Journal articles: 'Amyloid beta deposition'

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Head, Elizabeth, and Ira T. Lott. "Down syndrome and beta-amyloid deposition." Current Opinion in Neurology 17, no. 2 (April 2004): 95–100. http://dx.doi.org/10.1097/00019052-200404000-00003.

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Vlassenko, Andrei, Tyler Blazey, Yi Su, Chengjie Xiong, Tammie Benzinger, and John Morris. "P2-204: Regional beta-amyloid deposition several years prior to beta-amyloid positivity." Alzheimer's & Dementia 9 (July 2013): P431—P432. http://dx.doi.org/10.1016/j.jalz.2013.05.850.

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Rodrigue, Karen M., Kristen M. Kennedy, and Denise C. Park. "Beta-Amyloid Deposition and the Aging Brain." Neuropsychology Review 19, no. 4 (November 12, 2009): 436–50. http://dx.doi.org/10.1007/s11065-009-9118-x.

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Stein, Thor D., Philip H. Montenigro, Victor E. Alvarez, Weiming Xia, John F. Crary, Yorghos Tripodis, Daniel H. Daneshvar, et al. "Beta-amyloid deposition in chronic traumatic encephalopathy." Acta Neuropathologica 130, no. 1 (May 6, 2015): 21–34. http://dx.doi.org/10.1007/s00401-015-1435-y.

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Shin, Soo Jung, Yuon Jeong, Seong Gak Jeon, Sujin Kim, Seong-kyung Lee, Hong Seok Choi, Cheong Su Im, et al. "Uncaria rhynchophylla ameliorates amyloid beta deposition and amyloid beta-mediated pathology in 5XFAD mice." Neurochemistry International 121 (December 2018): 114–24. http://dx.doi.org/10.1016/j.neuint.2018.10.003.

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Bubak, Andrew N., Christina N. Como, James E. Hassell, Teresa Mescher, Seth E. Frietze, Christy S. Niemeyer, Randall J. Cohrs, and Maria A. Nagel. "Targeted RNA Sequencing of VZV-Infected Brain Vascular Adventitial Fibroblasts Indicates That Amyloid May Be Involved in VZV Vasculopathy." Neurology - Neuroimmunology Neuroinflammation 9, no. 1 (November 10, 2021): e1103. http://dx.doi.org/10.1212/nxi.0000000000001103.

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Background and ObjectivesCompared with stroke controls, patients with varicella zoster virus (VZV) vasculopathy have increased amyloid in CSF, along with increased amylin (islet amyloid polypeptide [IAPP]) and anti-VZV antibodies. Thus, we examined the gene expression profiles of VZV-infected primary human brain vascular adventitial fibroblasts (HBVAFs), one of the initial arterial cells infected in VZV vasculopathy, to determine whether they are a potential source of amyloid that can disrupt vasculature and potentiate inflammation.MethodsMock- and VZV-infected quiescent HBVAFs were harvested at 3 days postinfection. Targeted RNA sequencing of the whole-human transcriptome (BioSpyder Technologies, TempO-Seq) was conducted followed by gene set enrichment and pathway analysis. Selected pathways unique to VZV-infected cells were confirmed by enzyme-linked immunoassays, migration assays, and immunofluorescence analysis (IFA) that included antibodies against amylin and amyloid-beta, as well as amyloid staining by Thioflavin-T.ResultsCompared with mock, VZV-infected HBVAFs had significantly enriched gene expression pathways involved in vascular remodeling and vascular diseases; confirmatory studies showed secretion of matrix metalloproteinase-3 and -10, as well increased migration of infected cells and uninfected cells when exposed to conditioned media from VZV-infected cells. In addition, significantly enriched pathways involved in amyloid-associated diseases (diabetes mellitus, amyloidosis, and Alzheimer disease), tauopathy, and progressive neurologic disorder were identified; predicted upstream regulators included amyloid precursor protein, apolipoprotein E, microtubule-associated protein tau, presenilin 1, and IAPP. Confirmatory IFA showed that VZV-infected HBVAFs contained amyloidogenic peptides (amyloid-beta and amylin) and intracellular amyloid.DiscussionGene expression profiles and pathway enrichment analysis of VZV-infected HBVAFs, as well as phenotypic studies, reveal features of pathologic vascular remodeling (e.g., increased cell migration and changes in the extracellular matrix) that can contribute to cerebrovascular disease. Furthermore, the discovery of amyloid-associated transcriptional pathways and intracellular amyloid deposition in HBVAFs raise the possibility that VZV vasculopathy is an amyloid disease. Amyloid deposition may contribute to cell death and loss of vascular wall integrity, as well as potentiate chronic inflammation in VZV vasculopathy, with disease severity and recurrence determined by the host's ability to clear virus infection and amyloid deposition and by the coexistence of other amyloid-associated diseases (i.e., Alzheimer disease and diabetes mellitus).

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Brancaccio, D., G. M. Ghiggeri, P. Braidotti, A. Garberi, M. Gallieni, V. Bellotti, U. Zoni, R. Gusmano, and G. Coggi. "Deposition of kappa and lambda light chains in amyloid filaments of dialysis-related amyloidosis." Journal of the American Society of Nephrology 6, no. 4 (October 1995): 1262–70. http://dx.doi.org/10.1681/asn.v641262.

