Ahmad Salehi

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. ncbi request reprint Alzheimer's disease and NGF signaling
    A Salehi
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA
    J Neural Transm 111:323-45. 2004
  2. ncbi request reprint Traffic at the intersection of neurotrophic factor signaling and neurodegeneration
    Ahmad Salehi
    Department of Neurology and Neurological Sciences, Stanford University Medical Center, 1201Welch Rd, MSLS Building, Stanford, CA 94305 5489, USA
    Trends Neurosci 26:73-80. 2003
  3. ncbi request reprint Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration
    Ahmad Salehi
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, California 94305, USA
    Neuron 51:29-42. 2006
  4. ncbi request reprint P75 neurotrophin receptor in the nucleus basalis of meynert in relation to age, sex, and Alzheimer's disease
    A Salehi
    Graduate School Neurosciences Amsterdam, Netherlands Institute for Brain Research, Amsterdam, The Netherlands
    Exp Neurol 161:245-58. 2000
  5. ncbi request reprint Using mouse models to explore genotype-phenotype relationship in Down syndrome
    Ahmad Salehi
    Department of Neurology and Neurological Sciences, Neuroscience Institute at Stanford, Stanford University, Stanford, California 94305, USA
    Ment Retard Dev Disabil Res Rev 13:207-14. 2007
  6. doi request reprint Restoration of norepinephrine-modulated contextual memory in a mouse model of Down syndrome
    A Salehi
    Department of Neurology and Neurological Sciences, Stanford Medical School, Stanford, CA 94305, USA
    Sci Transl Med 1:7ra17. 2009
  7. doi request reprint The "Down syndrome critical region" is sufficient in the mouse model to confer behavioral, neurophysiological, and synaptic phenotypes characteristic of Down syndrome
    Nadia P Belichenko
    Department of Neurology and Neurological Sciences and the Center for Research and Treatment of Down Syndrome, Stanford University Medical Center, Stanford, California 94305 5489, USA
    J Neurosci 29:5938-48. 2009
  8. doi request reprint Excitatory-inhibitory relationship in the fascia dentata in the Ts65Dn mouse model of Down syndrome
    Pavel V Belichenko
    Department of Neurology and Neurological Sciences, the Center for Research and Treatment of Down Syndrome and Neuroscience Institute at Stanford University, Stanford, California 94305 5489, USA
    J Comp Neurol 512:453-66. 2009
  9. ncbi request reprint Synaptic and cognitive abnormalities in mouse models of Down syndrome: exploring genotype-phenotype relationships
    Pavel V Belichenko
    Department of Neurology and Neurological Sciences and the Center for Research and Treatment of Down Syndrome, Stanford University Medical Center, Stanford, California 94305 5489, USA
    J Comp Neurol 504:329-45. 2007
  10. ncbi request reprint Trafficking the NGF signal: implications for normal and degenerating neurons
    Jean Dominique Delcroix
    Department of Neurology and Neurological Sciences and of Pediatrics, Program in Neuroscience, Stanford University, Stanford, CA 94305, USA
    Prog Brain Res 146:3-23. 2004

Detail Information

Publications20

  1. ncbi request reprint Alzheimer's disease and NGF signaling
    A Salehi
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA
    J Neural Transm 111:323-45. 2004
    ..We will speculate about the possible mechanisms of failed NGF retrograde transport and its relationship to AD pathology...
  2. ncbi request reprint Traffic at the intersection of neurotrophic factor signaling and neurodegeneration
    Ahmad Salehi
    Department of Neurology and Neurological Sciences, Stanford University Medical Center, 1201Welch Rd, MSLS Building, Stanford, CA 94305 5489, USA
    Trends Neurosci 26:73-80. 2003
    ....
  3. ncbi request reprint Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration
    Ahmad Salehi
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, California 94305, USA
    Neuron 51:29-42. 2006
    ..Our study thus provides evidence for a pathogenic mechanism for DS in which increased expression of App, in the context of trisomy, causes abnormal transport of NGF and cholinergic neurodegeneration...
