Giulio Maria Pasinetti

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Giulio Maria Pasinetti
Dr. GM Pasinetti TMII.png
Dr. Pasinetti presents: "Innate Neuroimmune Priming: Mechanisms and Potential Imaging Biomarkers" at TMII's STRIVE Seminar Series at Mount Sinai, YC in September 2018
NationalityAmerican, Italian
Alma materUniversity of Milan
Employer Icahn School of Medicine at Mount Sinai
Known for Biological psychiatry, Alzheimer's disease
Website http://www.mountsinai.org/profiles/giulio-m-pasinetti

Giulio Maria Pasinetti is the Program Director of the Center on Molecular Integrative Neuroresilience [1] and is the Saunders Family Chair in Neurology at the Icahn School of Medicine at Mount Sinai (ISMMS) in New York City. [2] Pasinetti is a Professor of Neurology, Psychiatry, Neuroscience, and Geriatrics and Palliative Medicine at ISMMS. [2]

Contents

As the Program Director of the NIH / NCCIH funded P50 Center on Molecular Integrative Neuroresilience, Pasinetti's focus is on understanding the molecular mechanisms and pathophysiology that may be at the basis of stress-induced mood disorders, including anxiety, depression, and other neuropsychiatric disorders, and their influence on cognitive dysfunction.

At the Veterans Health Administration, Pasinetti is the Director of the Basic and Biomedical Research and Training Program, Geriatric Research, Education, and Clinical Center (GRECC), as well as the Director of the Translational Neuroscience Laboratories at the James J. Peters Veterans Affairs Medical Center (JJPVAMC). [3]

Pasinetti has an h-index of 81, with over 20,000 citations. [4] He has published over 250 papers indexed in PubMed, as well as 6 book chapters. [5]

Biography

Education

Pasinetti received an M.D. from the Milan University School of Medicine (1982) and a Ph.D. in Pharmacology from the University of Milan (1988). He was a Research Fellow (Neuropharmacology, 1983-1984) at the University of Milan. Upon moving to the United States, he worked as a Research Associate (Neurogerontology, 1984-1988) and, eventually, as a Senior Research Associate (Neurogerontology, 1989-1990) at the University of Southern California in Los Angeles. [6]

Career

Pasinetti began his career as an assistant professor at the California School of Gerontology and Biological Sciences at the University of Southern California (1990–1995) in Los Angeles. Since 1996, he has been a faculty member of the Icahn School of Medicine at Mount Sinai where he served as the Aidekman Family Chair and Professor in Neurology until 2009. Pasinetti was also the chief of the Friedman Brain Institute Center of Excellence for Novel Approaches to Neurodiagnostics and Neurotherapeutics, as well as, from 2008 to 2014, the director and principal investigator of the NIH-funded Center of Excellence for Research on Complementary and Alternative Medicine (CERC) in Alzheimer's disease. [2]

Awards

Dr. Pasinetti's awards and honors include the Mount Sinai School of Medicine Faculty Council Award for Academic Excellence, the Charles Dana Alliance for Brain Initiatives Award from the Dana Foundation, [7] the Foundation Queen Sofia of Spain Research Center award on Alzheimer's Disease, [8] the Research Career Scientist Developmental Award from the Veterans Health Administration, [9] the Zenith Award from the Alzheimer's Association, [10] the Temple Foundation Discovery Award from the Alzheimer's Association, [10] the Nathan W. & Margaret T. Shock Aging Research Foundation Award from the Gerontological Society of America, the Turken Family fellowship from the Alzheimer's Association (Los Angeles Chapter) and the Nathan Shock New Investigator Award of the Gerontological Society of America. [11] Dr. Pasinetti was also awarded the 2017 Mary Swartz Rose Senior Investigator Award by The American Society for Nutrition and the American Society for Nutrition Foundation. Most recently, Dr. Pasinetti was named an Honorary Fellow of The University of Bergamo (Università degli Studi di Bergamo).