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beta 2-Microglobulin (beta 2m) is considered to be the amyloidogenic precursor in dialysis-related amyloidosis, although the implication of other relevant cofactors in the pathogenesis of this disease has also been hypothesized. It is conceivable that substances found in amyloid deposits might represent something more than simple codeposition, possibly playing a pathogenic role in amyloidogenesis. Along these lines, a detailed analysis of the protein composition of amyloid fibrils purified from synovial material surgically obtained from nine patients on long-term dialysis was carried out. By the use of sodium dodecyl sulfate-polyacrylamide gel electrophoresis, several other protein components, in addition to beta 2m, were found. These were characterized by NH2 amino-terminal sequencing and immunoblotting. In fibrils obtained by water extraction, which fulfill the electron microscopy criteria of highly pure amyloid material, polyclonal kappa and lambda light chains were detected with a concentration of 15 micrograms/mL in the water extraction material; the beta 2m concentration was 200 micrograms/mL. Light microscopy immunohistochemistry was performed on samples from five patients. Amyloid deposits reacted with anti-beta 2m, and anti-light (kappa, lambda), chain antibodies. The immunoreaction of amyloid filaments to anti-beta 2m, anti-lambda, and anti-kappa light chain antibodies was also tested by electron microscopy by use of the immunogold staining procedure. Amyloid filaments were labeled by the three antibodies and showed a different intensity of immunostaining apparently related to their different aggregation pattern. These observations demonstrate that polyclonal immunoglobulin light chains (kappa and lambda) are not contaminants but, together with beta 2m, represent a major constituent of amyloid deposits in dialysis-related osteoarticular amyloidosis, thus indicating their possible role in amyloidogenesis.

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MOON, MARY ANN. "Alzheimer's Allele Related to Early Beta-Amyloid Deposition." Clinical Psychiatry News 34, no. 10 (October 2006): 31. http://dx.doi.org/10.1016/s0270-6644(06)71805-7.

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Costassa, E. V., G. Zanusso, F. Ingravalle, S. Peletto, M. N. Chieppa, M. Gallo, C. Palmitessa, et al. "Characterization of Beta Amyloid Deposition in Cattle Brain." Journal of Comparative Pathology 146, no. 1 (January 2012): 61. http://dx.doi.org/10.1016/j.jcpa.2011.11.063.

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Marano, Christopher, Clifford Workman, Christopher Lyman, Tova Narrow, Yun Zhou, Cynthia Munro, Robert Dannals, et al. "Cortical Beta-Amyloid Deposition in Late-Life Depression." American Journal of Geriatric Psychiatry 21, no. 3 (March 2013): S127. http://dx.doi.org/10.1016/j.jagp.2012.12.169.

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Wang, S. M., D. W. Kang, Y. H. Um, N. Y. Kim, and H. K. Lim. "Plasma oligomeric beta-amyloid is associated with cerebral beta-amyloid deposition in cognitively normal older adults." Gerontechnology 21, s (October 23, 2022): 3. http://dx.doi.org/10.4017/gt.2022.21.s.822.3.sp3.

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Risacher, Shannon L., Noelia Fandos, Judith Romero, Ian Sherriff, Pedro Pesini, Andrew J. Saykin, and Liana G. Apostolova. "Plasma amyloid beta levels are associated with cerebral amyloid and tau deposition." Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring 11, no. 1 (July 27, 2019): 510–19. http://dx.doi.org/10.1016/j.dadm.2019.05.007.

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Jensen, P. H., E. S. Sørensen, T. E. Petersen, J. Gliemann, and L. K. Rasmussen. "Residues in the synuclein consensus motif of the α-synuclein fragment, NAC, participate in transglutaminase-catalysed cross-linking to Alzheimer-disease amyloid βA4 peptide." Biochemical Journal 310, no. 1 (August 15, 1995): 91–94. http://dx.doi.org/10.1042/bj3100091.

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The widespread deposition of amyloid plaques is one of the hallmarks of Alzheimer disease (AD). A recently described component of amyloid plaques is the 35-residue peptide, non-A beta component of AD amyloid, which is derived from a larger intracellular neuronal constituent, alpha-synuclein. We demonstrate that transglutaminase catalyses the formation of the covalent non-A beta component of AD amyloid polymers in vitro as well as polymers with beta-amyloid peptide, the major constituent of AD plaques. The transglutaminase-reactive amino acid residues in the non-A beta component of AD amyloid were identified as Gln79 and Lys80. Lys80 is localized in a consensus motif Lys-Thr-Lys-Glu-Gly-Val, which is conserved in the synuclein gene family. Thus transglutaminase might be involved in the formation of insoluble amyloid deposits and participate in the modification of other members of the synuclein family.

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Jalkute, Chidambar B., Sagar H. Barage, and Kailas D. Sonawane. "Insight into molecular interactions of Aβ peptide and gelatinase from Enterococcus faecalis: a molecular modeling approach." RSC Advances 5, no. 14 (2015): 10488–96. http://dx.doi.org/10.1039/c4ra09354b.

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Friedland, Robert P., Joseph D. McMillan, and Zimple Kurlawala. "What Are the Molecular Mechanisms by Which Functional Bacterial Amyloids Influence Amyloid Beta Deposition and Neuroinflammation in Neurodegenerative Disorders?" International Journal of Molecular Sciences 21, no. 5 (February 28, 2020): 1652. http://dx.doi.org/10.3390/ijms21051652.

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Despite the enormous literature documenting the importance of amyloid beta (Ab) protein in Alzheimer's disease, we do not know how Ab aggregation is initiated and why it has its unique distribution in the brain. In vivo and in vitro evidence has been developed to suggest that functional microbial amyloid proteins produced in the gut may cross-seed Ab aggregation and prime the innate immune system to have an enhanced and pathogenic response to neuronal amyloids. In this commentary, we summarize the molecular mechanisms by which the microbiota may initiate and sustain the pathogenic processes of neurodegeneration in aging.

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Gentile, M. T., R. Poulet, A. Maffei, G. Russo, and G. Lembo. "HYPERTENSION INDUCES BETA AMYLOID DEPOSITION IN SELECTED BRAIN AREAS." Journal of Hypertension 22, Suppl. 2 (June 2004): S292. http://dx.doi.org/10.1097/00004872-200406002-01014.

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Yamada, T., Y. Tsuboi, and M. Takahashi. "Interrelationship between Beta-Amyloid Deposition and Complement-Activated Oligodendroglia." Dementia and Geriatric Cognitive Disorders 8, no. 5 (1997): 267–72. http://dx.doi.org/10.1159/000106643.