  4. ncbi request reprint P75 neurotrophin receptor in the nucleus basalis of meynert in relation to age, sex, and Alzheimer's disease
    A Salehi
    Graduate School Neurosciences Amsterdam, Netherlands Institute for Brain Research, Amsterdam, The Netherlands
    Exp Neurol 161:245-58. 2000
    ....
  5. ncbi request reprint Using mouse models to explore genotype-phenotype relationship in Down syndrome
    Ahmad Salehi
    Department of Neurology and Neurological Sciences, Neuroscience Institute at Stanford, Stanford University, Stanford, California 94305, USA
    Ment Retard Dev Disabil Res Rev 13:207-14. 2007
    ..An important conclusion is that uncovering these relationships is enhanced by working from carefully defined phenotypes to the genes responsible...
  6. doi request reprint Restoration of norepinephrine-modulated contextual memory in a mouse model of Down syndrome
    A Salehi
    Department of Neurology and Neurological Sciences, Stanford Medical School, Stanford, CA 94305, USA
    Sci Transl Med 1:7ra17. 2009
    ..Our findings raise the possibility that restoring norepinephrine-mediated neurotransmission could reverse cognitive dysfunction in Down syndrome...
  7. doi request reprint The "Down syndrome critical region" is sufficient in the mouse model to confer behavioral, neurophysiological, and synaptic phenotypes characteristic of Down syndrome
    Nadia P Belichenko
    Department of Neurology and Neurological Sciences and the Center for Research and Treatment of Down Syndrome, Stanford University Medical Center, Stanford, California 94305 5489, USA
    J Neurosci 29:5938-48. 2009
    ..The stage is now set for studies to decipher the gene(s) that play a conspicuous role in creating these phenotypes...
  8. doi request reprint Excitatory-inhibitory relationship in the fascia dentata in the Ts65Dn mouse model of Down syndrome
    Pavel V Belichenko
    Department of Neurology and Neurological Sciences, the Center for Research and Treatment of Down Syndrome and Neuroscience Institute at Stanford University, Stanford, California 94305 5489, USA
    J Comp Neurol 512:453-66. 2009
    ..The results demonstrate a significant alteration of inhibitory synapses in the fascia dentata of Ts65Dn mice...
  9. ncbi request reprint Synaptic and cognitive abnormalities in mouse models of Down syndrome: exploring genotype-phenotype relationships
    Pavel V Belichenko
    Department of Neurology and Neurological Sciences and the Center for Research and Treatment of Down Syndrome, Stanford University Medical Center, Stanford, California 94305 5489, USA
    J Comp Neurol 504:329-45. 2007
    ..The analysis of data from this and earlier studies points to genotype-phenotype linkages in DS whose complexity ranges from relatively simple to quite complex...
  10. ncbi request reprint Trafficking the NGF signal: implications for normal and degenerating neurons
    Jean Dominique Delcroix
    Department of Neurology and Neurological Sciences and of Pediatrics, Program in Neuroscience, Stanford University, Stanford, CA 94305, USA
    Prog Brain Res 146:3-23. 2004
    ..It is important to define further the significance of signaling endosomes in the biology of both normal and degenerating neurons...
  11. ncbi request reprint Synaptic structural abnormalities in the Ts65Dn mouse model of Down Syndrome
    Pavel V Belichenko
    Department of Neurology and Neurological Sciences and the Center for Research and Treatment of Down Syndrome, Stanford University Medical Center, 1201 Welch Road, Stanford, California 94305 5489, USA
    J Comp Neurol 480:281-98. 2004
    ..They establish the Ts65Dn mouse as a model for abnormal synapse structure and function in Down syndrome and point to the importance of studies to elucidate the mechanisms responsible for synapse enlargement...