Grants and Research

Pasinetti investigates the biological processes that occur when, during aging, subjects with normal cognitive function convert into the very earliest stages of Alzheimer's disease (AD) and then to frank dementia. He identified type 2 diabetes (T2D) as one of the major risk factors that might affect AD neuropathology and synaptic plasticity in part through epigenetic mechanisms. [12] By conducting genome wide association studies to clarify the molecular mechanisms in subjects with T2D who might be predisposed to the onset of Alzheimer's disease, [13] Pasinetti found that a subpopulation of individuals with T2D have a genetic predisposition to AD based on the evidence of shared common T2D/AD single nucleotide polymorphisms in gene pathways involved in chromatin modification enzymes, among others. Through this research, Pasinetti and his colleagues provided the basis for novel therapeutic targets towards the preservation of cognitive health in a subset of T2D subjects at risk for developing AD. [12] [14] [15] [16]

With his group, Pasinetti has led research investigations on the neuromolecular mechanisms underlying age-related cognitive decline, dementia, and stress-induced psychological and cognitive impairment with the goal of utilizing repurposed natural products, specifically polyphenols, to promote resilience to such conditions. [17] [18] [19] [20] With this in mind, Pasinetti initiated a drug repurposing study for AD, screening FDA-approved drugs and natural compounds for amyloid-lowering and anti-Aβ aggregation activities, and identified candidates for in vivo testing in AD animal models. [21] [22] [23] [24] As a result of this study, Pasinetti's laboratory identified antihypertensive drugs lacking cardiovascular side effects but with enhanced anti-Aβ oligomerization activity. [25] [26] Pasinetti's research has also validated that repurposing drugs that have already been well-characterized in terms of tolerability and safety profile may have several advantages over novel drugs. These studies provide new information about the potentially detrimental role of commonly prescribed drugs that can be used as a reference for physicians to consider, particularly when treating chronic degenerative disorders such as AD. [27] [28] [29]

Following these findings, as Chief of the Friedman Brain Institute Center of Excellence for Novel Approaches to Neurodiagnostics and Neurotherapeutics, Pasinetti developed drug discovery programs for Alzheimer's disease. [17] [26] [30] Here, he led a primary translational Center to determine whether interventions which appear to work in the preclinical animal model of the disease also show promise in treating patients who have the disease. [27] [29] [31]

Pasinetti is the Director of the NIH funded Botanical Center in Neuroresilience. [1] This Center supports three major projects which are being conducted through interdisciplinary collaborative efforts from Mount Sinai Hospital's Department of Neuroscience, Department of Neurology, Department of Genetics and Genomic Sciences, and the Friedman Brain Institute. [32] [33] One project is the efficacy of using polyphenols specifically as dietary supplements to promote resilience against stressful events and clarifying the role of the microbiome at the genomic level in the promotion of cognitive and psychological health. [31] [33] This research is leading to safe and efficacious treatments of dietary botanical supplements to promote resilience in response to psychological and cognitive impairment. [32]

In a study released on February 2, 2018, scientists from the Icahn School of Medicine at Mount Sinai, led by Dr. Giulio Maria Pasinetti, described an extensive analysis of two novel grape-derived phytochemicals, or natural essential nutrients, dihydrocaffeic acid (DHCA) and malvidin-3’-O-glucoside (Mal-gluc), which might be developed as therapeutic agents for the treatment of depression. The study demonstrated that DHCA reversed improper epigenetic modifications that have been shown to promote the DNA transcription of numerous pro-inflammatory genes, such as interleukin 6 (IL-6). Mal-gluc was found to increase the transcription of the Rac1 gene, which influences the expression of genes responsible for synaptic plasticity in the brain. It was demonstrated that treatment with both DHCA and Mal-gluc is effective in attenuating depression-like phenotypes in a mouse model of increased systemic inflammation induced by transplantation of cells from the bone marrow of stress-susceptible mice. This Mount Sinai study provides novel preclinical evidence supporting the targeting of multiple key disease mechanisms through DNA epigenetic modification for the treatment of depression and strongly supports the need to test and identify novel compounds that target alternative pathologic mechanisms, such as inflammation and synaptic maladaptation, for individuals who are resistant to currently available treatments. [34]