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Rutgers, Kim S., Alexandra van Remoortere, Mark A. van Buchem, C. Theo Verrips, Steven M. Greenberg, Brian J. Bacskai, Matthew P. Frosch, Sjoerd G. van Duinen, Marion L. Maat-Schieman, and Silvère M. van der Maarel. "Differential recognition of vascular and parenchymal beta amyloid deposition." Neurobiology of Aging 32, no. 10 (October 2011): 1774–83. http://dx.doi.org/10.1016/j.neurobiolaging.2009.11.012.

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Kim, Jinhee, Christine Ghadery, Sang Soo Cho, Alexander Mihaescu, Leigh Christopher, Mikaeel Valli, Sylvain Houle, and Antonio P. Strafella. "Network Patterns of Beta-Amyloid Deposition in Parkinson’s Disease." Molecular Neurobiology 56, no. 11 (May 20, 2019): 7731–40. http://dx.doi.org/10.1007/s12035-019-1625-z.

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Vieira, Daniela, João Durães, Inês Baldeiras, Beatriz Santiago, Diana Duro, Marisa Lima, Maria João Leitão, Miguel Tábuas-Pereira, and Isabel Santana. "Lower CSF Amyloid-Beta1–42 Predicts a Higher Mortality Rate in Frontotemporal Dementia." Diagnostics 9, no. 4 (October 25, 2019): 162. http://dx.doi.org/10.3390/diagnostics9040162.

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Frontotemporal lobar degeneration, the neuropathological substrate of frontotemporal dementia (FTD), is characterized by the deposition of protein aggregates, including tau. Evidence has shown concomitant amyloid pathology in some of these patients, which seems to contribute to a more aggressive disease. Our aim was to evaluate cerebrospinal fluid (CSF) amyloid-beta as a predictor of the mortality of FTD patients. We included 99 patients diagnosed with FTD—both behavioral and language variants—with no associated motor neuron disease, from whom a CSF sample was collected. These patients were followed prospectively in our center, and demographic and clinical data were obtained. The survival analysis was carried through a Cox regression model. Patients who died during follow up had a significantly lower CSF amyloid-beta1–42 than those who did not. The survival analysis demonstrated that an increased death rate was associated with a lower CSF amyloid-beta1–42 (HR = 0.999, 95% CI = [0.997, 1.000], p = 0.049). Neither demographic nor clinical variables, nor CSF total tau or p-tau were significantly associated with this endpoint. These results suggest that amyloid deposition in FTD patients may be associated with a higher mortality.

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Armstrong, Nicole, Yurun Cai, Hang Wang, Jennifer Schrack, Yuri Agrawal, Eleanor Simonsick, and Susan Resnick. "Sensory Impairment and Beta-Amyloid Deposition in the Baltimore Longitudinal Study of Aging." Innovation in Aging 5, Supplement_1 (December 1, 2021): 437. http://dx.doi.org/10.1093/geroni/igab046.1698.

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Abstract Studies have demonstrated a link between sensory impairment and dementia risk, but little is known about the presence of beta-amyloid plaques in individuals with single and multisensory impairments. Sensory function (combinations of vision, hearing, vestibular function, and proprioception) and amyloid PET imaging were measured in 170 BLSA participants (age=78± 9 years; 53% women; 77% white; 28% amyloid positive) from 2012 to 2019. Log-binomial regression models were used to examine the prevalence ratios (PR) of amyloid positivity for individual sensory impairments and across categories of impairments. While crude associations indicate associations of vision impairment (PR=1.72, p=0.04) and impairments in all four senses (PR=2.38, p=0.03) with amyloid positivity, these associations were insignificant after adjusting for age, sex, race, and education. There were no other crude and adjusted associations. These results suggest sensory impairments may be related to dementia independent of AD pathology. Future studies with larger sample sizes are warranted.

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Peters, Douglas G., Alexis N. Pollack, Keith C. Cheng, Dongxiao Sun, Takaomi Saido, Michael P. Haaf, Qing X. Yang, James R. Connor, and Mark D. Meadowcroft. "Dietary lipophilic iron alters amyloidogenesis and microglial morphology in Alzheimer's disease knock-in APP mice." Metallomics 10, no. 3 (2018): 426–43. http://dx.doi.org/10.1039/c8mt00004b.

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Carter, Chris. "Alzheimer's Disease: APP, Gamma Secretase, APOE, CLU, CR1, PICALM, ABCA7, BIN1, CD2AP, CD33, EPHA1, and MS4A2, and Their Relationships with Herpes Simplex,C. Pneumoniae, Other Suspect Pathogens, and the Immune System." International Journal of Alzheimer's Disease 2011 (2011): 1–34. http://dx.doi.org/10.4061/2011/501862.

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Alzheimer's disease susceptibility genes, APP and gamma-secretase, are involved in the herpes simplex life cycle, and that of other suspect pathogens (C. pneumoniae,H. pylori,C. neoformans,B. burgdorferri,P. gingivalis) or immune defence. Such pathogens promote beta-amyloid deposition andtauphosphorylation and may thus be causative agents, whose effects are conditioned by genes. The antimicrobial effects of beta-amyloid, the localisation of APP/gamma-secretase in immunocompetent dendritic cells, and gamma secretase cleavage of numerous pathogen receptors suggest that this network is concerned with pathogen disposal, effects which may be abrogated by the presence of beta-amyloid autoantibodies in the elderly. These autoantibodies, as well as those to nerve growth factor andtau, also observed in Alzheimer's disease, may well be antibodies to pathogens, due to homology between human autoantigens and pathogen proteins. NGF ortauantibodies promote beta-amyloid deposition, neurofibrillary tangles, or cholinergic neuronal loss, and, with other autoantibodies, such as anti-ATPase, are potential agents of destruction, whose formation is dictated by sequence homology between pathogen and human proteins, and thus by pathogen strain and human genes. Pathogen elimination in the ageing population and removal of culpable autoantibodies might reduce the incidence and offer hope for a cure in this affliction.

