Andrea Fuso
Università degli Studi "La Sapienza" di Roma, Psychology, Faculty Member
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Publication Date: 2006
Publication Name: Alzheimer's & Dementia
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Publication Date: 2008
Publication Name: Protein and Peptide Letters
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Publication Date: 2012
Publication Name: The Cerebellum
Research Interests: Cognitive Science, Neurogenesis, Transcription Factors, Gene Silencing, Cell Differentiation, and 13 moreCerebellum, Mice, Animals, Male, Neurons, In vitro culture, Primary Cell Culture, Subcellular Fractions, Cerebellar Cortex, Neurosciences, Granule cell layer, Nuclear Localization, and Purkinje cell
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S-adenosylmethionine reduces the progress of the Alzheimer-like features induced by B-vitamin deficiency in micemore
by Elisa Isopi and Andrea Fuso
Publication Date: 2012
Publication Name: Neurobiology of Aging
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by Andrea Fuso and Maria Teresa Fiorenza
We have previously shown that a nutritional model of B vitamin deficiency and homocysteine cycle alteration could lead to increased amyloid β deposition, due to PSEN1 and BACE over-expression and consequent increase in secretase activity.... more
We have previously shown that a nutritional model of B vitamin deficiency and homocysteine cycle alteration could lead to increased amyloid β deposition, due to PSEN1 and BACE over-expression and consequent increase in secretase activity. We hypothesize that nutritional factors causing homocysteine cycle alterations (ie hyperhomocysteinemia) could induce sequence-specific DNA hypomethylation and “aberrant” gene activation.
Journal Name: Neurobiology of aging
Publication Date: Feb 28, 2011
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Identification of Spermatogonial Stem Cell Subsets by Morphological Analysis and Prospective Isolationmore
by Ilaria Falciatori and Andrea Fuso
Publication Date: 2009
Publication Name: Stem Cells
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Publication Date: 2006
Publication Name: Alzheimer's & Dementia
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B-vitamin deprivation induces hyperhomocysteinemia and brain S-adenosylhomocysteine, depletes brain S-adenosylmethionine, and enhances PS1 and BACE expression and amyloid-β deposition in micemore
by Gemma Calamandrei and Andrea Fuso
Publication Date: 2008
Publication Name: Molecular and Cellular Neuroscience
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Publication Date: 2006
Publication Name: Alzheimer's & Dementia
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by Andrea Fuso and Sigfrido Scarpa
High homocysteine (Hcy) together with low S-adenosylmethionine (SAM) levels are often observed in Alzheimer disease (AD), and this could be a sign of alteration of SAM/Hcy metabolism. It has already been shown that DNA methylation is... more
High homocysteine (Hcy) together with low S-adenosylmethionine (SAM) levels are often observed in Alzheimer disease (AD), and this could be a sign of alteration of SAM/Hcy metabolism. It has already been shown that DNA methylation is involved in amyloid-β-protein precursor (AβPP) processing and amyloid-β(Aβ) production through the regulation of Presenilin 1 (PS1) expression and that exogenous SAM can silence the
Publication Date: 2006
Research Interests: Cognitive Science, RNA, Aging, Membrane Proteins, Gene expression, and 13 moreHumans, DNA methylation, Central Nervous System, Homocysteine, Clinical Sciences, High Pressure Liquid Chromatography, Neuroblastoma, Presenilin-2, Cdna Microarray, S-Adenosylmethionine, Alzheimer Disease, Neurosciences, and Amyloid Beta Precursor Protein
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by Andrea Fuso and Sigfrido Scarpa
Alzheimer disease (AD) is among the few diseases that may display high homocysteine (HCY) and low B12 and folate in blood. This observation has raised the suspect that amyloid-β overproduction and accumulation, which may be the cause of... more
Alzheimer disease (AD) is among the few diseases that may display high homocysteine (HCY) and low B12 and folate in blood. This observation has raised the suspect that amyloid-β overproduction and accumulation, which may be the cause of the disease, could be due to the loss of epigenetic control in the expression of the genes involved in AβPP (amyloid-β protein
Publication Date: 2006
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Widely confirmed reports were published on association between hyperhomocysteinemia, B vitamin deficiency, oxidative stress, and amyloid-β in Alzheimer's disease (AD). Homocysteine, cysteine, cysteinylglycine and glutathione are... more
Widely confirmed reports were published on association between hyperhomocysteinemia, B vitamin deficiency, oxidative stress, and amyloid-β in Alzheimer's disease (AD). Homocysteine, cysteine, cysteinylglycine and glutathione are metabolically interrelated thiols that may be potential indicators of health status and disease risk; they all participate in the metabolic pathway of homocysteine. Previous data obtained in one of our laboratories showed that B vitamin deficiency induced exacerbation of AD-like features in TgCRND8 AD mice; these effects were counteracted by S-adenosylmethionine (SAM) supplementation, through the modulation of DNA methylation and antioxidant pathways. Since the cellular response to oxidative stress typically involves alteration in thiols content, a rapid and sensitive HPLC method with fluorescence detection was here used to evaluate the effect of SAM and superoxide-dismutase (SOD) supplementation on thiols level in plasma, in TgCRND8 mice. The quantitati...