With his involvement at the Veterans Administration, Pasinetti and his lab identified biomarkers to help diagnose the two signature injuries of the recent wars in Iraq and Afghanistan: mild traumatic brain injury (mTBI) and post-traumatic stress disorder (PTSD). The focus was on four specific non-coding miRNA which were all found at significantly lower levels in those Veterans who had comorbid TBI plus PTSD, when compared to subjects who had only PTSD. [35] [36] The availability of such biomarkers could provide more precise benchmarks and outcome measures in clinical trials of different TBI or PTSD therapies.

Pasinetti's lab is now working on tracing "downstream" molecular pathways in preclinical rodent models of mTBI, to eventually tie them back to TBI or PTSD symptoms and allow for identification of potential new drug targets to be further developed in the clinical setting. [37]

Taken together, the focus of Dr. Pasinetti's research determining the molecular basis of neurodegenerative disorders and TBI to provide targets for novel therapies has the ultimate goal of identifying unique treatment strategies that can be translated to improve pharmacological treatment in clinical care.

Publications (Partial List)

Related Research Articles

<span class="mw-page-title-main">Cognitive disorder</span> Mental health condition affecting cognitive functions

Cognitive disorders (CDs), also known as neurocognitive disorders (NCDs), are a category of mental health disorders that primarily affect cognitive abilities including learning, memory, perception, and problem-solving. Neurocognitive disorders include delirium, mild neurocognitive disorders, and major neurocognitive disorder. They are defined by deficits in cognitive ability that are acquired, typically represent decline, and may have an underlying brain pathology. The DSM-5 defines six key domains of cognitive function: executive function, learning and memory, perceptual-motor function, language, complex attention, and social cognition.

<span class="mw-page-title-main">Tau protein</span> Group of six protein isoforms produced from the MAPT gene

The tau proteins are a group of six highly soluble protein isoforms produced by alternative splicing from the gene MAPT. They have roles primarily in maintaining the stability of microtubules in axons and are abundant in the neurons of the central nervous system (CNS), where the cerebral cortex has the highest abundance. They are less common elsewhere but are also expressed at very low levels in CNS astrocytes and oligodendrocytes.

<span class="mw-page-title-main">Amyloid beta</span> Group of peptides

Amyloid beta denotes peptides of 36–43 amino acids that are the main component of the amyloid plaques found in the brains of people with Alzheimer's disease. The peptides derive from the amyloid-beta precursor protein (APP), which is cleaved by beta secretase and gamma secretase to yield Aβ in a cholesterol-dependent process and substrate presentation. Aβ molecules can aggregate to form flexible soluble oligomers which may exist in several forms. It is now believed that certain misfolded oligomers can induce other Aβ molecules to also take the misfolded oligomeric form, leading to a chain reaction akin to a prion infection. The oligomers are toxic to nerve cells. The other protein implicated in Alzheimer's disease, tau protein, also forms such prion-like misfolded oligomers, and there is some evidence that misfolded Aβ can induce tau to misfold.

<span class="mw-page-title-main">Beta-secretase 1</span> Enzyme

Beta-secretase 1, also known as beta-site amyloid precursor protein cleaving enzyme 1, beta-site APP cleaving enzyme 1 (BACE1), membrane-associated aspartic protease 2, memapsin-2, aspartyl protease 2, and ASP2, is an enzyme that in humans is encoded by the BACE1 gene. Expression of BACE1 is observed mainly in neurons.

The biochemistry of Alzheimer's disease, the most common cause of dementia, is not yet very well understood. Alzheimer's disease (AD) has been identified as a proteopathy: a protein misfolding disease due to the accumulation of abnormally folded amyloid beta (Aβ) protein in the brain. Amyloid beta is a short peptide that is an abnormal proteolytic byproduct of the transmembrane protein amyloid-beta precursor protein (APP), whose function is unclear but thought to be involved in neuronal development. The presenilins are components of proteolytic complex involved in APP processing and degradation.

