D J Selkoe

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Toward a comprehensive theory for Alzheimer's disease. Hypothesis: Alzheimer's disease is caused by the cerebral accumulation and cytotoxicity of amyloid beta-protein
    D J Selkoe
    Department of Neurology, Harvard Medical School, and Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Ann N Y Acad Sci 924:17-25. 2000
  2. ncbi request reprint FAD mutations in presenilin-1 or amyloid precursor protein decrease the efficacy of a gamma-secretase inhibitor: evidence for direct involvement of PS1 in the gamma-secretase cleavage complex
    W Xia
    Department of Neurology, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Neurobiol Dis 7:673-81. 2000
  3. pmc Presenilin complexes with the C-terminal fragments of amyloid precursor protein at the sites of amyloid beta-protein generation
    W Xia
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 97:9299-304. 2000
  4. ncbi request reprint Presenilin 1 regulates the processing of beta-amyloid precursor protein C-terminal fragments and the generation of amyloid beta-protein in endoplasmic reticulum and Golgi
    W Xia
    Department of Neurology, Harvard Medical School, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Biochemistry 37:16465-71. 1998
  5. ncbi request reprint Two transmembrane aspartates in presenilin-1 required for presenilin endoproteolysis and gamma-secretase activity
    M S Wolfe
    Center for Neurologic Diseases, Harvard Medical School and Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Nature 398:513-7. 1999
  6. ncbi request reprint The intracellular domain of the beta-amyloid precursor protein is stabilized by Fe65 and translocates to the nucleus in a notch-like manner
    W T Kimberly
    Department of Neurology, Harvard Medical School, Brigham and Women s Hospital, Boston, MA 02115, USA
    J Biol Chem 276:40288-92. 2001
  7. ncbi request reprint Presenilin proteins undergo heterogeneous endoproteolysis between Thr291 and Ala299 and occur as stable N- and C-terminal fragments in normal and Alzheimer brain tissue
    M B Podlisny
    Center for Neurologic Diseases, Harvard Medical School, Boston, Massachusetts, 02115, USA
    Neurobiol Dis 3:325-37. 1997
  8. ncbi request reprint Aspartate mutations in presenilin and gamma-secretase inhibitors both impair notch1 proteolysis and nuclear translocation with relative preservation of notch1 signaling
    O Berezovska
    Alzheimer s Disease Research Laboratory, Department of Neurology, Harvard Medical School and Massachusetts General Hospital, Charlestown, California, USA
    J Neurochem 75:583-93. 2000
  9. pmc The AMY antigen co-occurs with abeta and follows its deposition in the amyloid plaques of Alzheimer's disease and down syndrome
    C A Lemere
    Center for Neurologic Diseases, Harvard Medical School and Brigham and Women s Hospital, Boston, Massachusetts, USA
    Am J Pathol 155:29-37. 1999
  10. ncbi request reprint Neurons regulate extracellular levels of amyloid beta-protein via proteolysis by insulin-degrading enzyme
    K Vekrellis
    Center for Neurologic Diseases, Harvard Medical School and Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Neurosci 20:1657-65. 2000

Collaborators

Detail Information

Publications50

  1. ncbi request reprint Toward a comprehensive theory for Alzheimer's disease. Hypothesis: Alzheimer's disease is caused by the cerebral accumulation and cytotoxicity of amyloid beta-protein
    D J Selkoe
    Department of Neurology, Harvard Medical School, and Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Ann N Y Acad Sci 924:17-25. 2000
    ..Mounting evidence from many laboratories supports an A beta accumulation in limbic and association cortices as the fundamental initiator of the disease, with attendant therapeutic implications...
  2. ncbi request reprint FAD mutations in presenilin-1 or amyloid precursor protein decrease the efficacy of a gamma-secretase inhibitor: evidence for direct involvement of PS1 in the gamma-secretase cleavage complex
    W Xia
    Department of Neurology, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Neurobiol Dis 7:673-81. 2000
    ..Taken together, these findings suggest that PS1 participates physically in a complex with APP during the gamma-secretase cleavage event...
  3. pmc Presenilin complexes with the C-terminal fragments of amyloid precursor protein at the sites of amyloid beta-protein generation
    W Xia
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 97:9299-304. 2000
    ..Thus, PSs are complexed with the gamma-secretase substrates C83 and C99 in the subcellular locations where Abeta is generated, indicating that PSs are directly involved in the pathogenically critical intramembranous proteolysis of APP...