Publication Date: 2015
Publication Name: Journal of Alzheimer's disease : JAD
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Multiple aspects of homocysteine metabolism were studied to understand the mechanism responsible for hyperhomocysteinemia toxicity in Alzheimer disease. Besides oxidative stress and vascular damage, homocysteine has also a great... more
Multiple aspects of homocysteine metabolism were studied to understand the mechanism responsible for hyperhomocysteinemia toxicity in Alzheimer disease. Besides oxidative stress and vascular damage, homocysteine has also a great importance in regulating DNA methylation through S-adenosylmethionine, the main methyl donor in eukaryotes. Alterations of S-adenosylmethionine and methylation were evidenced in Alzheimer disease and in elderly. In order to clarify whether DNA methylation can provide the basis for amyloid-beta overproduction, we used human SK-N-BE neuroblastoma and A172 glioblastoma cell lines. We tested the effects of folate, B12 and B6 deprivation and S-adenosylmethionine addition on methylation metabolism. Our results indicate that homocysteine accumulation induced through vitamin B deprivation could impair the "Methylation Potential" with consequent presenilin 1, BACE and amyloid-beta upregulation. Moreover, we found that homocysteine alterations had an effect ...
Publication Date: 2007
Publication Name: Journal of Alzheimer's disease : JAD
Research Interests: Cognitive Science, Oxidative Stress, Folic acid, Western blotting, Antioxidants, and 14 moreHumans, Glioblastoma, Polymerase Chain Reaction, DNA methylation, Homocysteine, Clinical Sciences, Neuroblastoma, Aged, Presenilin-2, S-Adenosylmethionine, Alzheimer Disease, Neurosciences, vitamin B deficiency, and Amyloid Beta Precursor Protein
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S-adenosylmethionine Inhibits Ubiquitin-Proteasome System In Vitro and on Rat Vascular Smooth Muscle Cellsmore
by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2008
Publication Name: Protein and Peptide Letters
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γ�Secretase is Differentially Modulated by Alterations of Homocysteine Cycle in Neuroblastoma and Glioblastoma Cellsmore
by Andrea Fuso and Sigfrido Scarpa
Multiple aspects of homocysteine metabolism were studied to understand the mechanism responsible for hyperho- mocysteinemia toxicity in Alzheimer disease. Besides oxidative stress and vascular damage, homocysteine has also a great... more
Multiple aspects of homocysteine metabolism were studied to understand the mechanism responsible for hyperho- mocysteinemia toxicity in Alzheimer disease. Besides oxidative stress and vascular damage, homocysteine has also a great importance in regulating DNA methylation through S-adenosylmethionine, the main methyl donor in eukaryotes. Alterations of S-adenosylmethionine and methylation were evidenced in Alzheimer disease and in elderly. In order to clarify
Publication Date: 2000
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Chromatin-modifying agents increase transcription of CYP46A1, a key player in brain cholesterol eliminationmore
by Andrea Fuso and Sigfrido Scarpa
The major mechanism of brain cholesterol elimination is the conversion of cholesterol into 24S-hydroxycholesterol by CYP46A1, a neuron-specific cytochrome P450. Since increasing evidence suggests that upregulation of CYP46A1 may be... more
The major mechanism of brain cholesterol elimination is the conversion of cholesterol into 24S-hydroxycholesterol by CYP46A1, a neuron-specific cytochrome P450. Since increasing evidence suggests that upregulation of CYP46A1 may be relevant for the treatment of Alzheimer's disease, we aim to identify the molecular mechanisms involved in CYP46A1 transcription. Our previous studies demonstrated the role of Sp transcription factors in basal expression and histone deacetylase (HDAC) inhibitor-dependent derepression of CYP46A1. Here, we show that the demethylating agent 5'-Aza-2'-deoxycytidine (DAC) is a CYP46A1 inducer and that pre-treatment with DAC causes a marked synergistic activation of CYP46A1 transcription by trichostatin A. Surprisingly, bisulfite sequencing analysis revealed that the CYP46A1 core promoter is completely unmethylated in both human brain and non-neuronal human tissues where CYP46A1 is not expressed. Therefore, we have investigated Sp expression levels ...
