Plasma β amyloid and impaired CO2-induced cerebral vasomotor reactivity

[1]  A. Hofman,et al.  Cerebral hypoperfusion and clinical onset of dementia: The Rotterdam study , 2005, Annals of neurology.

[2]  A. Hofman,et al.  Plasma amyloid β, apolipoprotein E, lacunar infarcts, and white matter lesions , 2004, Annals of neurology.

[3]  A. Hofman,et al.  Determinants of disease and disability in the elderly: The Rotterdam elderly study , 1991, European Journal of Epidemiology.

[4]  C. Iadecola,et al.  Cerebrovascular autoregulation is profoundly impaired in mice overexpressing amyloid precursor protein. , 2002, American journal of physiology. Heart and circulatory physiology.

[5]  D. Holtzman,et al.  Plaque‐associated disruption of CSF and plasma amyloid‐β (Aβ) equilibrium in a mouse model of Alzheimer's disease , 2002, Journal of neurochemistry.

[6]  D. Holtzman,et al.  Brain to Plasma Amyloid-β Efflux: a Measure of Brain Amyloid Burden in a Mouse Model of Alzheimer's Disease , 2002, Science.

[7]  P. Mehta,et al.  Amyloid β protein 1–40 and 1–42 levels in matched cerebrospinal fluid and plasma from patients with Alzheimer disease , 2001, Neuroscience Letters.

[8]  D. Selkoe.  Alzheimer's disease: genes, proteins, and therapy. , 2001, Physiological reviews.

[9]  A. Fagan,et al.  Apolipoprotein E facilitates neuritic and cerebrovascular plaque formation in an Alzheimer's disease model , 2000, Annals of neurology.

[10]  H. Fukuyama,et al.  Brain arteriolosclerosis and hemodynamic disturbance may induce leukoaraiosis , 1999, Neurology.

[11]  B Engvall,et al.  Cerebrospinal fluid Aβ42 is increased early in sporadic Alzheimer's disease and declines with disease progression , 1999, Annals of neurology.

[12]  A Hofman,et al.  Cerebral vasomotor reactivity and cerebral white matter lesions in the elderly , 1999, Neurology.

[13]  B. Guschlbauer,et al.  CO2 reactivity testing without blood pressure monitoring? , 1999, Stroke.

[14]  Yu-Min Kuo,et al.  Cerebral amyloid angiopathy: amyloid beta accumulates in putative interstitial fluid drainage pathways in Alzheimer's disease. , 1998, The American journal of pathology.

[15]  R. Panerai,et al.  Can cerebrovascular reactivity be assessed without measuring blood pressure in patients with carotid artery disease? . , 1998, Stroke.

[16]  M. Mullan,et al.  Characteristics of thein VitroVasoactivity of β-Amyloid Peptides , 1998, Experimental Neurology.

[17]  S. Paul,et al.  Lack of apolipoprotein E dramatically reduces amyloid β-peptide deposition , 1997, Nature Genetics.

[18]  T. Tokuda,et al.  Plasma Levels of amyloid β proteins Aβ1–40 and Aβ1–42(43) are elevated in Down's syndrome , 1997 .

[19]  G. Schellenberg,et al.  Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease , 1996, Nature Medicine.

[20]  M. Mullan,et al.  β-Amyloid-mediated vasoactivity and vascular endothelial damage , 1996, Nature.

[21]  B. Hyman,et al.  Apolipoprotein E ϵ4 and cerebral hemorrhage associated with amyloid angiopathy , 1995 .

[22]  A Hofman,et al.  Cerebral white matter lesions and atherosclerosis in the Rotterdam Study , 1993, The Lancet.

[23]  PhilipR. Wenham,et al.  Apolipoprotein E genotyping by one-stage PCR , 1991, The Lancet.

[24]  S. Otis,et al.  Intraoperative transcranial Doppler: limitations of the method. , 1989, Journal of vascular surgery.

[25]  P A Schneider,et al.  Noninvasive assessment of CO2-induced cerebral vasomotor response in normal individuals and patients with internal carotid artery occlusions. , 1988, Stroke.

[26]  H. Vinters.  Cerebral amyloid angiopathy. A critical review. , 1987, Stroke.

[27]  R. Escourolle,et al.  Leukoencephalopathy in diffuse hemorrhagic cerebral amyloid angiopathy , 1985, Annals of neurology.