Brain ventricular volume and cerebrospinal fluid biomarkers of Alzheimer's disease.

The frequent co-occurrence of Alzheimer's disease (AD) pathology in patients with normal pressure hydrocephalus suggests a possible link between ventricular dilation and AD. If enlarging ventricles serve as a marker of faulty cerebrospinal fluid (CSF) clearance mechanisms, then a relationship may be demonstrable between increasing ventricular volume and decreasing levels of amyloid-beta peptide (Abeta) in CSF in preclinical and early AD. CSF biomarker data (Abeta, tau, and phosphorylated tau) as well as direct measurements of whole brain and ventricular volumes were obtained from the Alzheimer's Disease Neuroimaging Initiative dataset. The ratio of ventricular volume to whole brain volume was derived as a secondary independent measure. Baseline data were used for the group analyses of 288 subjects classified as being either normal (n=87), having the syndrome of mild cognitive impairment (n=136), or mild AD (n=65). Linear regression models were derived for each biomarker as the dependent variable, using the MRI volume measures and age as independent variables. For controls, ventricular volume was negatively associated with CSF Abeta in APOE epsilon4 positive subjects. A different pattern was seen in AD subjects, in whom ventricular volume was negatively associated with tau, but not Abeta in epsilon4 positive subjects. Increased ventricular volume may be associated with decreased levels of CSF Abeta in preclinical AD. The basis for the apparent effect of APOE epsilon4 genotype on the relationship of ventricular volume to Abeta and tau levels is unknown, but could involve altered CSF-blood-brain barrier function during the course of disease.

[1]  M. Folstein,et al.  Clinical diagnosis of Alzheimer's disease: Report of the NINCDS—ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease , 2011, Neurology.

[2]  Joseph V. Hajnal,et al.  A robust method to estimate the intracranial volume across MRI field strengths (1.5T and 3T) , 2010, NeuroImage.

[3]  Anders M. Dale,et al.  Regional Shape Abnormalities in Mild Cognitive Impairment and Alzheimer's Disease , 2009, NeuroImage.

[4]  C. Jack,et al.  MRI and CSF biomarkers in normal, MCI, and AD subjects , 2009, Neurology.

[5]  Michael Weiner,et al.  Mapping correlations between ventricular expansion and CSF amyloid and tau biomarkers in 240 subjects with Alzheimer's disease, mild cognitive impairment and elderly controls , 2009, NeuroImage.

[6]  D. Galimberti,et al.  Faculty Opinions recommendation of Decreased cerebrospinal fluid Abeta(42) correlates with brain atrophy in cognitively normal elderly. , 2009 .

[7]  R. Petersen,et al.  Cerebrospinal fluid biomarker signature in Alzheimer's disease neuroimaging initiative subjects , 2009, Annals of neurology.

[8]  Nick C Fox,et al.  Hippocampal atrophy rates in Alzheimer disease , 2009, Neurology.

[9]  R. Deane,et al.  Clearance of amyloid-β peptide across the blood-brain barrier: Implication for therapies in Alzheimer’s disease , 2009 .

[10]  Miles C. Miller,et al.  Evidence of TAU pathology in kaolin-induced hydrocephalus model of the aged rat , 2009, Cerebrospinal Fluid Research.

[11]  Katie Hamm,et al.  apoE isoform-specific disruption of amyloid beta peptide clearance from mouse brain. , 2008, The Journal of clinical investigation.

[12]  Jeffrey A. James,et al.  Frequent amyloid deposition without significant cognitive impairment among the elderly. , 2008, Archives of neurology.

[13]  Sakari Savolainen,et al.  Assessment of beta-amyloid in a frontal cortical brain biopsy specimen and by positron emission tomography with carbon 11-labeled Pittsburgh Compound B. , 2008, Archives of neurology.

[14]  R. Bartha,et al.  Ventricular enlargement as a possible measure of Alzheimer's disease progression validated using the Alzheimer's disease neuroimaging initiative database. , 2008, Brain : a journal of neurology.

[15]  S. Nidhinandana,et al.  The effect of whole body position on lumbar cerebrospinal fluid opening pressure , 2008, Cerebrospinal Fluid Research.

[16]  C. Johanson,et al.  Apolipoprotein E, Amyloid-&bgr;, and Blood-Brain Barrier Permeability in Alzheimer Disease , 2008, Journal of neuropathology and experimental neurology.

[17]  S. Salloway,et al.  Cerebral Cortical Arteriolar Angiopathy, Vascular Beta-Amyloid, Smooth Muscle Actin, Braak Stage, and APOE Genotype , 2008, Stroke.

[18]  P. Deyn,et al.  Alzheimer's disease-related changes in diseases characterized by elevation of intracranial or intraocular pressure , 2008, Clinical Neurology and Neurosurgery.

[19]  Leslie M. Shaw,et al.  PENN Biomarker Core of the Alzheimer’s Disease Neuroimaging Initiative , 2007, Neurosignals.

[20]  Sharon E. Lee,et al.  Cerebral Ventricular Changes Associated With Transitions Between Normal Cognitive Function, Mild Cognitive Impairment, and Dementia , 2007, Alzheimer disease and associated disorders.

