

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Cerebrovascular dysfunction contributes to the pathology and progression of Alzheimer's disease (AD), but the mechanisms are not completely understood. Using transgenic mouse models of AD (TgCRND8, PDAPP, and Tg2576), we evaluated blood–brain barrier damage and the role of fibrin and fibrinolysis in the progression of amyloid-β pathology. These mouse models showed age-dependent fibrin deposition coincident with areas of blood–brain barrier permeability as demonstrated by Evans blue extravasation. Three lines of evidence suggest that fibrin contributes to the pathology. First, AD mice with only one functional plasminogen gene, and therefore with reduced fibrinolysis, have increased neurovascular damage relative to AD mice. Conversely, AD mice with only one functional fibrinogen gene have decreased blood–brain barrier damage. Second, treatment of AD mice with the plasmin inhibitor tranexamic acid aggravated pathology, whereas removal of fibrinogen from the circulation of AD mice with ancrod treatment attenuated measures of neuroinflammation and vascular pathology. Third, pretreatment with ancrod reduced the increased pathology from plasmin inhibition. These results suggest that fibrin is a mediator of inflammation and may impede the reparative process for neurovascular damage in AD. Fibrin and the mechanisms involved in its accumulation and clearance may present novel therapeutic targets in slowing the progression of AD.

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Pappolla, M. A., E. Matsubara, R. Vidal, J. Pacheco-Quinto, B. Poeggeler, M. Zagorski, and K. Sambamurti. "Melatonin Treatment Enhances Aβ Lymphatic Clearance in a Transgenic Mouse Model of Amyloidosis." Current Alzheimer Research 15, no. 7 (May 9, 2018): 637–42. http://dx.doi.org/10.2174/1567205015666180411092551.

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Background: It has been postulated that inadequate clearance of the amyloid β protein (Aβ) plays an important role in the accumulation of Aβ in sporadic late onset Alzheimer's disease (AD). While the blood brain barrier (BBB) has taken the center stage in processes involving Aβ clearance, little information is available about the role of the lymphatic system. We previously reported that Aβ is cleared through the lymphatic system. We now assessed lymphatic Aβ clearance by treating a mouse model of AD amyloidosis with melatonin, an Aβ aggregation inhibitor and immuno-regulatory neurohormone. Objective: To confirm and expand our initial finding that Aβ is cleared through the lymphatic system. Lymphatic clearance of metabolic and cellular “waste” products from the brain into the peripheral lymphatic system has been known for a long time. However, except for our prior report, there is no additional experimental data published about Aβ being cleared into peripheral lymph nodes. Methods: For these experiments, we used a transgenic mouse model (Tg2576) that over-expresses a mutant form of the Aβ precursor protein (APP) in the brain. We examined levels of Aβ in plasma and in lymph nodes of transgenic mice as surrogate markers of vascular and lymphatic clearance, respectively. Aβ levels were also measured in the brain and in multiple tissues. Results: Clearance of Aβ peptides through the lymphatic system was confirmed in this study. Treatment with melatonin led to the following changes: 1-A statistically significant increase in soluble monomeric Aβ40 and an increasing trend in Aβ42 in cervical and axillary lymph nodes of treated mice. 2- Statistically significant decreases in oligomeric Aβ40 and a decreasing trend Aβ42 in the brain. Conclusion: The data expands on our prior report that the lymphatic system participates in Aβ clearance from the brain. We propose that abnormalities in Aβ clearance through the lymphatic system may contribute to the development of cerebral amyloidosis. Melatonin and related indole molecules (i.e., indole- 3-propionic acid) are known to inhibit Aβ aggregation although they do not reverse aggregated Aβ or amyloid fibrils. Therefore, these substances should be further explored in prevention trials for delaying the onset of cognitive impairment in high risk populations.