<span class="mw-page-title-main">Kalirin</span> Protein-coding gene in the species Homo sapiens

Kalirin, also known as Huntingtin-associated protein-interacting protein (HAPIP), protein duo (DUO), or serine/threonine-protein kinase with Dbl- and pleckstrin homology domain, is a protein that in humans is encoded by the KALRN gene. Kalirin was first identified in 1997 as a protein interacting with huntingtin-associated protein 1. Is also known to play an important role in nerve growth and axonal development.

<span class="mw-page-title-main">VGF</span> Mammalian protein found in Homo sapiens

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<span class="mw-page-title-main">PTPN5</span> Protein-coding gene in the species Homo sapiens

Protein tyrosine phosphatase non-receptor type 5 is an enzyme that in humans is encoded by the PTPN5 gene.

<span class="mw-page-title-main">Kenneth L. Davis</span>

Kenneth L. Davis is chief executive officer of the Mount Sinai Health System in New York City, an American author and medical researcher who developed the Alzheimer's Disease Assessment Scale, the most widely used tool to test the efficacy of treatments for Alzheimer's disease designed specifically to evaluate the severity of cognitive and noncognitive behavioral dysfunctions characteristic to persons with Alzheimer's disease. His research led to four of the first five FDA-approved drugs for Alzheimer's.

<span class="mw-page-title-main">Alzheimer's disease</span> Progressive neurodegenerative disease

Alzheimer's disease (AD) is a neurodegenerative disease that usually starts slowly and progressively worsens, and is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation, mood swings, loss of motivation, self-neglect, and behavioral issues. As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the typical life expectancy following diagnosis is three to nine years.

Samuel E. Gandy, is a neurologist, cell biologist, Alzheimer's disease (AD) researcher and expert in the metabolism of the sticky substance called amyloid that clogs the brain in patients with Alzheimer's. His team discovered the first drugs that could lower the formation of amyloid.

Ming-Ming Zhou is an American scientist who focuses on structural and chemical biology, NMR spectroscopy, and drug design. He is the Dr. Harold, Golden Lamport Professor, and Chairman of the Department of Pharmacological Sciences. He is also the Co-Director of the Drug Discovery Institute at the Icahn School of Medicine at Mount Sinai and Mount Sinai Health System in New York City, as well as Professor of Sciences.

<span class="mw-page-title-main">Eric Schadt</span> American scientist

Eric Emil Schadt is an American mathematician and computational biologist. He is founder and former chief executive officer of Sema4, a patient-centered health intelligence company, and dean for precision medicine and Mount Sinai Professor in Predictive Health and Computational Biology at the Icahn School of Medicine at Mount Sinai. He was previously founding director of the Icahn Institute for Genomics and Multiscale Biology and chair of the Department of Genetics and Genomics Sciences at the Icahn School of Medicine at Mount Sinai.

The Icahn Genomics Institute is a biomedical and genomics research institute within the Icahn School of Medicine at Mount Sinai in New York City. Its aim is to establish a new generation of medicines that can better treat diseases afflicting the world, including cancer, heart disease and infectious pathogens. To do this, the institute’s doctors and scientists are developing and employing new types of treatments that utilize DNA and RNA based therapies, such as CRISPR, siRNA, RNA vaccines, and CAR T cells, and searching for novel drug targets through the use of functional genomics and data science. The institute is led by Brian Brown, a leading expert in gene therapy, genetic engineering, and molecular immunology.

Joseph D. Buxbaum is an American molecular and cellular neuroscientist, autism researcher, and the Director of the Seaver Autism Center at the Icahn School of Medicine at Mount Sinai. Buxbaum is also, along with Simon Baron-Cohen, the co-editor of the BioMed Central journal Molecular Autism, and is a member of the scientific advisory board of the Autism Science Foundation. Buxbaum is a Professor of Psychiatry, Neuroscience, and Genetics and Genomic Sciences. He is also the Vice Chair for Research and for Mentoring in the Department of Psychiatry at the Icahn School of Medicine at Mount Sinai.