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Lv, Wu, Jialin Zhang, Ao Jiao, Bowen Wang, Baomin Chen, and Jie Lin. "Resveratrol attenuates hIAPP amyloid formation and restores the insulin secretion ability in hIAPP-INS1 cell line via enhancing autophagy." Canadian Journal of Physiology and Pharmacology 97, no. 2 (February 2019): 82–89. http://dx.doi.org/10.1139/cjpp-2016-0686.

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It has been proved that human islet amyloid polypeptide (hIAPP), the main constituent of islet amyloid deposition, is one of the important factors that can induce type 2 diabetes or graft failure after islet transplantation. As there is no research on whether resveratrol degrading the amyloid deposition by its special chemical structure or enhancing autophagy had been published, we decided to detect the function of resveratrol in degrading the amyloid deposition in pancreatic beta cells. We established stable hIAPP-INS1 cell line via transfecting INS1 cells by lentivirus that overexpresses hIAPP. Our research demonstrates that amyloid deposition existed in hIAPP-INS1 cell by the thioflavin S fluorescent staining, meanwhile the function of insulin secretion of hIAPP-INS1 cells was decreased significantly (p < 0.01). After treatment with resveratrol (20 μM) for 24 h, amyloid deposition in hIAPP-INS1 cells was decreased significantly, and the insulin secretion was restored significantly (p < 0.01). Once inhibited the autophagy of hIAPP-INS1 cells by 3-methyladenine for 24 h, resveratrol does not effectively remove hIAPP deposits again, and cannot improve the function of insulin secretion. These results provide a novel thought that resveratrol can degrade the amyloid deposition in type 2 diabetes and the graft after islet transplantation.

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Godara, Amandeep, Andy Y. Wang, Knarik Arkun, Teresa Fogaren, Adnan S. Qamar, Ellen D. McPhail, James Kryzanski, Ron Riesenburger, and Raymond Comenzo. "Unraveling a rare cause of spinal stenosis: Coexistent AL and ATTR amyloidosis involving the ligamentum flavum." Surgical Neurology International 13 (January 12, 2022): 12. http://dx.doi.org/10.25259/sni_1235_2021.

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Background: Amyloidosis is a protein misfolding disorder that leads to the deposition of beta-pleated sheets of a fibrillar derivative of various protein precursors. Identification of the type of precursor protein is integral in treatment decision-making. The presence of two different types of amyloid in the same patient is unusually rare, and there are no previous reports of two different types of amyloid deposition in the ligamentum flavum (LF) in the same patient. Case Description: Here, we describe two patients with spinal stenosis who underwent laminectomies and were found to have AL and ATTR amyloid deposits in the LF. Conclusion: As the spine is becoming recognized as a site for ATTRwt amyloid deposition, patients undergoing spinal decompression surgery may potentially benefit from evaluation for amyloidosis in the LF.

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Makino, Mitsuhiro, Kaori Ito-Takahashi, Akira Yano, Yoshikatsu Miwa, Yoshito Kanazawa, Akiko Chiba, Akira Kanda, and Shinji Murata. "P2-395: Effect of a novel beta-amyloid peptide vaccine on brain beta-amyloid deposition in Tg2576 mice." Alzheimer's & Dementia 9 (July 2013): P502—P503. http://dx.doi.org/10.1016/j.jalz.2013.05.1044.

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Uéda, K., H. Fukushima, E. Masliah, Y. Xia, A. Iwai, M. Yoshimoto, D. A. Otero, J. Kondo, Y. Ihara, and T. Saitoh. "Molecular cloning of cDNA encoding an unrecognized component of amyloid in Alzheimer disease." Proceedings of the National Academy of Sciences 90, no. 23 (December 1, 1993): 11282–86. http://dx.doi.org/10.1073/pnas.90.23.11282.

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A neuropathological hallmark of Alzheimer disease (AD) is a widespread amyloid deposition. We analyzed the entire amino acid sequences in an amyloid preparation and found, in addition to the major beta/A4-protein (A beta) fragment, two unknown peptides. We raised antibodies against synthetic peptides using subsequences of these peptides. These antibodies immunostained amyloid in neuritic and diffuse plaques as well as vascular amyloid. Electron microscopic analysis demonstrated that the immunostaining was localized on amyloid fibrils. We have isolated an apparently full-length cDNA encoding a 140-amino-acid protein within which two previously unreported amyloid sequences are encoded in tandem in the most hydrophobic domain. We tentatively named this 35-amino acid peptide NAC (non-A beta component of AD amyloid) and its precursor NACP. NAC is the second component, after A beta, identified chemically in the purified AD amyloid preparation. Secondary structure predictions indicate that the NAC peptide sequence has a strong tendency to form beta-structures consistent with its association with amyloid. NACP is detected as a M(r) 19,000 protein in the cytosolic fraction of brain homogenates and comigrates on immunoblots with NACP synthesized in Escherichia coli from NACP cDNA. NACP mRNA is expressed principally in brain but is also expressed in low concentrations in all tissues examined except in liver, suggesting its ubiquitous and brain-specific functions. The availability of the cDNA encoding full-length NACP should help to elucidate the mechanisms of amyloidosis in AD.

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Smith, Gwenn S., Hiroto Kuwabara, Ayon Nandi, Neda F. Gould, Najilla Nassery, Alena Savonenko, Jin Hui Joo, et al. "Molecular imaging of beta-amyloid deposition in late-life depression." Neurobiology of Aging 101 (May 2021): 85–93. http://dx.doi.org/10.1016/j.neurobiolaging.2021.01.002.

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Lucchini, Roberto, Somaiyeh Azmoun, Cheuk Tang, Donatella Placidi, Giuseppa Cagna, Manuale Oppini, Carlo Rodella, et al. "Diffuse brain deposition of beta-amyloid among italian ferroalloy workers." Safety and Health at Work 13 (January 2022): S57—S58. http://dx.doi.org/10.1016/j.shaw.2021.12.906.

