LUCIANO D'ADAMIO

Summary

Affiliation: Albert Einstein College of Medicine
Country: USA

Publications

  1. pmc The interactome of the amyloid beta precursor protein family members is shaped by phosphorylation of their intracellular domains
    Robert Tamayev
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA
    Mol Neurodegener 4:28. 2009
  2. pmc CD74 interacts with APP and suppresses the production of Abeta
    Shuji Matsuda
    Albert Einstein College of Medicine, Department of Microbiology and Immunology, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Mol Neurodegener 4:41. 2009
  3. pmc Evidence that the Amyloid beta Precursor Protein-intracellular domain lowers the stress threshold of neurons and has a "regulated" transcriptional role
    Luca Giliberto
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA
    Mol Neurodegener 3:12. 2008
  4. ncbi request reprint The familial dementia BRI2 gene binds the Alzheimer gene amyloid-beta precursor protein and inhibits amyloid-beta production
    Shuji Matsuda
    Albert Einstein College of Medicine, Bronx, NY 10461, USA
    J Biol Chem 280:28912-6. 2005
  5. ncbi request reprint Processing of beta-amyloid precursor-like protein-1 and -2 by gamma-secretase regulates transcription
    Meir H Scheinfeld
    Albert Einstein College of Medicine, Department of Microbiology and Immunology, Bronx, New York 10461, USA
    J Biol Chem 277:44195-201. 2002
  6. ncbi request reprint Amyloid-beta protein precursor (AbetaPP) intracellular domain-associated protein-1 proteins bind to AbetaPP and modulate its processing in an isoform-specific manner
    Enrico Ghersi
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA
    J Biol Chem 279:49105-12. 2004
  7. pmc BRI3 inhibits amyloid precursor protein processing in a mechanistically distinct manner from its homologue dementia gene BRI2
    Shuji Matsuda
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 1046, USA
    J Biol Chem 284:15815-25. 2009
  8. ncbi request reprint Amyloid beta protein precursor (AbetaPP), but not AbetaPP-like protein 2, is bridged to the kinesin light chain by the scaffold protein JNK-interacting protein 1
    Shuji Matsuda
    Albert Einstein College of Medicine, Department of Microbiology and Immunology, Bronx, New York 10461, USA
    J Biol Chem 278:38601-6. 2003
  9. pmc BRI2 inhibits amyloid beta-peptide precursor protein processing by interfering with the docking of secretases to the substrate
    Shuji Matsuda
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Neurosci 28:8668-76. 2008
  10. pmc APP heterozygosity averts memory deficit in knockin mice expressing the Danish dementia BRI2 mutant
    Robert Tamayev
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA
    EMBO J 30:2501-9. 2011