Publication Date: 2010
Publication Name: Journal of Alzheimer's disease : JAD
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Identification of Spermatogonial Stem Cell Subsets by Morphological Analysis and Prospective Isolationmore
by Andrea Fuso
Spermatogenesis is maintained by a pool of spermatogonial stem cells (SSCs). Analyses of the molecular profile of SSCs have revealed the existence of subsets, indicating that the stem cell population is more heterogeneous than previously... more
Spermatogenesis is maintained by a pool of spermatogonial stem cells (SSCs). Analyses of the molecular profile of SSCs have revealed the existence of subsets, indicating that the stem cell population is more heterogeneous than previously believed. However, SSC subsets are poorly characterized. In rodents, the first steps in spermatogenesis have been extensively investigated, both under physiological conditions and during the regenerative phase that follows germ cell damage. In the widely accepted model, the SSCs are type Asingle (As) spermatogonia. Here, we tested the hypothesis that As spermatogonia are phenotypically heterogeneous by analyzing glial cell line-derived neurotrophic factor (GDNF) family receptor alpha1 (GFRA1) expression in whole-mounted seminiferous tubules, via cytofluorimetric analysis and in vivo colonogenic assays. GFRA1 is a coreceptor for GDNF, a Sertoli cell-derived factor essential for SSC self-renewal and proliferation. Morphometric analysis demonstrated that 10% of As spermatogonia did not express GFRA1 but were colonogenic, as shown by germ cell transplantation assay. In contrast, cells selected for GFRA1 expression were not colonogenic in vivo. In human testes, GFRA1 was also heterogeneously expressed in Adark and in Apale spermatogonia, the earliest spermatogonia. In vivo 5-bromo-2'-deoxyuridine administration showed that both GFRA1(+) and GFRA1(-) As spermatogonia were engaged in the cell cycle, a finding supported by the lack of long-term label-retaining As spermatogonia. GFRA1 expression was asymmetric in 5% of paired cells, suggesting that As subsets may be generated by asymmetric cell division. Our data support the hypothesis of the existence of SSC subsets and reveal a previously unrecognized heterogeneity in the expression profile of As spermatogonia in vivo.
Publication Date: 2009
Publication Name: Stem Cells
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Publication Date: 2012
Publication Name: Reproduction
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by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2004
Publication Name: Neurobiology of Aging
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by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2000
Publication Name: Neurobiology of Aging
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P4-394 DNA methylation and HCY/SAM cycle alterations modulate PS1, bace and beta-amyloid levels in Alzheimer's diseasemore
by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2004
Publication Name: Neurobiology of Aging
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by Andrea Fuso and Sigfrido Scarpa
The sporadic form of Alzheimer disease, late onset Alzheimer's disease (LOAD), is a multifactorial disease; a strong link between nutritional and genetic factors with normal aging and dementia is supported by... more
The sporadic form of Alzheimer disease, late onset Alzheimer's disease (LOAD), is a multifactorial disease; a strong link between nutritional and genetic factors with normal aging and dementia is supported by studies on nutrition, metabolism, and neurodegeneration. Specifically, the involvement of homocysteine (HCY) and its dietary determinants (vitamins B6, B12, and folate, besides methionine) in dementia has been a topic of intense investigation. In this Commentary we would like to highlight the role of 1-carbon metabolism in epigenetics and Alzheimer's disease and evidence the co-involvement of this metabolism in amyloid and tau pathways.