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Allué, José Antonio, Leticia Sarasa, María Izco, Virginia Pérez-Grijalba, Noelia Fandos, María Pascual-Lucas, Samuel Ogueta, Pedro Pesini, and Manuel Sarasa. "Outstanding Phenotypic Differences in the Profile of Amyloid-β between Tg2576 and APPswe/PS1dE9 Transgenic Mouse Models of Alzheimer’s Disease." Journal of Alzheimer's Disease 53, no. 3 (August 3, 2016): 773–85. http://dx.doi.org/10.3233/jad-160280.

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30

Kim, Tae-Kyung, Jung-Eun Lee, Sun-Kyu Park, Kang-Woo Lee, Ji-Seon Seo, Joo-Young Im, Sang-Tae Kim, et al. "Analysis of differential plaque depositions in the brains of Tg2576 and Tg-APPswe/PS1dE9 transgenic mouse models of Alzheimer disease." Experimental & Molecular Medicine 44, no. 8 (2012): 492. http://dx.doi.org/10.3858/emm.2012.44.8.056.

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31

Sly, L. M., R. F. Krzesicki, J. R. Brashler, A. E. Buhl, D. D. McKinley, D. B. Carter, and J. E. Chin. "Endogenous brain cytokine mRNA and inflammatory responses to lipopolysaccharide are elevated in the Tg2576 transgenic mouse model of Alzheimer’s disease." Brain Research Bulletin 56, no. 6 (December 2001): 581–88. http://dx.doi.org/10.1016/s0361-9230(01)00730-4.

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32

Kawarabayashi, Takeshi, Linda H. Younkin, Takaomi C. Saido, Mikio Shoji, Karen Hsiao Ashe, and Steven G. Younkin. "Age-Dependent Changes in Brain, CSF, and Plasma Amyloid β Protein in the Tg2576 Transgenic Mouse Model of Alzheimer's Disease." Journal of Neuroscience 21, no. 2 (January 15, 2001): 372–81. http://dx.doi.org/10.1523/jneurosci.21-02-00372.2001.

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33

Moncaster, Juliet, Noel Casey, Timothy Connelly, Mark Wojnarowicz, Olga Minaeva, Srikant Sarangi, and Lee Goldstein. "P2-250: High-resolution multi-elemental metallomic mapping of the brain in the tg2576 transgenic mouse model of Alzheimer's disease." Alzheimer's & Dementia 7 (July 2011): S391—S392. http://dx.doi.org/10.1016/j.jalz.2011.05.1113.

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34

Go, Jun, Sun Il Choi, Ji Eun Kim, Young Ju Lee, Moon Hwa Kwak, Eun Kyoung Koh, Sung Hwa Song, Ji Eun Sung, and Dae Youn Hwang. "Effect of Reserpine on the Behavioral Defects, Aβ-42 Deposition and NGF Metabolism in Tg2576 Transgenic Mouse Model for Alzheimer's Disease." Journal of Life Science 23, no. 6 (June 30, 2013): 812–24. http://dx.doi.org/10.5352/jls.2013.23.6.812.

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35

Comes, Gemma, Yasmina Manso, Anna Escrig, Olaya Fernandez-Gayol, Paula Sanchis, Amalia Molinero, Mercedes Giralt, Javier Carrasco, and Juan Hidalgo. "Influence of Transgenic Metallothionein-1 on Gliosis, CA1 Neuronal Loss, and Brain Metal Levels of the Tg2576 Mouse Model of Alzheimer’s Disease." International Journal of Molecular Sciences 18, no. 2 (January 26, 2017): 251. http://dx.doi.org/10.3390/ijms18020251.

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36

Zhang, Lei, Wei Lu, Lin Chen, Xuan Qiu, Chen Li, Chun-xia Huang, Xia Gong, et al. "The early changes in behavior and the myelinated fibers of the white matter in the Tg2576 transgenic mouse model of Alzheimer's disease." Neuroscience Letters 555 (October 2013): 112–17. http://dx.doi.org/10.1016/j.neulet.2013.09.030.

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37

Apelt, Jenny, Ashok Kumar, and Reinhard Schliebs. "Impairment of cholinergic neurotransmission in adult and aged transgenic Tg2576 mouse brain expressing the Swedish mutation of human β-amyloid precursor protein." Brain Research 953, no. 1-2 (October 2002): 17–30. http://dx.doi.org/10.1016/s0006-8993(02)03262-6.