  4. ncbi request reprint Presenilin 1 regulates the processing of beta-amyloid precursor protein C-terminal fragments and the generation of amyloid beta-protein in endoplasmic reticulum and Golgi
    W Xia
    Department of Neurology, Harvard Medical School, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Biochemistry 37:16465-71. 1998
    ..Our results indicate PS1 and APP can interact in the ER and Golgi, where PS1 is required for proper gamma-secretase processing of APP CTFs, and that PS1 mutations augment Abeta42 levels principally in Golgi-like vesicles...
  5. ncbi request reprint Two transmembrane aspartates in presenilin-1 required for presenilin endoproteolysis and gamma-secretase activity
    M S Wolfe
    Center for Neurologic Diseases, Harvard Medical School and Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Nature 398:513-7. 1999
    ....
  6. ncbi request reprint The intracellular domain of the beta-amyloid precursor protein is stabilized by Fe65 and translocates to the nucleus in a notch-like manner
    W T Kimberly
    Department of Neurology, Harvard Medical School, Brigham and Women s Hospital, Boston, MA 02115, USA
    J Biol Chem 276:40288-92. 2001
    ..These findings strongly support the hypothesis that APP signals in the nucleus in a manner analogous to the function of Notch...
  7. ncbi request reprint Presenilin proteins undergo heterogeneous endoproteolysis between Thr291 and Ala299 and occur as stable N- and C-terminal fragments in normal and Alzheimer brain tissue
    M B Podlisny
    Center for Neurologic Diseases, Harvard Medical School, Boston, Massachusetts, 02115, USA
    Neurobiol Dis 3:325-37. 1997
    ..Our results indicate that presenilins are rapidly processed to N- and C-terminal fragments in both neural and nonneural cells and that interference with this processing is not an obligatory feature of FAD-causing mutations...
  8. ncbi request reprint Aspartate mutations in presenilin and gamma-secretase inhibitors both impair notch1 proteolysis and nuclear translocation with relative preservation of notch1 signaling
    O Berezovska
    Alzheimer s Disease Research Laboratory, Department of Neurology, Harvard Medical School and Massachusetts General Hospital, Charlestown, California, USA
    J Neurochem 75:583-93. 2000
    ..The latter is an important finding from the perspective of therapeutic treatment of Alzheimer's disease by targeting gamma-secretase processing of APP to reduce Abeta production...
  9. pmc The AMY antigen co-occurs with abeta and follows its deposition in the amyloid plaques of Alzheimer's disease and down syndrome
    C A Lemere
    Center for Neurologic Diseases, Harvard Medical School and Brigham and Women s Hospital, Boston, Massachusetts, USA
    Am J Pathol 155:29-37. 1999
    ..We conclude that AMY IR represents an amyloid-associated antigen that co-deposits in most but not all Abeta plaques in AD and DS and that accumulation of the AMY antigen follows Abeta deposition in plaques...
  10. ncbi request reprint Neurons regulate extracellular levels of amyloid beta-protein via proteolysis by insulin-degrading enzyme
    K Vekrellis
    Center for Neurologic Diseases, Harvard Medical School and Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Neurosci 20:1657-65. 2000
    ..Our results support a principal role for membrane-associated and secreted IDE isoforms in the degradation and clearance of naturally secreted Abeta by neurons and microglia...
  11. pmc Evidence that the 42- and 40-amino acid forms of amyloid beta protein are generated from the beta-amyloid precursor protein by different protease activities
    M Citron
    Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, MA, USA
    Proc Natl Acad Sci U S A 93:13170-5. 1996
    ....
  12. ncbi request reprint The transmembrane aspartates in presenilin 1 and 2 are obligatory for gamma-secretase activity and amyloid beta-protein generation
    W T Kimberly
    Department of Neurology, Harvard Medical School and Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Biol Chem 275:3173-8. 2000
    ..We conclude that presenilins, and their TM aspartates in particular, are attractive targets for lowering Abeta therapeutically to prevent Alzheimer's disease...
  13. ncbi request reprint The role of APP processing and trafficking pathways in the formation of amyloid beta-protein
    D J Selkoe
    Centre for Neurologic Diseases, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Ann N Y Acad Sci 777:57-64. 1996
    ..In conclusion, studies of the regulation of A beta production and aggregation in cell culture can provide information under physiological conditions that can complement analyses of these processes in vivo...
  14. pmc The lysosomal cysteine protease, cathepsin S, is increased in Alzheimer's disease and Down syndrome brain. An immunocytochemical study
    C A Lemere
    Department of Neurology, Harvard Medical School, Boston, Massachusetts, USA
    Am J Pathol 146:848-60. 1995
    ..The association of cat S immunoreactivity with tangle-bearing neurons, astrocytes, and rare senile plaques implies a role for altered cat S activity in the pathogenesis of AD...