Publication Date: 2011
Publication Name: Neurobiology of Aging
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by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2011
Publication Name: Neurobiology of Aging
Research Interests: Neurobiology, Gene expression, Brain, Humans, Mutation, and 15 moreMice, Animals, DNA methylation, Homocysteine, Clinical Sciences, Analysis of Variance, Presenilin-2, Transfection, Genome sequence, Neurobiology of Aging, S-Adenosylmethionine, Neurosciences, vitamin B deficiency, Gene Expression Regulation, and Amyloid Beta Precursor Protein
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S-adenosylmethionine/homocysteine cycle alterations modify DNA methylation status with consequent deregulation of PS1 and BACE and beta-amyloid productionmore
by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2005
Publication Name: Molecular and Cellular Neuroscience
Research Interests: Cognitive Science, Membrane Proteins, Gene expression, Brain, Molecular and cellular biology, and 13 moreHumans, DNA methylation, Homocysteine, SAM, Presenilin-2, App, Cellular and Molecular Neuroscience, S-Adenosylmethionine, Alzheimer Disease, Neurosciences, vitamin B deficiency, Ad, and Amyloid Beta Precursor Protein
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B-vitamin deprivation induces hyperhomocysteinemia and brain S-adenosylhomocysteine, depletes brain S-adenosylmethionine, and enhances PS1 and BACE expression and amyloid-β deposition in micemore
by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2008
Publication Name: Molecular and Cellular Neuroscience
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Corrigendum to “S-adenosylmethionine/homocysteine cycle alterations modify DNA methylation status with consequent deregulation of PS1 and BACE and beta-amyloid production” [Mol. Cell. Neurosci. 28 (2005) 195–204]more
by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2006
Publication Name: Molecular and Cellular Neuroscience
Research Interests: Cognitive Science, Membrane Proteins, Gene expression, Brain, Molecular and cellular biology, and 13 moreHumans, DNA methylation, Homocysteine, SAM, Presenilin-2, App, Cellular and Molecular Neuroscience, S-Adenosylmethionine, Alzheimer Disease, Neurosciences, vitamin B deficiency, Ad, and Amyloid Beta Precursor Protein
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Evaluation of chemical and diastereoisomeric stability of S-adenosylmethionine in aqueous solution by capillary electrophoresismore
by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2005
Publication Name: Journal of Pharmaceutical and Biomedical Analysis
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DNA methylase and demethylase activities are modulated by one-carbon metabolism in Alzheimer's disease models☆☆☆more
by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2011
Publication Name: The Journal of Nutritional Biochemistry
Research Interests: Genetics, Nutrition and Dietetics, Carbon, Folic acid, Epigenomics, and 18 moreCell line, Humans, Mice, Methylation, Female, Animals, Male, DNA methylation, Nutritional Biochemistry, Analysis of Variance, Carbon Metabolism, Food Sciences, S-Adenosylmethionine, Alzheimer Disease, DNA binding proteins, Biochemistry and cell biology, vitamin B deficiency, and Experimental Model
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Publication Date: 2010
Publication Name: Journal of Cancer Research and Clinical Oncology
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Publication Date: 2001
Publication Name: Journal of Biological Chemistry
Research Interests: RNA, Skeletal muscle biology, DNA replication, Biological Chemistry, Molecular Mechanics, and 15 moreBiological Sciences, Spleen, Cell line, Cell Differentiation, Brain, Mice, Animals, DNA methylation, CpG islands, Muscles, CHEMICAL SCIENCES, Rats, Time Factors, S-Adenosylmethionine, and Tissue Specificity
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by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2001
Publication Name: FEBS Letters
Research Interests: Transcription Regulation, Transcription Factors, Gene expression, Gene Silencing, Cell Division, and 13 moreCell line, Cell Differentiation, Mice, Regulation of Gene Expression, Animals, Polymerase Chain Reaction, DNA methylation, Muscles, Creatine Kinase, Molecular weight, S-Adenosylmethionine, Culture Media, and Biochemistry and cell biology
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A reassessment of semiquantitative analytical procedures for DNA methylation: Comparison of bisulfite- and HpaII polymerase-chain-reaction-based methodsmore
by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2006
Publication Name: Analytical Biochemistry
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Publication Date: 2006
Publication Name: Alzheimer's & Dementia
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S-adenosylmethionine and Superoxide-dismutase are effective in amyloidosis reduction in TgCRND8 micemore
by Andrea Fuso and Sigfrido Scarpa
Alzheimer's & Dementia: The Journal of the Alzheimer's Association, Volume 7, Issue 4, Pages S478-S479, July 2011, Authors:Andrea Fuso; Rosaria Cavallaro; Vincenzina Nicolia; Maria Teresa Fiorenza;... more
Alzheimer's & Dementia: The Journal of the Alzheimer's Association, Volume 7, Issue 4, Pages S478-S479, July 2011, Authors:Andrea Fuso; Rosaria Cavallaro; Vincenzina Nicolia; Maria Teresa Fiorenza; Sigfrido Scarpa.
Publication Date: 2011
Publication Name: Alzheimer's & Dementia
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Publication Date: 2008
Publication Name: Alzheimer's & Dementia
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P4-181: Homocysteine, S-adenosylmethionine/s-adenosylhomocysteine ratio, glutathione and nitric oxide levels in TgCRDND8 mice fed with B vitamin–deficient dietmore
by Andrea Fuso and Sigfrido Scarpa
Publication Date: 2008
Publication Name: Alzheimer's & Dementia
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Publication Date: 2006
Publication Name: Alzheimer's & Dementia
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P2-165: The equilibrium between Gsk3β and PP2A activities is regulated by B vitamins in Alzheimer's diseasemore
by Andrea Fuso and Sigfrido Scarpa