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38

Sarsoza, Floyd, Tommy Saing, Rakez Kayed, Robert Dahlin, Malcolm Dick, Camille Broadwater-Hollifield, Scott Mobley, et al. "A fibril-specific, conformation-dependent antibody recognizes a subset of Aβ plaques in Alzheimer disease, Down syndrome and Tg2576 transgenic mouse brain." Acta Neuropathologica 118, no. 4 (April 10, 2009): 505–17. http://dx.doi.org/10.1007/s00401-009-0530-3.

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39

Reimers, Diana, Manuela Vallejo-Muñoz, María José Casarejos, Adriano Jimenez-Escrig, Rafael Gonzalo-Gobernado, and Eulalia Bazan. "Immunohistochemical Study of ASC Expression and Distribution in the Hippocampus of an Aged Murine Model of Alzheimer’s Disease." International Journal of Molecular Sciences 22, no. 16 (August 13, 2021): 8697. http://dx.doi.org/10.3390/ijms22168697.

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Neuroinflammation is involved in the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease (AD), and is notably dependent on age. One important inflammatory pathway exerted by innate immune cells of the nervous system in response to danger signals is mediated by inflammasomes (IF) and leads to the generation of potent pro-inflammatory cytokines. The protein “apoptosis-associated speck-like protein containing a caspase recruitment domain” (ASC) modulates IF activation but has also other functions which are crucial in AD. We intended to characterize immunohistochemically ASC and pattern recognition receptors (PRR) of IF in the hippocampus (HP) of the transgenic mouse model Tg2576 (APP), in which amyloid-beta (Aβ) pathology is directly dependent on age. We show in old-aged APP a significant amount of ASC in microglia and astrocytes associated withAβ plaques, in the absence of PRR described by others in glial cells. In addition, APP developed foci with clusters of extracellular ASC granules not spatiallyrelated to Aβ plaques, which density correlated with the advanced age of mice and AD development. Clusters were associated withspecific astrocytes characterized by their enlarged ring-shaped process terminals, ASC content, and frequent perivascular location. Their possible implication in ASC clearance and propagation of inflammation is discussed.

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Wang, Fu-Hua, Paulina Appelkvist, Tomas Klason, Olle Gissberg, Anna Bogstedt, Kristina Eliason, Stefan Martinsson, et al. "Decreased axonal transport rates in the Tg2576 APP transgenic mouse: improvement with the gamma-secretase inhibitor MRK-560 as detected by manganese-enhanced MRI." European Journal of Neuroscience 36, no. 9 (September 10, 2012): 3165–72. http://dx.doi.org/10.1111/j.1460-9568.2012.08258.x.

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41

Nicolle, Michelle M., Mona L. Watson, Joseph A. McQuail, Kumar Sambamurti, Ashley E. Brady, Carrie Jones, P. Jeffrey Conn, and Craig W. Lindsey. "P3-276: Acute administration of a novel M1 receptor allosteric potentiator (BQCA) restores reversal learning in a transgenic mouse model of Alzheimer's disease (Tg2576)." Alzheimer's & Dementia 5, no. 4S_Part_14 (July 2009): P424. http://dx.doi.org/10.1016/j.jalz.2009.04.947.

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Bürger, Susanne, Monika Noack, Ludmil P. Kirazov, Evgeni P. Kirazov, Cyrill L. Naydenov, Elena Kouznetsova, Yousef Yafai, and Reinhard Schliebs. "Vascular endothelial growth factor (VEGF) affects processing of amyloid precursor protein and β‐amyloidogenesis in brain slice cultures derived from transgenic Tg2576 mouse brain." International Journal of Developmental Neuroscience 27, no. 6 (July 7, 2009): 517–23. http://dx.doi.org/10.1016/j.ijdevneu.2009.06.011.