<span class="mw-page-title-main">Joel Dudley</span>

Joel Dudley is currently Associate Professor of Genetics and Genomic Sciences and founding Director of the Institute for Next Generation Healthcare at the Icahn School of Medicine at Mount Sinai. In March, 2018 Dr. Dudley was named Executive Vice President for Precision Health for the Mount Sinai Health System (MSHS). In 2017 he was awarded an Endowed Professorship by Mount Sinai in Biomedical Data Science. Prior to Mount Sinai, he held positions as Co-founder and Director of Informatics at NuMedii, Inc. and Consulting Professor of Systems Medicine in the Department of Pediatrics at Stanford University School of Medicine. His work is focused at the nexus of -omics, digital health, artificial intelligence (AI), scientific wellness, and healthcare delivery. His work has been featured in the Wall Street Journal, Scientific American, MIT Technology Review, CNBC, and other popular media outlets. He was named in 2014 as one of the 100 most creative people in business by Fast Company magazine. He is co-author of the book Exploring Personal Genomics from Oxford University Press. Dr. Dudley received a BS in Microbiology from Arizona State University and an MS and PhD in Biomedical Informatics from Stanford University School of Medicine.

Li-Huei Tsai is an American neuroscientist and the director of the Picower Institute for Learning and Memory in the Department of Brain and Cognitive Sciences at the Massachusetts Institute of Technology.

Dena Dubal is the David A. Coulter Endowed Chair in Ageing and Neurodegenerative Disease at University of California, San Francisco. Dubal has demonstrated that the hormone Klotho can enhance cognition and protect the brain from neurodegenerative decline.

<span class="mw-page-title-main">Changjoon Justin Lee</span>

Changjoon Justin Lee is an American neuroscientist specializing in the field of glioscience. He served as the Director of Center for Neuroscience at the Korea Institute of Science and Technology and later founded the WCI Center for Functional Connectomics as part of the World Class Institute Program. In 2015, he established the Center for Glia-Neuron Interaction before becoming co-director of the IBS Center for Cognition and Sociality and head of the Cognitive Glioscience Group in 2018. He has been on the editorial boards of the journals Molecular Brain and Molecular Pain and is a chief editor of Experimental Neurobiology.

<span class="mw-page-title-main">LILRA5</span> Protein-coding gene in the species Homo sapiens

Leukocyte immunoglobulin-like receptor subfamily A member 5 (LILR-A5) also known as CD85 antigen-like family member F (CD85f), immunoglobulin-like transcript 7 (ILT-7), and leukocyte immunoglobulin-like receptor 9 (LIR-9) is a protein that in humans is encoded by the LILRA5 gene. This gene is one of the leukocyte receptor genes that form a gene cluster on the chromosomal region 19q13.4. Four alternatively spliced transcript variants encoding distinct isoforms have been described.