Collaborators

Detail Information

Publications31

  1. pmc The interactome of the amyloid beta precursor protein family members is shaped by phosphorylation of their intracellular domains
    Robert Tamayev
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA
    Mol Neurodegener 4:28. 2009
    ..abstract:..
  2. pmc CD74 interacts with APP and suppresses the production of Abeta
    Shuji Matsuda
    Albert Einstein College of Medicine, Department of Microbiology and Immunology, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Mol Neurodegener 4:41. 2009
    ..abstract:..
  3. pmc Evidence that the Amyloid beta Precursor Protein-intracellular domain lowers the stress threshold of neurons and has a "regulated" transcriptional role
    Luca Giliberto
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA
    Mol Neurodegener 3:12. 2008
    ..Also, we have studied the susceptibility of primary neurons from such mice to stress and pro-apoptotic agents...
  4. ncbi request reprint The familial dementia BRI2 gene binds the Alzheimer gene amyloid-beta precursor protein and inhibits amyloid-beta production
    Shuji Matsuda
    Albert Einstein College of Medicine, Bronx, NY 10461, USA
    J Biol Chem 280:28912-6. 2005
    ..Finding that BRI2 pathogenic mutations alter the regulatory function of BRI2 on A(beta)PP processing would define dysregulation of A(beta)PP cleavage as a pathogenic mechanism common to AD, FDD, and FBD...
  5. ncbi request reprint Processing of beta-amyloid precursor-like protein-1 and -2 by gamma-secretase regulates transcription
    Meir H Scheinfeld
    Albert Einstein College of Medicine, Department of Microbiology and Immunology, Bronx, New York 10461, USA
    J Biol Chem 277:44195-201. 2002
    ....
  6. ncbi request reprint Amyloid-beta protein precursor (AbetaPP) intracellular domain-associated protein-1 proteins bind to AbetaPP and modulate its processing in an isoform-specific manner
    Enrico Ghersi
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA
    J Biol Chem 279:49105-12. 2004
    ..Furthermore, we provide data supporting a possible function for AIDA-1a as a modulator of AbetaPP processing...
  7. pmc BRI3 inhibits amyloid precursor protein processing in a mechanistically distinct manner from its homologue dementia gene BRI2
    Shuji Matsuda
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 1046, USA
    J Biol Chem 284:15815-25. 2009
    ..Competitive inhibition of APP processing by BRI3 may provide a new approach to AD therapy and prevention...
  8. ncbi request reprint Amyloid beta protein precursor (AbetaPP), but not AbetaPP-like protein 2, is bridged to the kinesin light chain by the scaffold protein JNK-interacting protein 1
    Shuji Matsuda
    Albert Einstein College of Medicine, Department of Microbiology and Immunology, Bronx, New York 10461, USA
    J Biol Chem 278:38601-6. 2003
    ..Our data suggest that kinesin-I-dependent neuronal AbetaPP transport, which controls AbetaPP processing, may be regulated by JIP1...
  9. pmc BRI2 inhibits amyloid beta-peptide precursor protein processing by interfering with the docking of secretases to the substrate
    Shuji Matsuda
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Neurosci 28:8668-76. 2008
    ..Alterations of BRI2 by gene targeting or transgenic expression regulate Abeta levels and AD pathology in mouse models of AD. Competitive inhibition of APP processing by BRI2 may provide a new approach to AD therapy and prevention...
  10. pmc APP heterozygosity averts memory deficit in knockin mice expressing the Danish dementia BRI2 mutant
    Robert Tamayev
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA
    EMBO J 30:2501-9. 2011
    ..This evidence establishes a pathogenic sameness between familial Danish and Alzheimer's dementias...
  11. ncbi request reprint Amyloid beta protein precursor is phosphorylated by JNK-1 independent of, yet facilitated by, JNK-interacting protein (JIP)-1
    Meir H Scheinfeld
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    J Biol Chem 278:42058-63. 2003
    ..Understanding the connection between AbetaPP phosphorylation and the JNK signaling pathway, which mediates cell response to stress may have important implications in understanding the pathogenesis of Alzheimer's disease...
  12. pmc β- but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia
    Robert Tamayev
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA
    EMBO Mol Med 4:171-9. 2012
    ..Our data and the failures of anti-Aβ therapies in humans advise against targeting γ-secretase cleavage of APP and/or Aβ...
  13. pmc Generation and initial characterization of FDD knock in mice
    Luca Giliberto
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York, USA
    PLoS ONE 4:e7900. 2009
    ..The interaction between the two precursors, APP and BRI(2), and possibly between Abeta and ABri or ADan, could be important in influencing the rate of amyloid production or the tendency of these peptides to aggregate...
  14. ncbi request reprint Growth factor receptor-bound protein 2 interaction with the tyrosine-phosphorylated tail of amyloid beta precursor protein is mediated by its Src homology 2 domain
    Dawang Zhou
    Albert Einstein College of Medicine, Department of Microbiology and Immunology, Bronx, New York 10461, USA
    J Biol Chem 279:25374-80. 2004
    ....
  15. pmc Caspase-9 mediates synaptic plasticity and memory deficits of Danish dementia knock-in mice: caspase-9 inhibition provides therapeutic protection
    Robert Tamayev
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Mol Neurodegener 7:60. 2012
    ..It was previously shown that FAD mutations in APP and PSENs promote activation of caspases leading to the hypothesis that aberrant caspase activation could participate in AD pathogenesis...
  16. pmc Danish dementia mice suggest that loss of function and not the amyloid cascade causes synaptic plasticity and memory deficits
    Robert Tamayev
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 107:20822-7. 2010
    ..Together, the data suggest that clinical dementia in Danish patients occurs via a loss of function mechanism and not as a result of amyloidosis and tauopathy...
  17. pmc Increased AβPP processing in familial Danish dementia patients
    Shuji Matsuda
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA
    J Alzheimers Dis 27:385-91. 2011
    ....
  18. ncbi request reprint The intracellular localization of amyloid beta protein precursor (AbetaPP) intracellular domain associated protein-1 (AIDA-1) is regulated by AbetaPP and alternative splicing
    Enrico Ghersi
    Albert Einstein College of Medicine, Department of Microbiology and Immunology, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    J Alzheimers Dis 6:67-78. 2004
    ....
  19. pmc Maturation of BRI2 generates a specific inhibitor that reduces APP processing at the plasma membrane and in endocytic vesicles
    Shuji Matsuda
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Neurobiol Aging 32:1400-8. 2011
    ..Thus, BRI2 is a specific inhibitor that reduces secretases' access to APP in the intracellular compartments where APP is normally processed...
  20. ncbi request reprint Evidence for a role of the nerve growth factor receptor TrkA in tyrosine phosphorylation and processing of beta-APP
    Philip E Tarr
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Ullmann 1209, Bronx, NY 10461, USA
    Biochem Biophys Res Commun 295:324-9. 2002
    ..Thus, tyrosine phosphorylation of APP may functionally link APP processing and neurotrophic signaling to intracellular pathways associated with cellular differentiation and survival...
  21. pmc An intracellular threonine of amyloid-β precursor protein mediates synaptic plasticity deficits and memory loss
    Franco Lombino
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York, United States of America
    PLoS ONE 8:e57120. 2013
    ..These data are consistent with a role for the carboxyl-terminal APP domain in the pathogenesis of dementia and suggest that averting the noxious role of Thr(668) is a viable therapeutic strategy for human dementias...
  22. pmc Inhibition of γ-secretase worsens memory deficits in a genetically congruous mouse model of Danish dementia
    Robert Tamayev
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Mol Neurodegener 7:19. 2012
    ..However, inhibiting Aβ production did not rescue the deficits of FDDKI mice, suggesting that sAPPβ/β-CTF, and not Aβ, are the toxic species causing memory loss...
  23. pmc Memory deficits of British dementia knock-in mice are prevented by Aβ-precursor protein haploinsufficiency
    Robert Tamayev
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Neurosci 32:5481-5. 2012
    ..This evidence establishes a mechanistic connection between Familial British and Alzheimer's dementias...
  24. pmc The gamma-secretase-generated intracellular domain of beta-amyloid precursor protein binds Numb and inhibits Notch signaling
    Roberta Roncarati
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 99:7102-7. 2002
    ..Thus, gamma-secretase may have opposing effects on Notch signaling; positive by cleaving Notch and generating NICD, and negative by processing APP and generating AID, which inhibits the function of NICD...
  25. pmc Memory deficits due to familial British dementia BRI2 mutation are caused by loss of BRI2 function rather than amyloidosis
    Robert Tamayev
    Department of Microbiology and Immunology, Einstein College of Medicine, Bronx, New York 10461, USA
    J Neurosci 30:14915-24. 2010
    ..Collectively, these results indicate that the British BRI2 mutation underlies abnormal memory due to loss of BRI2 function and independently of histopathological alterations typically evident in advanced neurodegenerative disease...
  26. pmc The intracellular threonine of amyloid precursor protein that is essential for docking of Pin1 is dispensable for developmental function
    Alessia P M Barbagallo
    Department of Microbiology and Immunology, Einstein College of Medicine, Bronx, New York, United States of America
    PLoS ONE 6:e18006. 2011
    ..Thr residue at amino acid 668 of the APP intracellular domain (AID) is highly conserved. When phosphorylated, this residue generates a binding site for Pin1. The interaction of APP with Pin1 has been involved in AD pathogenesis...
  27. pmc JNK-interacting protein-1 promotes transcription of A beta protein precursor but not A beta precursor-like proteins, mechanistically different than Fe65
    Meir H Scheinfeld
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 100:1729-34. 2003
    ..This activity for the AID fragment may help explain the unique functions of A beta PP relative to its other family members, and changes in gene expression found in Alzheimer's disease...
  28. ncbi request reprint Tyrosine phosphorylation of the beta-amyloid precursor protein cytoplasmic tail promotes interaction with Shc
    Philip E Tarr
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Biol Chem 277:16798-804. 2002
    ..Thus, APP and Shc proteins interact in vitro, in cells, and in the mouse brain. Tyrosine phosphorylation of APP may promote the interaction with Shc proteins...
  29. pmc A single tyrosine residue in the amyloid precursor protein intracellular domain is essential for developmental function
    Alessia P M Barbagallo
    Department of Microbiology and Immunology, Einstein College of Medicine, Bronx, New York 10461, USA
    J Biol Chem 286:8717-21. 2011
    ..Our results demonstrate that a single residue in the APP intracellular region, Tyr(682), is indispensable for the essential function of APP in developmental regulation...
  30. ncbi request reprint Autosomal recessive hypercholesterolemia protein interacts with and regulates the cell surface level of Alzheimer's amyloid beta precursor protein
    Cristiana Noviello
    Albert Einstein College of Medicine, Department of Microbiology and Immunology, Bronx, New York 10461, USA
    J Biol Chem 278:31843-7. 2003
    ..Moreover, we show that reduction of ARH expression by RNA interference results in increased levels of cell membrane A beta PP. These data assert a physiological role for ARH in A beta PP internalization, transport, and/or processing...
  31. pmc Tyr(682) in the intracellular domain of APP regulates amyloidogenic APP processing in vivo
    Alessia P M Barbagallo
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York, United States of America
    PLoS ONE 5:e15503. 2010
    ..For example, normal Aβ generation and secretion are dependent upon Tyr(682) in vitro. However, physiological functions of Tyr(682) are unknown...