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Kim, Jee Wook, Min Soo Byun, Jun Ho Lee, Dahyun Yi, So Yeon Jeon, Bo Kyung Sohn, Jun-Young Lee, et al. "Serum albumin and beta-amyloid deposition in the human brain." Neurology 95, no. 7 (July 20, 2020): e815-e826. http://dx.doi.org/10.1212/wnl.0000000000010005.

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ObjectivesTo investigate the relationships of serum albumin with in vivo Alzheimer disease (AD) pathologies, including cerebral β-amyloid (Aβ) protein deposition, neurodegeneration of AD-signature regions, and cerebral white matter hyperintensities (WMH), in the human brain.MethodsA total of 396 older adults without dementia underwent comprehensive clinical assessments, measurement of serum albumin level, and multimodal brain imaging, including [11C] Pittsburgh compound B-PET, 18F-fluorodeoxyglucose-PET, and MRI. Serum albumin was categorized as follows: <4.4 g/dL (low albumin), 4.4 to 4.5 g/dL (middle albumin), and >4.5 g/dL (high albumin; used as a reference category). Aβ positivity, AD-signature region cerebral glucose metabolism (AD-CM), AD-signature region cortical thickness (AD-CT), and WMH volume were used as outcome measures.ResultsSerum albumin level (as a continuous variable) was inversely associated with Aβ deposition and Aβ positivity. The low albumin group showed a significantly higher Aβ positivity rate compared to the high albumin group (odds ratio 3.40, 95% confidence interval 1.67–6.92, p = 0.001), while the middle albumin group showed no difference (odds ratio 1.74, 95% confidence interval 0.80–3.77, p = 0.162). Neither serum albumin level (as a continuous variable) nor albumin categories were related to AD-CM, AD-CT, or WMH volume.ConclusionsLow serum albumin may increase the risk of AD dementia by elevating amyloid accumulation. In terms of AD prevention, more attention needs to be paid to avoid a low serum albumin level, even within the clinical normal range, by clinicians.

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Miyoshi, Michie, Hitoshi Shinotoh, Hitoshi Shimada, Kouichi Sato, Kiyoshi Fukushi, Hiroshi Ito, Tetsuya Suhara, Masayasu Matsumoto, and Toshiaki Irie. "P1-266: Changes in beta-amyloid deposition by pet study." Alzheimer's & Dementia 4 (July 2008): T294—T295. http://dx.doi.org/10.1016/j.jalz.2008.05.856.

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Bartzokis, George, Po H. Lu, and Jim Mintz. "Human brain myelination and amyloid beta deposition in Alzheimer's disease." Alzheimer's & Dementia 3, no. 2 (April 2007): 122–25. http://dx.doi.org/10.1016/j.jalz.2007.01.019.

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Mazzitelli, Sonia. "P3-054: Requirement of active JNK for beta-amyloid deposition." Alzheimer's & Dementia 7 (July 2011): S531. http://dx.doi.org/10.1016/j.jalz.2011.05.1493.

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Guo, Jian-Ping, and Patrick McGeer. "P1-330: Simple in vitro screening assays for agents that inhibit beta-amyloid deposition or promote beta-amyloid phagocytosis." Alzheimer's & Dementia 8, no. 4S_Part_6 (July 2012): P221. http://dx.doi.org/10.1016/j.jalz.2012.05.2016.

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Michels, Lars, Geoffrey Warnock, Alfred Buck, Gianluca Macauda, Sandra E. Leh, Andrea M. Kaelin, Florian Riese, et al. "Arterial spin labeling imaging reveals widespread and Aβ-independent reductions in cerebral blood flow in elderly apolipoprotein epsilon-4 carriers." Journal of Cerebral Blood Flow & Metabolism 36, no. 3 (September 30, 2015): 581–95. http://dx.doi.org/10.1177/0271678x15605847.

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Changes in cerebral blood flow are an essential feature of Alzheimer’s disease and have been linked to apolipoprotein E-genotype and cerebral amyloid-deposition. These factors could be interdependent or influence cerebral blood flow via different mechanisms. We examined apolipoprotein E-genotype, amyloid beta-deposition, and cerebral blood flow in amnestic mild cognitive impairment using pseudo-continuous arterial spin labeling MRI in 27 cognitively normal elderly and 16 amnestic mild cognitive impairment participants. Subjects underwent Pittsburgh Compound B (PiB) positron emission tomography and apolipoprotein E-genotyping. Global cerebral blood flow was lower in apolipoprotein E ɛ4-allele carriers (apolipoprotein E4+) than in apolipoprotein E4− across all subjects (including cognitively normal participants) and within the group of cognitively normal elderly. Global cerebral blood flow was lower in subjects with mild cognitive impairment compared with cognitively normal. Subjects with elevated cerebral amyloid-deposition (PiB+) showed a trend for lower global cerebral blood flow. Apolipoprotein E-status exerted the strongest effect on global cerebral blood flow. Regional analysis indicated that local cerebral blood flow reductions were more widespread for the contrasts apolipoprotein E4+ versus apolipoprotein E4− compared with the contrasts PiB+ versus PiB− or mild cognitive impairment versus cognitively normal. These findings suggest that apolipoprotein E-genotype exerts its impact on cerebral blood flow at least partly independently from amyloid beta-deposition, suggesting that apolipoprotein E also contributes to cerebral blood flow changes outside the context of Alzheimer’s disease.

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Byun, Kyunghee, Younghee Maeng, and Bonghee Lee. "A study on changes of the CNS pathway to the entorhinal cortex by amyloid beta 1-42." Journal of Medicine and Life Science 4, no. 1 (June 1, 2006): 61–71. http://dx.doi.org/10.22730/jmls.2006.4.1.61.