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43

Chang, Kang-Wei, Shih-Ying Lee, and Chia-Chieh Chen. "Transgenic Mouse (Tg2576) Is an Ideal Model for the Biological Characterization of [<sup>18</sup>F]-FDDNP for Identifying Alzheimer’s Disease." Journal of Biosciences and Medicines 03, no. 12 (2015): 1–6. http://dx.doi.org/10.4236/jbm.2015.312001.

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44

Hartlage-Rübsamen, Maike, Jenny Apelt, and Reinhard Schliebs. "Fibrillary beta-amyloid deposits are closely associated with atrophic nitric oxide synthase (NOS)-expressing neurons but do not upregulate the inducible NOS in transgenic Tg2576 mouse brain with Alzheimer pathology." Neuroscience Letters 302, no. 2-3 (April 2001): 73–76. http://dx.doi.org/10.1016/s0304-3940(01)01652-4.

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45

Apelt, Jenny, Katrin Ach, and Reinhard Schliebs. "Aging-related down-regulation of neprilysin, a putative β-amyloid-degrading enzyme, in transgenic Tg2576 Alzheimer-like mouse brain is accompanied by an astroglial upregulation in the vicinity of β-amyloid plaques." Neuroscience Letters 339, no. 3 (March 2003): 183–86. http://dx.doi.org/10.1016/s0304-3940(03)00030-2.

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46

Latvala, Sari, Bjoern Jacobsen, Michael B. Otteneder, Annika Herrmann, and Sven Kronenberg. "Distribution of FcRn Across Species and Tissues." Journal of Histochemistry & Cytochemistry 65, no. 6 (April 12, 2017): 321–33. http://dx.doi.org/10.1369/0022155417705095.

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The neonatal Fc receptor (FcRn) is a major histocompatibility complex class I type molecule that binds to, transports, and recycles immunoglobulin G (IgG) and albumin, thereby protecting them from lysosomal degradation. Therefore, besides the knowledge of FcRn affinity, FcRn protein expression is critical in understanding the pharmacokinetic behavior of Fc-containing biotherapeutics such as monoclonal antibodies. The goal of this investigation was to achieve for the first time a comparative assessment of FcRn distribution across a variety of tissues and species. FcRn was mapped in about 20 tissues including placenta from human and the most frequently used species in non-clinical safety testing of monoclonal antibodies (mouse, rat, cynomolgus monkey). In addition, the FcRn expression pattern was characterized in two humanized transgenic mouse lines (Tg32 and Tg276) expressing human FcRn under different promoters, and in the severe combined immunodeficient (SCID) mouse. Consecutive sections were stained with specific markers, namely, anti-CD68 for macrophages and anti–von Willebrand Factor for endothelial cells. Overall, the FcRn expression pattern was comparable across species and tissues with consistent expression of FcRn in endothelial cells and interstitial macrophages, Kupffer cells, alveolar macrophages, enterocytes, and choroid plexus epithelium. The human FcRn transgenic mouse Tg276 showed a different and much more widespread staining pattern of FcRn. In addition, immunodeficiency and lack of IgG in SCID mice had no negative effect on FcRn expression compared with wild-type mice.

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47

Arora, Shitij, Mohammad Husain, Dileep Kumar, Hitesh Patni, Shresh Pathak, Devi Mehrotra, Vivek Kathi Reddy, et al. "Human immunodeficiency virus downregulates podocyte apoE expression." American Journal of Physiology-Renal Physiology 297, no. 3 (September 2009): F653—F661. http://dx.doi.org/10.1152/ajprenal.90668.2008.