Research Grants12

  1. Signaling Function by APP Processing and Release of AID
    LUCIANO D ADAMIO; Fiscal Year: 2006
    ..Lastly, regulation of APP endocytosis and processing by Numb/Nbl proteins might provide potential new targets for compounds aimed to reduce Abeta production. ..
  2. BR12 Familial British and Danish Dementias and Alzheimer's Disease
    LUCIANO D ADAMIO; Fiscal Year: 2009
    ..We hope that our studies will translate into a program to develop drug for altering the course of the disease versus simply treating the symptoms like all of the approved drugs for AD currently are. ..
  3. Cellular signaling and Trafficking of APP Family Members
    LUCIANO D ADAMIO; Fiscal Year: 2003
    ..These studies may clarify the biological role of APP family members and have important practical applications in the development of new compounds for the cure and or prevention of Alzheimer's disease. ..
  4. Novel Animal Models of Familial British, Danish and Alzheimer's Dementia
    LUCIANO D ADAMIO; Fiscal Year: 2007
    ....
  5. Cellular signaling and Trafficking of APP Family Members
    LUCIANO D ADAMIO; Fiscal Year: 2007
    ..These studies may clarify the biological role of APP family members and have important practical applications in the development of new compounds for the cure and or prevention of Alzheimer's disease. ..
  6. Cellular signaling and Trafficking of APP Family Members
    LUCIANO D ADAMIO; Fiscal Year: 2006
    ..These studies may clarify the biological role of APP family members and have important practical applications in the development of new compounds for the cure and or prevention of Alzheimer's disease. ..
  7. Signaling Function by APP Processing and Release of AID
    LUCIANO D ADAMIO; Fiscal Year: 2005
    ..Lastly, regulation of APP endocytosis and processing by Numb/Nbl proteins might provide potential new targets for compounds aimed to reduce Abeta production. ..
  8. Cellular signaling and Trafficking of APP Family Members
    LUCIANO D ADAMIO; Fiscal Year: 2005
    ..These studies may clarify the biological role of APP family members and have important practical applications in the development of new compounds for the cure and or prevention of Alzheimer's disease. ..
  9. Signaling Function by APP Processing and Release of AID
    LUCIANO D ADAMIO; Fiscal Year: 2004
    ..Lastly, regulation of APP endocytosis and processing by Numb/Nbl proteins might provide potential new targets for compounds aimed to reduce Abeta production. ..
  10. Cellular signaling and Trafficking of APP Family Members
    LUCIANO D ADAMIO; Fiscal Year: 2004
    ..These studies may clarify the biological role of APP family members and have important practical applications in the development of new compounds for the cure and or prevention of Alzheimer's disease. ..
  11. Signaling Function by APP Processing and Release of AID
    LUCIANO D ADAMIO; Fiscal Year: 2003
    ..Lastly, regulation of APP endocytosis and processing by Numb/Nbl proteins might provide potential new targets for compounds aimed to reduce Abeta production. ..
  12. BR12 Familial British and Danish Dementias and Alzheimer's Disease
    LUCIANO D apos ADAMIO; Fiscal Year: 2010
    ..We hope that our studies will translate into a program to develop drug for altering the course of the disease versus simply treating the symptoms like all of the approved drugs for AD currently are. ..