  15. ncbi request reprint The cell biology of beta-amyloid precursor protein and presenilin in Alzheimer's disease
    D J Selkoe
    Center for Neurologic Diseases, Harvard Medical School, Brigham and Women s Hospital, Boston, MA 02115, USA
    Trends Cell Biol 8:447-53. 1998
    ..This review discusses the current understanding of the cell biology of two proteins crucial for the pathogenesis of AD, the beta-amyloid precursor protein and presenilin...
  16. ncbi request reprint A de novo designed helix-turn-helix peptide forms nontoxic amyloid fibrils
    Y Fezoui
    Department of Neurology Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Struct Biol 7:1095-9. 2000
    ..These results suggest that the potential to form fibrils under physiologic conditions is not limited to those proteins associated with amyloidoses and that fibril formation alone is not predictive of cytotoxic activity...
  17. ncbi request reprint Nasal vaccination with beta-amyloid peptide for the treatment of Alzheimer's disease
    C A Lemere
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    DNA Cell Biol 20:705-11. 2001
    ..Examples of other intranasal vaccines and mucosal adjuvants are presented. Taken together, these data have implications for the future development of an intranasal Abeta vaccine for humans...
  18. ncbi request reprint Enhancer function and novel DNA binding protein activity in the near upstream betaAPP gene promoter
    H W Querfurth
    Division of Neurology, St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA
    Gene 232:125-41. 1999
    ..An interaction model involving both domains and looping of interjacent DNA is proposed. We conclude that this newly described binding protein-enhancer complex is required for full betaAPP promoter activation...
  19. ncbi request reprint Trafficking of cell-surface amyloid beta-protein precursor. II. Endocytosis, recycling and lysosomal targeting detected by immunolocalization
    T Yamazaki
    Department of Neurology, Harvard Medical School, Boston, MA 02115, USA
    J Cell Sci 109:999-1008. 1996
    ....
  20. pmc Interaction between amyloid precursor protein and presenilins in mammalian cells: implications for the pathogenesis of Alzheimer disease
    W Xia
    Department of Neurology, Harvard Medical School, Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 94:8208-13. 1997
    ....
  21. ncbi request reprint Alzheimer's disease: genes, proteins, and therapy
    D J Selkoe
    Department of Neurology and Program in Neuroscience, Harvard Medical School, Boston, Massachusetts, USA
    Physiol Rev 81:741-66. 2001
    ..The progress reviewed here, coupled with better ability to diagnose the disease early, bode well for the successful development of therapeutic and preventative drugs for this major public health problem...
  22. pmc Immune hyporesponsiveness to amyloid beta-peptide in amyloid precursor protein transgenic mice: implications for the pathogenesis and treatment of Alzheimer's disease
    A Monsonego
    Center for Neurologic Diseases, Harvard Medical School and Brigham and Women's Hospital, 77 Avenue Louis Pasteur, HIM 730, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 98:10273-8. 2001
    ..Moreover, humans with life-long elevation of brain and peripheral Abeta (e.g., patients with presenilin mutations or Down syndrome) could have reduced immune responses to Abeta vaccination...
  23. ncbi request reprint Regulation of rat magnocellular neurosecretory system by D-aspartate: evidence for biological role(s) of a naturally occurring free D-amino acid in mammals
    H Wang
    Department of Neurology, Harvard Medical School and Center for Neurologic Diseases, Brigham and Women s Hospital, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA
    J Endocrinol 167:247-52. 2000
    ..These results provide evidence for the role(s) of naturally occurring free D-Asp in mammalian physiology. The findings argue against the conventional concept that only L-stereoisomers of amino acids are functional in higher species...
  24. pmc alpha-Synuclein occurs in lipid-rich high molecular weight complexes, binds fatty acids, and shows homology to the fatty acid-binding proteins
    R Sharon
    Center for Neurologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 98:9110-5. 2001
    ....
  25. ncbi request reprint Cell surface amyloid beta-protein precursor colocalizes with beta 1 integrins at substrate contact sites in neural cells
    T Yamazaki
    Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 17:1004-10. 1997
    ..These results are consistent with the putative role of beta PP in cell adhesion and suggests that beta PP either interacts with selected integrins or shares similar cellular machinery to promote cell adhesion...
  26. ncbi request reprint Insulin-degrading enzyme regulates extracellular levels of amyloid beta-protein by degradation
    W Q Qiu
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, Massachusetts 02115 5716, USA
    J Biol Chem 273:32730-8. 1998
    ..We conclude that a principal protease capable of down-regulating the levels of secreted Abeta extracellularly is IDE...