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Apolipoprotein E ( apoE) has been demonstrated to play an important role in providing protection against mesangial cell injury. In the present study, we evaluated the role of apoE and its associated downstream effects in human immunodeficiency virus (HIV)-associated nephropathy (HIVAN). Control ( n = 6) and age- and sex-matched HIV-1 transgenic mice (Tg26, n = 6) were evaluated for their renal cortical expression of apoE. Renal tissue from Tg26 mice not only showed decreased apoE expression but also displayed downregulation of perlecan mRNA expression. In in vitro studies, conditionally immortalized human podocytes (CIHPs) were transduced with either NL4-3HIV (an HIV-1 construct lacking gag and pol, used for the development of Tg26 mouse model; NL4-3/CIHP) or empty vector (EV/CIHP); NL4-3/CIHPs and EV/CIHPs were studied for apoE mRNA expression. NL4-3/CIHPs showed reduction in apoE expression compared with EV/CIHPs. To evaluate the role of HIV-1 genes in the modulation of apoE expression, conditionally immortalized mouse podocytes (CIMPs) were transduced with individual HIV-1 gene constructs. Only nef-transduced CIMPs showed a decrease in apoE expression. To confirm this effect of nef in CIHPs, microarray analysis was performed in stable colonies of nef/CIHPs and EV/CIHPs. nef/CIHPs showed a 60% decrease in apoE and a 90% reduction in heparan sulfate mRNA expression. Moreover, nef transgenic mice showed a decrease in renal tissue expression of both apoE and perlecan. Both Tg26 and nef transgenic mice also showed areas of mesangial cell proliferation. These findings suggest that HIV-1-induced reduction in podocyte apoE expression and associated downregulation of podocyte perlecan might be contributing to mesangial cell (MC) phenotype in HIVAN.

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Carroll, Virginia A., Mark K. Lafferty, Luigi Marchionni, Joseph L. Bryant, Robert C. Gallo, and Alfredo Garzino-Demo. "Expression of HIV-1 matrix protein p17 and association with B-cell lymphoma in HIV-1 transgenic mice." Proceedings of the National Academy of Sciences 113, no. 46 (October 31, 2016): 13168–73. http://dx.doi.org/10.1073/pnas.1615258113.

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HIV-1 infection is associated with increased risk for B-cell lymphomas. How HIV infection promotes the development of lymphoma is unclear, but it may involve chronic B-cell activation, inflammation, and/or impaired immunity, possibly leading to a loss of control of oncogenic viruses and reduced tumor immunosurveillance. We hypothesized that HIV structural proteins may contribute to lymphomagenesis directly, because they can persist long term in lymph nodes in the absence of viral replication. The HIV-1 transgenic mouse Tg26 carries a noninfectious HIV-1 provirus lacking part of the gag-pol region, thus constituting a model for studying the effects of viral products in pathogenesis. Approximately 15% of Tg26 mice spontaneously develop leukemia/lymphoma. We investigated which viral proteins are associated with the development of leukemia/lymphoma in the Tg26 mouse model, and performed microarray analysis on RNA from spleen and lymph nodes to identify potential mechanisms of lymphomagenesis. Of the viral proteins examined, only expression of HIV-1 matrix protein p17 was associated with leukemia/lymphoma development and was highly expressed in bone marrow before disease. The tumor cells resembled pro-B cells, and were CD19+IgM−IgD−CD93+CD43+CD21−CD23−VpreB+CXCR4+. Consistent with the pro-B-cell stage of B-cell development, microarray analysis revealed enrichment of transcripts, including Rag1, Rag2, CD93, Vpreb1, Vpreb3, and Igll1. We confirmed RAG1 expression in Tg26 tumors, and hypothesized that HIV-1 matrix protein p17 may directly induce RAG1 in B cells. Stimulation of human activated B cells with p17 enhanced RAG1 expression in three of seven donors, suggesting that intracellular signaling by p17 may lead to genomic instability and transformation.

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Tremblay, Patrick, Haydn L. Ball, Kiyotoshi Kaneko, Darlene Groth, Ramanujan S. Hegde, Fred E. Cohen, Stephen J. DeArmond, Stanley B. Prusiner, and Jiri G. Safar. "Mutant PrPSc Conformers Induced by a Synthetic Peptide and Several Prion Strains." Journal of Virology 78, no. 4 (February 15, 2004): 2088–99. http://dx.doi.org/10.1128/jvi.78.4.2088-2099.2004.