References

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  14. Hao, Ke; Di Narzo, Antonio Fabio; Ho, Lap; Luo, Wei; Li, Shuyu; Chen, Rong; Li, Tongbin; Dubner, Lauren; Pasinetti, Giulio Maria (June 2015). "Shared genetic etiology underlying Alzheimer's disease and type 2 diabetes". Molecular Aspects of Medicine. 43–44: 66–76. doi:10.1016/j.mam.2015.06.006. PMC   6021176 . PMID   26116273.
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  18. "Study Finds Hope in Treating Alzheimer's With Wine Polyphenol" . Retrieved 28 September 2016.{{cite journal}}: Cite journal requires |journal= (help)
  19. "Calorie Restriction May Prevent Alzheimer's Through Promotion Of Longevity Program In The Brain". www.sciencedaily.com. Retrieved 28 September 2016.
  20. "Smart chocolate may eventually be used to treat Alzheimer's, says neurologist" . Retrieved 28 September 2016.{{cite journal}}: Cite journal requires |journal= (help)
  21. Jun, Wang; Merina, Varghese; Kenjiro, Ono; Masahito, Yamada; Samara, Levine; Nikos, Tzavaras; Bing, Gong; J., Hurst, William; D., Blitzer, Robert; Maria, Pasinetti, Giulio (1 January 2014). "Cocoa Extracts Reduce Oligomerization of Amyloid-β: Implications for Cognitive Improvement in Alzheimer's Disease". Journal of Alzheimer's Disease. 41 (2): 643–50. doi:10.3233/JAD-132231. ISSN   1387-2877. PMID   24957018 . Retrieved 28 September 2016.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  22. Wang, Jun; Bi, Weina; Cheng, Alice; Freire, Daniel; Vempati, Prashant; Zhao, Wei; Gong, Bing; Janle, Elsa M.; Chen, Tzu-Ying; Ferruzzi, Mario G.; Schmeidler, James; Ho, Lap; Pasinetti, Giulio M. (14 March 2014). "Targeting multiple pathogenic mechanisms with polyphenols for the treatment of Alzheimer's disease-experimental approach and therapeutic implications". Frontiers in Aging Neuroscience. 6: 42. doi: 10.3389/fnagi.2014.00042 . PMC   3954102 . PMID   24672477.
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  24. Pasinetti, Giulio (11 March 2015). "Novel role of red wine-derived polyphenols in the prevention of Alzheimerʼs disease dementia and brain pathology: experimental approaches and clinical implications". Planta Medica. 78 (15): E24. doi:10.1055/s-0035-1545846. PMID   25760447.
  25. Wang, Jun; Zhao, Zhong; Lin, Emi; Zhao, Wei; Qian, Xianjuan; Freire, Daniel; Bilski, Amanda E.; Cheng, Alice; Vempati, Prashant; Ho, Lap; Ono, Kenjiro; Yamada, Masahito; Pasinetti, Giulio M. (6 June 2013). "Unintended Effects of Cardiovascular Drugs on the Pathogenesis of Alzheimer's Disease". PLOS ONE. 8 (6): e65232. Bibcode:2013PLoSO...865232W. doi: 10.1371/journal.pone.0065232 . ISSN   1932-6203. PMC   3675203 . PMID   23762322.
  26. 1 2 Giulio, Pasinetti; Paul, Rosenberg. "Pilot Trial of Carvedilol in Alzheimer's Disease".{{cite journal}}: Cite journal requires |journal= (help)
  27. 1 2 Ward, Libby; Pasinetti, Giulio Maria (24 June 2016). "Recommendations for Development of Botanical Polyphenols as "Natural Drugs" for Promotion of Resilience Against Stress-Induced Depression and Cognitive Impairment". NeuroMolecular Medicine. 18 (3): 487–495. doi:10.1007/s12017-016-8418-6. PMC   4985489 . PMID   27342633.
  28. Wang, Jun; Tang, Cheuk; Ferruzzi, Mario G.; Gong, Bing; Song, Brian J.; Janle, Elsa M.; Chen, Tzu-Ying; Cooper, Bruce; Varghese, Merina; Cheng, Alice; Freire, Daniel; Bilski, Amanda; Roman, Jessica; Nguyen, Tuyen; Ho, Lap; Talcott, Stephen T.; Simon, James E.; Wu, Qingli; Pasinetti, Giulio M. (December 2013). "Role of standardized grape polyphenol preparation as a novel treatment to improve synaptic plasticity through attenuation of features of metabolic syndrome in a mouse model". Molecular Nutrition & Food Research. 57 (12): 2091–2102. doi:10.1002/mnfr.201300230. PMC   3855562 . PMID   23963661.
