Multimodal techniques for diagnosis and prognosis of Alzheimer's disease

Alzheimer's disease affects millions of people around the world. Currently, there are no treatments that prevent or slow the disease. Like other neurodegenerative diseases, Alzheimer's disease is characterized by protein misfolding in the brain. This process and the associated brain damage begin years before the substantial neurodegeneration that accompanies dementia. Studies using new neuroimaging techniques and fluid biomarkers suggest that Alzheimer's disease pathology can be detected preclinically. These advances should allow the design of new clinical trials and early mechanism-based therapeutic intervention.

[1]  Z. Khachaturian.  Diagnosis of Alzheimer's disease. , 1985, Archives of neurology.

[2]  L. Wolfson,et al.  Clinico‐pathologic studies in dementia , 1988, Neurology.

[3]  L. Berg.  Clinical Dementia Rating (CDR). , 1988, Psychopharmacology bulletin.

[4]  R. Mohs,et al.  Consortium to establish a registry for Alzheimer's disease (CERAD) clinical and neuropsychological assessment of Alzheimer's disease. , 2002, Psychopharmacology bulletin.

[5]  D. Selkoe,et al.  Immunochemical identification of the serine protease inhibitor α 1-antichymotrypsin in the brain amyloid deposits of Alzheimer's disease , 1988, Cell.

[6]  M. Albert,et al.  Prevalence of Alzheimer's disease in a community population of older persons. Higher than previously reported. , 1989, JAMA.

[7]  S. M. Sumi,et al.  The Consortium to Establish a Registry for Alzheimer's Disease (CERAD) , 1991, Neurology.

[8]  J. Morris.  The Clinical Dementia Rating (CDR) , 1993, Neurology.

[9]  Jan Six,et al.  Detection of Proteins in Normal and Alzheimer's Disease Cerebrospinal Fluid with a Sensitive Sandwich Enzyme‐Linked Immunosorbent Assay , 1993 .

[10]  M. Vandermeeren,et al.  Detection of tau proteins in normal and Alzheimer's disease cerebrospinal fluid with a sensitive sandwich enzyme-linked immunosorbent assay. , 1993, Journal of neurochemistry.

[11]  C. Cotman,et al.  Decreased levels of C1q in cerebrospinal fluid of living Alzheimer patients correlate with disease state , 1994, Neurobiology of Aging.

[12]  J. Morris,et al.  Handbook of dementing illnesses , 1995 .

[13]  R. Wolfert,et al.  Reduction of β‐amyloid peptide42 in the cerebrospinal fluid of patients with Alzheimer's disease , 1995 .

[14]  J. Morris,et al.  Profound Loss of Layer II Entorhinal Cortex Neurons Occurs in Very Mild Alzheimer’s Disease , 1996, The Journal of Neuroscience.

[15]  D. Thal,et al.  The subunits of α 2-macroglobulin receptor/low density lipoprotein receptor-related protein, native and transformed α 2-macroglobulin and interleukin 6 in Alzheimer's disease , 1997, Brain Research.

[16]  M. Bobinski,et al.  Frequency of Stages of Alzheimer-Related Lesions in Different Age Categories , 1997, Neurobiology of Aging.

[17]  J. Trojanowski,et al.  Editorial on Consensus Recommendations for the Postmortem Diagnosis of Alzheimer Disease from the National Institute on Aging and the Reagan Institute Working Group on Diagnostic Criteria for the Neuropathological Assessment of Alzheimer Disease , 1997, Journal of neuropathology and experimental neurology.

[18]  H. Braak,et al.  Frequency of Stages of Alzheimer-Related Lesions in Different Age Categories , 1997, Neurobiology of Aging.

[19]  D. Loeffler,et al.  Cerebrospinal Fluid C3a Increases with Age, But Does Not Increase Further in Alzheimer’s Disease , 1997, Neurobiology of Aging.

[20]  J. Trojanowski,et al.  Increased F2‐isoprostanes in Alzheimer's disease: evidence for enhanced lipid peroxidation in vivo , 1998, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[21]  Nick C Fox,et al.  Serial magnetic resonance imaging of cerebral atrophy in preclinical Alzheimer's disease , 1999, The Lancet.

[22]  W R Markesbery,et al.  The magnitude of brain lipid peroxidation correlates with the extent of degeneration but not with density of neuritic plaques or neurofibrillary tangles or with APOE genotype in Alzheimer's disease patients. , 1999, The American journal of pathology.

[23]  E. Tangalos,et al.  Mild Cognitive Impairment Clinical Characterization and Outcome , 1999 .

[24]  H. Wiśniewski,et al.  Plasma amyloid β‐peptide 1–42 and incipient Alzheimer's disease , 1999 .

[25]  T. Montine,et al.  No difference in plasma or urinary F2‐isoprostanes among patients with Huntington's disease or Alzheimer's disease and controls , 2000, Annals of neurology.