  27. ncbi request reprint Amyloid beta-peptide is transported on lipoproteins and albumin in human plasma
    A L Biere
    Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts 02115, USA
    J Biol Chem 271:32916-22. 1996
    ..Abeta distribution in plasma was not significantly influenced by apolipoprotein E genotype. We conclude that Abeta is normally bound to and transported by albumin and specific lipoproteins in human plasma under physiological conditions...
  28. ncbi request reprint Amyloid-beta oligomers: their production, toxicity and therapeutic inhibition
    D M Walsh
    Department of Neurology, Harvard Medical School and Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, MA 02115, USA
    Biochem Soc Trans 30:552-7. 2002
    ....
  29. ncbi request reprint The genetics and molecular pathology of Alzheimer's disease: roles of amyloid and the presenilins
    D J Selkoe
    Department of Neurology and Neuroscience, Harvard Medical School, Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Neurol Clin 18:903-22. 2000
    ..In this article, the exciting new understanding of the pathogenesis of AD is reviewed and its affect on the patient population is discussed...
  30. ncbi request reprint Clearing the brain's amyloid cobwebs
    D J Selkoe
    Center for Neurologic Diseases, Harvard Medical School, Brigham and Women s Hospital, Boston, MA 02115, USA
    Neuron 32:177-80. 2001
    ..This previously neglected topic has begun receiving serious attention. Understanding how proteolysis regulates Abeta levels in the cerebral cortex has implications for both the pathogenesis and the treatment of this protean disorder...
  31. ncbi request reprint Evidence for genetic linkage of Alzheimer's disease to chromosome 10q
    L Bertram
    Genetics and Aging Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Science 290:2302-3. 2000
    ..Furthermore, we found evidence for allele-specific association between the putative disease locus and marker D10S583, which has recently been located within 195 kilobases of the IDE gene...
  32. ncbi request reprint Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both transfected cells and transgenic mice
    M Citron
    Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, Massachusetts, USA
    Nat Med 3:67-72. 1997
    ..Our data demonstrate that the presenilin mutations cause a dominant gain of function and may induce AD by enhancing A beta 42 production, thus promoting cerebral beta-amyloidosis...
  33. pmc Presenilin, Notch, and the genesis and treatment of Alzheimer's disease
    D J Selkoe
    Center for Neurologic Diseases, Harvard Medical School, Brigham and Women s Hospital, 77 Avenue Louis Pasteur, HIM 730, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 98:11039-41. 2001
    ....
  34. ncbi request reprint The E280A presenilin 1 Alzheimer mutation produces increased A beta 42 deposition and severe cerebellar pathology
    C A Lemere
    Center for Neurologic Diseases, Harvard Medical School, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Nat Med 2:1146-50. 1996
    ....
  35. ncbi request reprint Notch and presenilins in vertebrates and invertebrates: implications for neuronal development and degeneration
    D J Selkoe
    Center for Neurologic Diseases, Harvard Medical School, Brigham and Women s Hospital, HIM 730, MA 02115, USA
    Curr Opin Neurobiol 10:50-7. 2000
    ....
  36. ncbi request reprint Amyloid beta-protein and the genetics of Alzheimer's disease
    D J Selkoe
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Biol Chem 271:18295-8. 1996
  37. ncbi request reprint Ubiquitination of a new form of alpha-synuclein by parkin from human brain: implications for Parkinson's disease
    H Shimura
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Science 293:263-9. 2001
    ..These findings demonstrate a critical biochemical reaction between the two PD-linked gene products and suggest that this reaction underlies the accumulation of ubiquitinated alpha-synuclein in conventional PD...
  38. ncbi request reprint Naturally occurring free D-aspartate is a nuclear component of cells in the mammalian hypothalamo-neurohypophyseal system
    H Wang
    Department of Neurology, Harvard Medical School and Center for Neurologic Diseases, Brigham and Women s Hospital, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    Neuroscience 109:1-4. 2002
    ..The findings provide new insight for the biological function of D-stereoisomers of amino acids as well as the organization of the nucleus of at least some eukaryotic cells...
  39. pmc Lysosomal processing of amyloid precursor protein to A beta peptides: a distinct role for cathepsin S
    J S Munger
    Department of Medicine, Brigham and Women s Hospital, Boston, MA 02115, USA
    Biochem J 311:299-305. 1995
    ..This pathway appears to be inducible, distinct from a constitutive pathway used by 293 and other cells to generate A beta, and may be relevant to the pathogenesis of Alzheimer's disease...