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ABSTRACT Gerstmann-Sträussler-Scheinker (GSS) disease is a dominantly inherited, human prion disease caused by a mutation in the prion protein (PrP) gene. One mutation causing GSS is P102L, denoted P101L in mouse PrP (MoPrP). In a line of transgenic mice denoted Tg2866, the P101L mutation in MoPrP produced neurodegeneration when expressed at high levels. MoPrPSc(P101L) was detected both by the conformation-dependent immunoassay and after protease digestion at 4°C. Transmission of prions from the brains of Tg2866 mice to those of Tg196 mice expressing low levels of MoPrP(P101L) was accompanied by accumulation of protease-resistant MoPrPSc(P101L) that had previously escaped detection due to its low concentration. This conformer exhibited characteristics similar to those found in brain tissue from GSS patients. Earlier, we demonstrated that a synthetic peptide harboring the P101L mutation and folded into a β-rich conformation initiates GSS in Tg196 mice (29). Here we report that this peptide-induced disease can be serially passaged in Tg196 mice and that the PrP conformers accompanying disease progression are conformationally indistinguishable from MoPrPSc(P101L) found in Tg2866 mice developing spontaneous prion disease. In contrast to GSS prions, the 301V, RML, and 139A prion strains produced large amounts of protease-resistant PrPSc in the brains of Tg196 mice. Our results argue that MoPrPSc(P101L) may exist in at least several different conformations, each of which is biologically active. Such conformations occurred spontaneously in Tg2866 mice expressing high levels of MoPrPC(P101L) as well as in Tg196 mice expressing low levels of MoPrPC(P101L) that were inoculated with brain extracts from ill Tg2866 mice, with a synthetic peptide with the P101L mutation and folded into a β-rich structure, or with prions recovered from sheep with scrapie or cattle with bovine spongiform encephalopathy.

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50

Salhan, Divya, Shresh Pathak, Mohammad Husain, Pranai Tandon, Dileep Kumar, Ashwani Malhotra, Leonard G. Meggs, and Pravin C. Singhal. "HIV gene expression deactivates redox-sensitive stress response program in mouse tubular cells both in vitro and in vivo." American Journal of Physiology-Renal Physiology 302, no. 1 (January 1, 2012): F129—F140. http://dx.doi.org/10.1152/ajprenal.00024.2011.

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Human immunodeficiency virus (HIV)-1 has been reported to cause tubular cell injury both in in vivo and in vitro studies. In the present study, we evaluated the role of oxidative stress in the induction of apoptosis in HIV gene expressing mouse tubular cells in in vivo (Tg26, a transgenic mouse model of HIV-associated nephropathy) and in vitro (tubular cells were transduced with pNL4-3: ΔG/P-GFP, VSV.G psueudo typed virus) studies. Although Tg26 mice showed enhanced tubular cell reactive oxygen species (ROS) generation and apoptosis, renal tissue did not display a robust antioxidant response in the form of enhanced free radical scavenger (MnSOD/catalase) expression. Tg26 mice not only showed enhanced tubular cell expression of phospho-p66ShcA but also displayed nuclear Foxo3a translocation to the cytoplasm. These findings indicated deactivation of tubular cell Foxo3A-dependent redox-sensitive stress response program (RSSRP) in Tg26 mice. In in vitro studies, NL4-3 (pNL4-3: ΔG/P-GFP, VSV.G pseudotyped virus)-transduced mouse proximal tubular cells (NL4-3/MPTEC) displayed enhanced phosphorylation of p66ShcA. NL4-3/MPTECs also displayed greater ( P < 0.01) ROS generation when compared with empty vector-transduced tubular cells; however, both diminution of p66ShcA and N-acetyl cysteine attenuated NL4-3-induced tubular cell ROS generation as well as apoptosis. In addition, both antioxidants and free radical scavengers partially inhibited HIV-induced tubular cell apoptosis. NL4-3/MPTEC displayed deactivation of RSSRP in the form of enhanced phosphorylation of Foxo3A and attenuated expression of superoxide dismutase (SOD) and catalase. Since both SOD and catalase were able to provide protection against HIV-1-induced tubular cell apoptosis, it suggests that HIV-1-induced proapoptotic effect may be a consequence of the deactivated RSSRP.

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