[26]  J. Trojanowski,et al.  Increased 8,12‐iso‐iPF2α‐VI in Alzheimer's disease: Correlation of a noninvasive index of lipid peroxidation with disease severity , 2000, Annals of neurology.

[27]  K. Blennow,et al.  Standardization of measurement of β-amyloid(1-42) in cerebrospinal fluid and plasma , 2000, Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis.

[28]  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.

[29]  M. Bobinski,et al.  Prediction of cognitive decline in normal elderly subjects with 2-[18F]fluoro-2-deoxy-d-glucose/positron-emission tomography (FDG/PET) , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[30]  M. Raichle,et al.  Searching for a baseline: Functional imaging and the resting human brain , 2001, Nature Reviews Neuroscience.

[31]  H. Tohgi,et al.  Remarkable increase in the concentration of 8‐hydroxyguanosine in cerebrospinal fluid from patients with Alzheimer's disease , 2002, Journal of neuroscience research.

[32]  J. Hardy,et al.  The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics , 2009 .

[33]  Kaj Blennow,et al.  Proteome analysis of cerebrospinal fluid proteins in Alzheimer patients , 2002, Neuroreport.

[34]  R. Malinow,et al.  APP Processing and Synaptic Function , 2003, Neuron.

[35]  S. Wisniewski,et al.  Plasma and cerebrospinal fluid α1‐antichymotrypsin levels in Alzheimer's disease: Correlation with cognitive impairment , 2003, Annals of neurology.

[36]  Trey Sunderland,et al.  Decreased beta-amyloid1-42 and increased tau levels in cerebrospinal fluid of patients with Alzheimer disease. , 2003, JAMA.

[37]  J. Baron,et al.  Mild cognitive impairment , 2003, Neurology.

[38]  Tetsuya Suhara,et al.  Development of a new radioligand, N-(5-fluoro-2-phenoxyphenyl)-N-(2-[18F]fluoroethyl-5-methoxybenzyl)acetamide, for pet imaging of peripheral benzodiazepine receptor in primate brain. , 2004, Journal of medicinal chemistry.

[39]  W. Klunk,et al.  Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound‐B , 2004, Annals of neurology.

[40]  H. Kimura,et al.  Expression of monoamine oxidase B activity in astrocytes of senile plaques , 2004, Acta Neuropathologica.

[41]  Hiroshi Matsuda,et al.  The prediction of rapid conversion to Alzheimer's disease in mild cognitive impairment using regional cerebral blood flow SPECT , 2005, NeuroImage.

[42]  David M Holtzman,et al.  Synaptic activity regulates interstitial fluid amyloid-beta levels in vivo. , 2005, Neuron.

[43]  J. Price,et al.  Complement Activation in Very Early Alzheimer Disease , 2005, Alzheimer disease and associated disorders.

[44]  Benjamin J. Shannon,et al.  Molecular, Structural, and Functional Characterization of Alzheimer's Disease: Evidence for a Relationship between Default Activity, Amyloid, and Memory , 2005, The Journal of Neuroscience.

[45]  Steven Mennerick,et al.  Synaptic Activity Regulates Interstitial Fluid Amyloid-β Levels In Vivo , 2005, Neuron.

[46]  Jing Zhang,et al.  Quantitative proteomics of cerebrospinal fluid from patients with Alzheimer disease. , 2005, Journal of Alzheimer's disease : JAD.

[47]  Gina N. LaRossa,et al.  [11C]PIB in a nondemented population , 2006, Neurology.

[48]  P. Thompson,et al.  PET of brain amyloid and tau in mild cognitive impairment. , 2006, The New England journal of medicine.

[49]  J. Julien,et al.  Bone Marrow-Derived Microglia Play a Critical Role in Restricting Senile Plaque Formation in Alzheimer's Disease , 2006, Neuron.

[50]  David M Holtzman,et al.  Human amyloid-β synthesis and clearance rates as measured in cerebrospinal fluid in vivo , 2006, Nature Medicine.

[51]  K. Blennow,et al.  Association between CSF biomarkers and incipient Alzheimer's disease in patients with mild cognitive impairment: a follow-up study , 2006, The Lancet Neurology.

[52]  Gina N. LaRossa,et al.  Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Aβ42 in humans , 2006, Annals of neurology.

[53]  D. Kiel,et al.  Inflammatory markers and the risk of Alzheimer disease , 2007, Neurology.

[54]  R. Mayeux,et al.  Hippocampal and entorhinal atrophy in mild cognitive impairment , 2007, Neurology.

[55]  M. J. Leon,et al.  Longitudinal CSF isoprostane and MRI atrophy in the progression to AD , 2007, Journal of Neurology.

[56]  J. Morris,et al.  Pathologic correlates of nondemented aging, mild cognitive impairment, and early-stage alzheimer’s disease , 2001, Journal of Molecular Neuroscience.