  40. ncbi request reprint The role of cell-derived oligomers of Abeta in Alzheimer's disease and avenues for therapeutic intervention
    D M Walsh
    Laboratory for Neurodegenerative Research, Conway Institute, University College Dublin, Republic of Ireland
    Biochem Soc Trans 33:1087-90. 2005
    ..In each case, compounds capable of reducing oligomer production or antibodies that avidly bind Abeta oligomers also ameliorate the synaptotoxic effects of these natural, cell-derived oligomers...
  41. pmc The Alzheimer's disease-associated presenilins are differentially phosphorylated proteins located predominantly within the endoplasmic reticulum
    J Walter
    Central Institute of Mental Health, Department of Molecular Biology, Mannheim, Germany
    Mol Med 2:673-91. 1996
    ..Mutations in the recently cloned Presenilin genes (PS-1 and PS-2) are by far the most common cause of early onset familial AD...
  42. ncbi request reprint Cell surface presenilin-1 participates in the gamma-secretase-like proteolysis of Notch
    W J Ray
    Departments of Psychiatry and Genetics, Washington University Medical School, St Louis, Missouri 63110, USA
    J Biol Chem 274:36801-7. 1999
    ..Thus, PS1 appears to function specifically in Notch proteolysis near the plasma membrane as an aspartyl protease or cofactor...
  43. ncbi request reprint Transforming growth factor-beta bound to soluble derivatives of the beta amyloid precursor protein of Alzheimer's disease
    S Bodmer
    Dept of Internal Medicine, University Hospital, Zurich, Switzerland
    Biochem Biophys Res Commun 171:890-7. 1990
    ..The complex formation between TGF beta and beta APP may have important implications in regulation of biological activity of the two proteins and in delivery or clearance of TGF beta and beta APP in the brain and other compartments...
  44. pmc In vitro studies of amyloid beta-protein fibril assembly and toxicity provide clues to the aetiology of Flemish variant (Ala692-->Gly) Alzheimer's disease
    D M Walsh
    Center for Neurologic Diseases, Brigham and Women's Hospital, 77 Avenue Louis Pasteur, Boston MA 02115, USA
    Biochem J 355:869-77. 2001
    ..Increased peptide solubility and assembly stability would favour formation of larger deposits and inhibit their elimination. In addition, increased concentrations of neurotoxic assemblies would accelerate neuronal injury and death...
  45. ncbi request reprint Ectodomain phosphorylation of beta-amyloid precursor protein at two distinct cellular locations
    J Walter
    Central Institute of Mental Health, Department of Molecular Biology, J5, 68159 Mannheim, Germany
    J Biol Chem 272:1896-903. 1997
    ..Therefore, this study revealed two distinct cellular locations for betaAPP phosphorylation...
  46. ncbi request reprint Mutagenesis identifies new signals for beta-amyloid precursor protein endocytosis, turnover, and the generation of secreted fragments, including Abeta42
    R G Perez
    Departments of Psychiatry and Neurobiology and Anatomy, Allegheny University of the Health Sciences, Pittsburgh, Pennsylvania 15212, USA
    J Biol Chem 274:18851-6. 1999
    ....
  47. ncbi request reprint The APP family of proteins: similarities and differences
    D M Walsh
    Laboratory for Neurodegenerative Research, Conway Institute, University College Dublin, Republic of Ireland
    Biochem Soc Trans 35:416-20. 2007
    ..Here, we will review how knowledge of the similarities and differences between APP and the APLPs may prove useful for the development of novel disease-modifying therapeutics...
  48. pmc Proteolytic processing of the Alzheimer disease-associated presenilin-1 generates an in vivo substrate for protein kinase C
    J Walter
    Central Institute of Mental Health, Department of Molecular Biology, J5, 68159 Mannheim, Germany
    Proc Natl Acad Sci U S A 94:5349-54. 1997
    ..The selective phosphorylation of the PS-1 CTF indicates that the physiological and/or pathological properties of the CTF are regulated by PKC activity...
  49. ncbi request reprint Skeletal and CNS defects in Presenilin-1-deficient mice
    J Shen
    Center for Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA
    Cell 89:629-39. 1997
    ..5. These results show that PS1 is required for proper formation of the axial skeleton, normal neurogenesis, and neuronal survival...
  50. ncbi request reprint Immunochemical identification of the serine protease inhibitor alpha 1-antichymotrypsin in the brain amyloid deposits of Alzheimer's disease
    C R Abraham
    Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115
    Cell 52:487-501. 1988
    ..Models by which alpha 1-antichymotrypsin could contribute to the development of Alzheimer amyloid deposits are discussed...