  29. 1 2 Dubner, Lauren; Wang, Jun; Ho, Lap; Ward, Libby; Pasinetti, Giulio M. (27 October 2015). "Recommendations for Development of New Standardized Forms of Cocoa Breeds and Cocoa Extract Processing for the Prevention of Alzheimer's Disease: Role of Cocoa in Promotion of Cognitive Resilience and Healthy Brain Aging". Journal of Alzheimer's Disease. 48 (4): 879–889. doi:10.3233/JAD-150536. PMID   26402120.
  30. Wang, Jun; Land, David; Ono, Kenjiro; Galvez, Jorge; Zhao, Wei; Vempati, Prashant; Steele, John W.; Cheng, Alice; Yamada, Masahito; Levine, Samara; Mazzola, Paolo; Pasinetti, Giulio M. (26 March 2014). "Molecular Topology as Novel Strategy for Discovery of Drugs with Aβ Lowering and Anti-Aggregation Dual Activities for Alzheimer's Disease". PLOS ONE. 9 (3): e92750. Bibcode:2014PLoSO...992750W. doi: 10.1371/journal.pone.0092750 . ISSN   1932-6203. PMC   3966818 . PMID   24671215.
  31. 1 2 Wang, Dongjie; Ho, Lap; Faith, Jeremiah; Ono, Kenjiro; Janle, Elsa M.; Lachcik, Pamela J.; Cooper, Bruce R.; Jannasch, Amber H.; D'Arcy, Bruce R.; Williams, Barbara A.; Ferruzzi, Mario G.; Levine, Samara; Zhao, Wei; Dubner, Lauren; Pasinetti, Giulio M. (June 2015). "Role of intestinal microbiota in the generation of polyphenol-derived phenolic acid mediated attenuation of Alzheimer's disease β-amyloid oligomerization". Molecular Nutrition & Food Research. 59 (6): 1025–1040. doi:10.1002/mnfr.201400544. PMC   4498582 . PMID   25689033.
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  34. Wang, Jun; Hodes, Georgoa E.; Hongxing, Zhang; Pasinetti, Giulio Maria (2018). "Epigenetic modulation of inflammation and synaptic plasticity promotes resilience against stress in mice". Nature Communications. 9 (1): 477. Bibcode:2018NatCo...9..477W. doi:10.1038/s41467-017-02794-5. PMC   5797143 . PMID   29396460.
  35. Ho, Lap; Lange, Gudrun; Zhao, Wei; Wang, Jun; Rooney, Robert; Patel, Divyen H.; Fobler, Malusha M.; Helmer, Drew A.; Elder, Gregory; Shaughness, Michael C.; Ahlers, Stephen T.; Russo, Scott J.; Pasinetti, Giulio Maria (1 January 2014). "Select small nucleolar RNAs in blood components as novel biomarkers for improved identification of comorbid traumatic brain injury and post-traumatic stress disorder in veterans of the conflicts in Afghanistan and Iraq". American Journal of Neurodegenerative Disease. 3 (3): 170–181. ISSN   2165-591X. PMC   4299721 . PMID   25628968.
  36. Pasinetti, Giulio M.; Ho, Lap; Dooley, Christopher; Abbi, Bhavna; Lange, Gudrun (1 January 2012). "Select non-coding RNA in blood components provide novel clinically accessible biological surrogates for improved identification of traumatic brain injury in OEF/OIF Veterans". American Journal of Neurodegenerative Disease. 1 (1): 88–98. ISSN   2165-591X. PMC   3560446 . PMID   22737634.
  37. Zhao, Wei; Ho, Lap; Varghese, Merina; Yemul, Shrishailam; Dams-O'Connor, Kristen; Gordon, Wayne; Knable, Lindsay; Freire, Daniel; Haroutunian, Vahram; Pasinetti, Giulio Maria (1 January 2013). "Decreased level of olfactory receptors in blood cells following traumatic brain injury and potential association with tauopathy". Journal of Alzheimer's Disease. 34 (2): 417–429. doi:10.3233/JAD-121894. ISSN   1875-8908. PMC   3968322 . PMID   23241557.