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Deposition of amyloid beta protein as amyloid fibrils or non fibrillar aggregations in senile plaques characterizes the Alzheimer disease brain. Microtubule associated protein tau is abnormally phosphorylated in AD and aggregates as paired helical filaments (PHFs) in neurofibrillary tangles. The purpose of this study were 1) to identify the entorhinal cortex pathway in the normal rat brain after PRV injection, 2) whether amyloid beta 1-42 injection caused the hyperphosphorylation of tau along the entorhinal cortex CNS pathway. For analysis, rats were sacrificed at 48 hours after PRV injection or cut, at 7 days after amyloid beta 1-42 injection. Brains were processed for immunohistochemistry against PRV. tau-P, or 6E10. PRV positive neurons were observed in several CNS nuclei including hippocampus, and tau-p neurons area appeared in several nuclei including TM. These data suggest that the hyperphosphorylated tau has been increased in the CNS nuclei along entorhinal cortex pathway, and this may cause memory disturbance in Alzheimer's disease patients.

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Deal, Jennifer A., Andreea Rawlings, A. Richey Sharrett, Nicholas Reed, Joshua Betz, Thomas Mosley, Frank Lin, and Rebecca Gottesman. "HEARING IMPAIRMENT, COGNITIVE PERFORMANCE, AND BETA-AMYLOID DEPOSITION IN THE ARIC-PET AMYLOID IMAGING STUDY." Innovation in Aging 3, Supplement_1 (November 2019): S551. http://dx.doi.org/10.1093/geroni/igz038.2032.

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Abstract Hearing impairment is a risk factor for dementia but the mechanism underlying this association is unknown. We investigated the relationship between hearing and cognitive performance and brain β-amyloid deposition in 252 adults aged 67-88 years (37% black race) without dementia from three U.S. communities. Global cortical standardized uptake value ratios (SUVRs) were calculated from florbetapir-positron emission tomography scans, with elevated SUVR defined as >1.2 (the median value). Air conduction hearing threshold levels for the frequencies of 0.5, 1, 2 and 4 kHz were obtained by pure tone audiometry and averaged for the better-hearing ear to yield a pure tone average (PTA) in decibels hearing level (dB). A composite cognitive score was created from ten neuropsychological tests summarized using latent variable methods. Multivariable-adjusted linear and Poisson regression with robust standard errors were used to estimate the average difference in cognitive scores and prevalence of elevated SUVR, respectively, by hearing impairment status. In analyses adjusted for age, sex, education and APOE ε4 status, hearing was not associated with elevated SUVR [prevalence ratio per 10 db increase (worse hearing) = 0.94 (95% CI: 0.84, 1.04)]. Results did not differ by race. In contrast, each 10 db increase in hearing impairment was associated with 0.08 standard deviation (95% CI: 0.02, 0.15) lower cognitive score, after adjustment for demographic and cardiovascular factors. Poorer hearing is associated with poorer cognitive performance but not with amyloid deposition, suggesting that the mechanism underlying the relationship between hearing and cognition may be independent of Alzheimer’s-related pathologic brain changes.

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Komaki, Alireza, Iraj Salehi, Arman Keymoradzadeh, Masoumeh Taheri Azandaryani, and Zoleikha Golipoor. "Effect of Long-term Exposure to Extremely Low-frequency Electromagnetic Fields on β-amyloid Deposition and Microglia Cells in an Alzheimer Model in Rats." Journal of Guilan University of Medical Sciences 30, no. 3 (October 1, 2021): 218–29. http://dx.doi.org/10.32598/jgums.30.3.1609.2.

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Background: Recently, researchers have considered extremely low-frequency electromagnetic fields (ELF-EMFs), as one of the non-invasive therapies, in the treatment of many severe neurological disorders, including Alzheimer Disease (AD). AD is a progressive neurodegenerative disease characterized by the deposition of amyloid plaques in the brain. However, the increase in microglial cells increases phagocytosis and the destruction of amyloid plaques. Therefore, the present study aimed to investigate the amount of β-amyloid precursor deposition and the number of microglia cells in the animal model of AD before and after exposure to ELF-EMFs. Objective: The aim of this study was to investigate the deposition of beta ameloid precursor and the number of microglial cells in the Alzheimer's animal model before and after exposure to magnetic waves. Methods: Fifty male adult rats were randomly grouped into 5: The control group, the ELF-EMFs group, the AD group, the treatment group 1, and the treatment group 2. After the study period, the animals were killed for immunohistochemistry assessment to detect and compare the deposition of β-amyloid and the production of allograft inflammatory factor 1 (Iba1) protein. Results: Exposure to ELF reduced the deposition of β-amyloid and increased microglia cells. However, these changes were not different between the control and ELF-EMFs groups (P<0.001). Conclusion: ELF-EMF can reduce the formation of β-amyloid plaques and induce the proliferation of microglia cells. Therefore, they can be used to treat brain damage caused by Alzheimer disease.

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Rabinovici, G. D., and W. J. Jagust. "Amyloid Imaging in Aging and Dementia: Testing the Amyloid HypothesisIn Vivo." Behavioural Neurology 21, no. 1-2 (2009): 117–28. http://dx.doi.org/10.1155/2009/609839.

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Amyloid imaging represents a major advance in neuroscience, enabling the detection and quantification of pathologic protein aggregations in the brain. In this review we survey current amyloid imaging techniques, focusing on positron emission tomography (PET) with ^{11}carbon-labelled Pittsburgh Compound-B (11C-PIB), the most extensively studied and best validated tracer. PIB binds specifically to fibrillar beta-amyloid (Aβ) deposits, and is a sensitive marker for Aβ pathology in cognitively normal older individuals and patients with mild cognitive impairment (MCI) and Alzheimer’s disease (AD). PIB-PET provides us with a powerful tool to examine in vivo the relationship between amyloid deposition, clinical symptoms, and structural and functional brain changes in the continuum between normal aging and AD. Amyloid imaging studies support a model in which amyloid deposition is an early event on the path to dementia, beginning insidiously in cognitively normal individuals, and accompanied by subtle cognitive decline and functional and structural brain changes suggestive of incipient AD. As patients progress to dementia, clinical decline and neurodegeneration accelerate and proceed independently of amyloid accumulation. In the future, amyloid imaging is likely to supplement clinical evaluation in selecting patients for anti-amyloid therapies, while MRI and FDG-PET may be more appropriate markers of clinical progression.