  12. pmc Failed retrograde transport of NGF in a mouse model of Down's syndrome: reversal of cholinergic neurodegenerative phenotypes following NGF infusion
    J D Cooper
    Department of Neurology and Neurological Sciences and the Program in Neuroscience, Stanford University, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 98:10439-44. 2001
    ..We suggest that age-related cholinergic neurodegeneration may be a treatable disorder of failed retrograde NGF signaling...
  13. ncbi request reprint Sleep/wake disruption in Alzheimer's disease: APOE status and longitudinal course
    Jerome A Yesavage
    National Institute of Aging Alzheimer s Disease Core Center, Palo Alto VA Health Care System 151Y, 3801 Miranda Avenue, Palo Alto, CA 94304, USA
    J Geriatr Psychiatry Neurol 17:20-4. 2004
    ..In these data, APOE status was associated with the progression of sleep/wake disturbances in AD. Overall, there was greater deterioration on sleep parameters in patients negative for the epsilon4 allele...
  14. pmc Increased efficiency of the GABAA and GABAB receptor-mediated neurotransmission in the Ts65Dn mouse model of Down syndrome
    Alexander M Kleschevnikov
    Department of Neurosciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
    Neurobiol Dis 45:683-91. 2012
    ..Thus, both GABAA and GABAB receptor-mediated synaptic efficiency is increased in the Ts65Dn DG, thus likely contributing to deficient synaptic plasticity and poor learning in DS...
  15. ncbi request reprint Diminished neuronal metabolic activity in Alzheimer's disease. Review article
    A Salehi
    Netherlands Institute for Brain Research, Amsterdam
    J Neural Transm 106:955-86. 1999
    ..Moreover, ApoE epsilon4 may participate in the pathogenesis of AD by decreasing neuronal metabolism. The main implication of these findings is that therapeutic strategies in AD should be focussed on reactivation of neuronal metabolism...
  16. ncbi request reprint Frameshift mutants of beta amyloid precursor protein and ubiquitin-B in Alzheimer's and Down patients
    F W Van Leeuwen
    Graduate School for Neurosciences Amsterdam, Netherlands Institute for Brain Research, 1105 AZ Amsterdam, The Netherlands
    Science 279:242-7. 1998
    ..This type of transcript mutation is likely an important factor in the widely occurring nonfamilial early- and late-onset forms of Alzheimer's disease...
  17. ncbi request reprint Reduced neuronal activity and reactivation in Alzheimer's disease
    D F Swaab
    Netherlands Institute for Brain Research, Amsterdam, The Netherlands
    Prog Brain Res 117:343-77. 1998
    ..A number of pharmacological and non-pharmacological studies support the concept that activation of the brain indeed has beneficial effects on several aspects of cognition and other central functions...
  18. ncbi request reprint Cells in human postmortem brain tissue slices remain alive for several weeks in culture
    Ronald W H Verwer
    Graduate School Neurosciences Amsterdam, The Netherlands
    FASEB J 16:54-60. 2002
    ..These slice cultures offer new opportunities to study the cellular and molecular mechanisms of neurological and psychiatric diseases and new therapeutic strategies...
  19. ncbi request reprint A sex difference and no effect of ApoE type on the amount of cytoskeletal alterations in the nucleus basalis of Meynert in Alzheimer's disease
    A Salehi
    Graduate School Neurosciences Amsterdam, Netherlands Institute for Brain Research
    Neurobiol Aging 19:505-10. 1998
    ..We also found a significant relationship between the number of Alz-50-stained neurons and the severity of dementia...
  20. pmc Aggravated decrease in the activity of nucleus basalis neurons in Alzheimer's disease is apolipoprotein E-type dependent
    A Salehi
    Graduate School Neurosciences Amsterdam, Netherlands Institute for Brain Research, Meibergdreef 33, 1105 AZ Amsterdam, The Netherlands
    Proc Natl Acad Sci U S A 95:11445-9. 1998
    ..Our data show that the decreased activity of nucleus basalis neurons in AD is ApoE epsilon4 dependent and suggest that ApoE epsilon4 participates in the pathogenesis of AD by decreasing neuronal metabolism...