[57]  R. Guerreiro,et al.  Peripheral Inflammatory Cytokines as Biomarkers in Alzheimer’s Disease and Mild Cognitive Impairment , 2007, Neurodegenerative Diseases.

[58]  Norman Relkin,et al.  Cerebrospinal fluid proteomic biomarkers for Alzheimer's disease , 2007, Annals of neurology.

[59]  R. Tibshirani,et al.  Classification and prediction of clinical Alzheimer's diagnosis based on plasma signaling proteins , 2007, Nature Medicine.

[60]  I. Sokal,et al.  CSF tau/Aβ42 ratio for increased risk of mild cognitive impairment , 2007, Neurology.

[61]  David M Holtzman,et al.  Identification and validation of novel CSF biomarkers for early stages of Alzheimer's disease , 2007, Proteomics. Clinical applications.

[62]  A. Fagan,et al.  Cerebrospinal fluid tau/beta-amyloid(42) ratio as a prediction of cognitive decline in nondemented older adults. , 2007, Archives of neurology.

[63]  R. Petersen,et al.  Association of Low Plasma Aβ42/Aβ40 Ratios With Increased Imminent Risk for Mild Cognitive Impairment and Alzheimer Disease , 2007 .

[64]  T. J. Grabowski,et al.  Proteome-based plasma biomarkers for Alzheimer's disease , 2007 .

[65]  D. Schacter,et al.  The Brain's Default Network , 2008, Annals of the New York Academy of Sciences.

[66]  David L. Brody,et al.  Amyloid-β Dynamics Correlate with Neurological Status in the Injured Human Brain , 2008, Science.

[67]  A. Fagan,et al.  Alzheimer’s disease risk variants show association with cerebrospinal fluid amyloid beta , 2009, neurogenetics.

[68]  Bradford C. Dickerson,et al.  Functional abnormalities of the medial temporal lobe memory system in mild cognitive impairment and Alzheimer's disease: Insights from functional MRI studies , 2008, Neuropsychologia.

[69]  Martin Rossor,et al.  Microglia, amyloid, and cognition in Alzheimer's disease: An [11C](R)PK11195-PET and [11C]PIB-PET study , 2008, Neurobiology of Disease.

[70]  Eileen Daly,et al.  Proteome-based identification of plasma proteins associated with hippocampal metabolism in early Alzheimer’s disease , 2008, Journal of Neurology.

[71]  Henrik Zetterberg,et al.  Characterization of tau in cerebrospinal fluid using mass spectrometry. , 2008, Journal of proteome research.

[72]  D. Holtzman,et al.  Rapid appearance and local toxicity of amyloid-β plaques in a mouse model of Alzheimer’s disease , 2008, Nature.

[73]  K. Blennow,et al.  Effect of phenserine treatment on brain functional activity and amyloid in Alzheimer's disease , 2008, Annals of neurology.

[74]  B. Gulyás,et al.  Functional neuroimaging in multiple sclerosis with radiolabelled glia markers: Preliminary comparative PET studies with [11C]vinpocetine and [11C]PK11195 in patients , 2008, Journal of the Neurological Sciences.

[75]  K. Blennow,et al.  Targeted proteomics in Alzheimer’s disease: focus on amyloid-β , 2008, Expert review of proteomics.

[76]  D. Holtzman,et al.  Amyloid-beta dynamics in the injured human brain , 2009, Alzheimer's & Dementia.

[77]  A. Fagan,et al.  Decreased cerebrospinal fluid Aβ42 correlates with brain atrophy in cognitively normal elderly , 2009, Annals of neurology.

[78]  Randall J Bateman,et al.  A γ‐secretase inhibitor decreases amyloid‐β production in the central nervous system , 2009, Annals of neurology.

[79]  Owen Carmichael,et al.  TRAJECTORIES OF BRAIN LOSS IN AGING AND THE DEVELOPMENT OF COGNITIVE IMPAIRMENT , 2009, Neurology.

[80]  Charles D. Smith,et al.  Neuropathology of nondemented aging: Presumptive evidence for preclinical Alzheimer disease , 2009, Neurobiology of Aging.

[81]  J. Hirvonen,et al.  Assessment of MAO‐B Occupancy in the Brain With PET and [11C]‐L‐Deprenyl‐D2: A Dose‐Finding Study With a Novel MAO‐B Inhibitor, EVT 301 , 2009, Clinical pharmacology and therapeutics.

[82]  David M. Holtzman,et al.  Biomarkers of Alzheimer's disease , 2009, Neurobiology of Disease.

[83]  R. Castellani,et al.  Alzheimer disease. , 2010, Disease-a-month : DM.

[84]  Hilkka Soininen,et al.  J-ADNI and selection of cognition measures , 2010, Alzheimer's & Dementia.

[85]  John C. Morris,et al.  Clinical Dementia Rating , 1994, Neurology.