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Baek, Min Seok, Narae Lee, Jin Woo Kim, and Jin Yong Hong. "Association of Hippocampal Subfield Volumes with Amyloid-Beta Deposition in Alzheimer’s Disease." Journal of Clinical Medicine 11, no. 6 (March 10, 2022): 1526. http://dx.doi.org/10.3390/jcm11061526.

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We investigated the relationship between hippocampal subfield volumes and cortical amyloid-beta (Aβ) deposition in Alzheimer’s disease (AD). Fifty participants (11 cognitively unimpaired [CU], 10 with mild cognitive impairment [MCI], and 29 with AD) who underwent 18F-florbetaben positron emission tomography, magnetic resonance imaging, and neuropsychological tests were enrolled. The hippocampal subfield volumes were obtained using an automated brain volumetry system with the Winterburn atlas and were compared among the diagnostic groups, and the correlations with the Aβ deposition and AD risk factors were determined. Patients with MCI and AD showed decreased volume in the stratum radiatum/lacunosum/moleculare (SRLM) of the cornu ammonis (CA)1 and CA4-dentate gyrus (DG) compared with the CU. Decreased SRLM and CA4-DG volumes were associated with an increased Aβ deposition in the global cortex (R = −0.459, p = 0.001; R = −0.393, p = 0.005, respectively). The SRLM and CA4-DG volumes aided in the distinction of AD from CU (areas under the receiver operating characteristic [AUROC] curve = 0.994 and 0.981, respectively, p < 0.001), and Aβ+ from Aβ− individuals (AUROC curve = 0.949 and 0.958, respectively, p < 0.001). Hippocampal subfield volumes demonstrated potential as imaging biomarkers in the diagnosis and detection of AD and Aβ deposition, respectively.

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Godoy, Maria Dantas Costa Lima, Marco Aurélio Fornazieri, Richard L. Doty, Fábio de Rezende Pinna, José Marcelo Farfel, Glaucia Bento dos Santos, Mariana Molina, et al. "Is Olfactory Epithelium Biopsy Useful for Confirming Alzheimer’s Disease?" Annals of Otology, Rhinology & Laryngology 128, no. 3 (December 2, 2018): 184–92. http://dx.doi.org/10.1177/0003489418814865.

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Objectives: The clinical symptoms of Alzheimer’s disease (AD) are preceded by a long asymptomatic period associated with “silent” deposition of aberrant paired helical filament (PHF)-tau and amyloid-beta proteins in brain tissue. Similar depositions have been reported within the olfactory epithelium (OE), a tissue that can be biopsied in vivo. The degree to which such biopsies are useful in identifying AD is controversial. This postmortem study had 3 main goals: first, to quantify the relative densities of AD-related proteins in 3 regions of the olfactory neuroepithelium, namely, the nasal septum, middle turbinate, and superior turbinate; second, to establish whether such densities are correlated among these epithelial regions as well as with semi-quantitative ratings of general brain cortex pathology; and third, to evaluate correlations between the protein densities and measures of antemortem cognitive function. Methods: Postmortem blocks of olfactory mucosa were obtained from 12 AD cadavers and 24 controls and subjected to amyloid-beta and PHF-tau immunohistochemistry. Results: We observed marked heterogeneity in the presence of the biomarkers of tau and amyloid-beta among the targeted olfactory epithelial regions. No significant difference was observed between the cadavers with AD and the controls regarding the concentration of these proteins in any of these epithelial regions. Only one correlation significant was evident, namely, that between the tau protein densities of the middle and the upper turbinate ( r = .58, P = .002). Conclusion: AD-related biomarker heterogeneity, which has not been previously demonstrated, makes comparisons across studies difficult and throws into question the usefulness of OE amyloid-beta and PHF-tau biopsies in detecting AD.

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Hosokawa, Masato, Yoshinori Tanaka, Tetsuaki Arai, Hiromi Kondo, Haruhiko Akiyama, and Masato Hasegawa. "Progranulin haploinsufficiency reduces amyloid beta deposition in Alzheimer’s disease model mice." Experimental Animals 67, no. 1 (2018): 63–70. http://dx.doi.org/10.1538/expanim.17-0060.

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Wilhelmus, Micha M. M., A. B. Smit, Maarten Loos, and Benjamin Drukarch. "Absence of tissue transglutaminase delays amyloid-beta deposition in Alzheimer's disease." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): OR4–3. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_or4-3.

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Collins, Thomas R. "Sleep Disruption Leads to Amyloid-Beta Deposition in Mice, Researchers Find." Neurology Today 15, no. 1 (January 2015): 11–12. http://dx.doi.org/10.1097/01.nt.0000460025.37121.3b.

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MIKLOSSY, J., A. KIS, A. RADENOVIC, L. MILLER, L. FORRO, R. MARTINS, K. REISS, N. DARBINIAN, P. DAREKAR, and L. MIHALY. "Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes." Neurobiology of Aging 27, no. 2 (February 2006): 228–36. http://dx.doi.org/10.1016/j.neurobiolaging.2005.01.018.

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Tabaton, Massimo, Claudia Caponnetto, Gianluigi Mancardi, and Carlo Loeb. "Amyloid beta protein deposition in brains from elderly subjects with leukoaraiosis." Journal of the Neurological Sciences 106, no. 2 (December 1991): 123–27. http://dx.doi.org/10.1016/0022-510x(91)90248-6.

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Myllykangas, Liisa, Tuomo Polvikoski, Karoliina Reunanen, Fabienne Wavrant-De Vrieze, Clare Ellis, Dena Hernandez, Raimo Sulkava, et al. "ApoE ?3-haplotype modulates Alzheimer beta-amyloid deposition in the brain." American Journal of Medical Genetics 114, no. 3 (March 18, 2002): 288–91. http://dx.doi.org/10.1002/ajmg.10202.

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Wang, Ming-Liang, Meng-Meng Yu, Wen-Bin Li, and Yue-Hua Li. "Longitudinal Association between White Matter Hyperintensities and White Matter Beta-Amyloid Deposition in Cognitively Unimpaired Elderly." Current Alzheimer Research 18, no. 1 (April 28, 2021): 8–13. http://dx.doi.org/10.2174/1567205018666210324125116.

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Background: White matter (WM) beta-amyloid uptake has been used as a reference region to calculate the cortical standard uptake value ratio (SUVr). However, white matter hyperintensities (WMH) may have an influence on WM beta-amyloid uptake. Our study aimed to investigate the associations between WMH and WM beta-amyloid deposition in cognitively unimpaired elderly. Methods: Data from 83 cognitively unimpaired individuals in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) dataset were analyzed. All participants had complete baseline and four-year follow-up information about WMH volume, WM 18F-AV-45 SUVr, and cognitive function, including ADNI-Memory (ADNI-Mem) and ADNI-Executive function (ADNI-EF) scores. Cross-sectional and longitudinal linear regression analyses were used to determine the associations between WMH and WM SUVr and cognitive measures. Results: Lower WM 18F-AV-45 SUVr at baseline was associated with younger age (β=0.01, P=0.037) and larger WMH volume (β=-0.049, P=0.048). The longitudinal analysis found an annual increase in WM 18F-AV-45 SUVr was associated with an annual decrease in WMH volume (β=-0.016, P=0.041). An annual decrease in the ADNI-Mem score was associated with an annual increase in WMH volume (β=-0.070, P=0.001), an annual decrease in WM 18F-AV-45 SUVr (β=0.559, P=0.030), and fewer years of education (β=0.011, P=0.044). There was no significant association between WM 18F-AV-45 SUVr and ADNI-EF (P>0.05). Conclusions: Reduced beta-amyloid deposition in WM was associated with higher WMH load and memory decline in cognitively unimpaired elderly. WMH volume should be considered when WM 18F-AV-45 SUVr is used as a reference for evaluating cortical 18F-AV-45 SUVr.

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Shimomura, K. "0103 Novel Prebiotic Enhances Sleep-Wake Cycle and Memory Consolidation in 5xFAD Mice." Sleep 43, Supplement_1 (April 2020): A41. http://dx.doi.org/10.1093/sleep/zsaa056.101.

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Abstract Introduction Prior studies have shown that the gut microbiomes of Alzheimer’s Disease (AD) patients differ from unaffected individuals. Sleep and circadian rhythm disturbances are common in AD and often precede dementia symptoms. Gut microbiome alterations have also been observed in models of circadian disruption. Therefore, we hypothesized that altering the gut microbiome could improve sleep/circadian rhythms and cognition in an AD mouse model. Methods Mice were given a dietary polysaccharide, Modified Resistant Maltodextrin (MRM), as a 1% solution in the drinking water beginning at 2 months of age. 5xFAD and wild-type (WT) littermates were tested. Sleep-wake was recorded by EEG/EMG, memory consolidation was tested by the Object-Location Memory test, and beta amyloid deposition in the brain was assayed (dot blot). Composition of the gut microbiota was determined from amplicon sequencing of the 16s ribosomal RNA gene from fecal DNA. Results MRM treatment reduced dark (active)-phase sleep and the phase scattering of REM sleep in 5xFAD mice, indices of circadian consolidation. 6-month-old 5xFAD mice given plain water exhibited no 24hr retention of object location memory. However, MRM-treated 5xFAD mice demonstrated 24-hour memory, even at 12 months of age. Both improved memory and increased consolidation of sleep were also observed in WT mice. Two unclassified species of bacteria from the family Tannerellaceae were significantly increased in MRM-treated 5xFAD and WT mice. At 12 months of age, synaptic and neuronal loss become prominent in this AD model. However, the level of beta amyloid deposition in the brain was not significantly different between MRM and water control groups. Conclusion MRM treatment altered the gut microbiome, improved circadian timing of sleep and memory retention, but did not impact beta amyloid deposition in 5xFAD mice. Because these effects were also present in WT mice, MRM-induced microbiome changes may affect sleep and cognition independently from beta amyloid. Support Northwestern University Feinberg School of Medicine Center for Circadian and Sleep Medicine

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Treyer, Valerie, Rafael S. Meyer, Andreas Buchmann, Giovanni A. G. Crameri, Sandro Studer, Antje Saake, Esmeralda Gruber, et al. "Physical activity is associated with lower cerebral beta-amyloid and cognitive function benefits from lifetime experience–a study in exceptional aging." PLOS ONE 16, no. 2 (February 19, 2021): e0247225. http://dx.doi.org/10.1371/journal.pone.0247225.

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Background Exceptional agers (85+ years) are characterized by preserved cognition presumably due to high cognitive reserve. In the current study, we examined whether personality, risk and protective factors for dementia as well as quality of life are associated with core features of Alzheimer’s disease (amyloid-deposition and hippocampal volume) as well as cognition in exceptional aging. Methods We studied 49 exceptional agers (average 87.8 years, range 84–94 years), with preserved activities of daily living and absence of dementia. All participants received a detailed clinical and neuropsychological examination. We used established questionnaires to measure lifetime experience, personality, recent physical and cognitive activity as well as quality of life. Cerebral amyloid-deposition was estimated by 18-[F]-Flutemetamol-PET and manual hippocampal volumetry was performed on 3D T1 MRI images. Results In this sample of exceptional agers with preserved activities of daily living, we found intact cognitive performance in the subjects with the highest amyloid-load in the brain, but a lower quality of life with respect to autonomy as well as higher neuroticism. Higher self-reported physical activity in the last twelve months went with a lower amyloid load. Higher self-reported leisure-time/ not work-related activity went with better executive functioning at older age. Conclusion Even in exceptional aging, high amyloid load may subtly influence personality and quality of life. Our findings support a close relationship between high physical activity and low amyloid-deposition and underscore the importance of extracurricular activities for executive functions. As executive functions are known to be a central resource for everyday functioning in fostering extracurricular activities may be effective in delaying the onset of dementia.

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Journal articles on the topic 'Amyloid beta deposition'

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