[21]  Miles C. Miller,et al.  RAGE, LRP-1, and amyloid-beta protein in Alzheimer’s disease , 2006, Acta Neuropathologica.

[22]  Antonio Federico,et al.  Cerebrospinal fluid tau, Aß, and phosphorylated tau protein for the diagnosis of Alzheimer's disease , 2006, Journal of cellular physiology.

[23]  Amir Samii,et al.  Brain amyloid accumulates in aged rats with kaolin-induced hydrocephalus , 2006, Neuroreport.

[24]  A. Dale,et al.  Effects of age on volumes of cortex, white matter and subcortical structures , 2005, Neurobiology of Aging.

[25]  C. Jack,et al.  Ways toward an early diagnosis in Alzheimer’s disease: The Alzheimer’s Disease Neuroimaging Initiative (ADNI) , 2005, Alzheimer's & Dementia.

[26]  D. Holtzman,et al.  Human Apolipoprotein E4 Alters the Amyloid-β 40:42 Ratio and Promotes the Formation of Cerebral Amyloid Angiopathy in an Amyloid Precursor Protein Transgenic Model , 2005, The Journal of Neuroscience.

[27]  Anders M. Dale,et al.  Sequence-independent segmentation of magnetic resonance images , 2004, NeuroImage.

[28]  E. Stopa,et al.  Homeostatic capabilities of the choroid plexus epithelium in Alzheimer's disease , 2004, Cerebrospinal Fluid Research.

[29]  D. Tate,et al.  Cerebral volume loss, cognitive deficit and neuropsychological performance: Comparative measures of brain atrophy: I. Dementia , 2004, Journal of the International Neuropsychological Society.

[30]  Charles DeCarli,et al.  Cerebrospinal fluid tau and beta-amyloid: how well do these biomarkers reflect autopsy-confirmed dementia diagnoses? , 2003, Archives of neurology.

[31]  G. Silverberg,et al.  Alzheimer's disease, normal‐pressure hydrocephalus, and senescent changes in CSF circulatory physiology: a hypothesis , 2003, The Lancet Neurology.

[32]  M. Béné,et al.  Choroid plexus, aging of the brain, and Alzheimer's disease. , 2003, Frontiers in bioscience : a journal and virtual library.

[33]  M. Béné,et al.  CHOROID PLEXUS, AGEING OF THE BRAIN, AND ALZHEIMER'S DISEASE , 2003 .

[34]  A. Dale,et al.  Whole Brain Segmentation Automated Labeling of Neuroanatomical Structures in the Human Brain , 2002, Neuron.

[35]  D F Tate,et al.  Brain Volume, Intracranial Volume, and Dementia , 2001, Investigative radiology.

[36]  T. Berzin,et al.  Human Choroid Plexus Growth Factors: What Are the Implications for CSF Dynamics in Alzheimer's Disease? , 2001, Experimental Neurology.

[37]  D. Selkoe,et al.  Toward a Comprehensive Theory for Alzheimer's Disease. Hypothesis: Alzheimer's Disease Is Caused by the Cerebral Accumulation and Cytotoxicity of Amyloid β‐Protein , 2000, Annals of the New York Academy of Sciences.

[38]  A. Kluger,et al.  Alzheimer's disease comorbidity in normal pressure hydrocephalus: prevalence and shunt response , 2000, Journal of neurology, neurosurgery, and psychiatry.

[39]  Anders M. Dale,et al.  Cortical Surface-Based Analysis I. Segmentation and Surface Reconstruction , 1999, NeuroImage.

[40]  J. Morris,et al.  Clinical Dementia Rating: A Reliable and Valid Diagnostic and Staging Measure for Dementia of the Alzheimer Type , 1997, International Psychogeriatrics.

[41]  S. Sorbi,et al.  Analysis of apolipoprotein E, α1-antichymotrypsin and presenilin-1 genes polymorphisms in dementia caused by normal pressure hydrocephalus in man , 1997, Neuroscience Letters.

[42]  J. Hardy,et al.  Alzheimer's disease: the amyloid cascade hypothesis. , 1992, Science.

[43]  M. Folstein,et al.  Clinical diagnosis of Alzheimer's disease , 1984, Neurology.

[44]  S. Folstein,et al.  “Mini-mental state”: A practical method for grading the cognitive state of patients for the clinician , 1975 .

[45]  R. Deane,et al.  Clearance of amyloid-beta peptide across the blood-brain barrier: implication for therapies in Alzheimer's disease. , 2009, CNS & neurological disorders drug targets.

[46]  A. Chakravarty.  Unifying concept for Alzheimer's disease, vascular dementia and normal pressure hydrocephalus - a hypothesis. , 2004, Medical hypotheses.

[47]  S. Savolainen,et al.  Prevalence of Alzheimer's Disease in Patients Investigated for Presumed Normal Pressure Hydrocephalus: A Clinical and Neuropathological Study , 1999, Acta Neurochirurgica.

[48]  D. Premkumar,et al.  Production and increased detection of amyloid beta protein and amyloidogenic fragments in brain microvessels, meningeal vessels and choroid plexus in Alzheimer's disease. , 1996, Brain research. Molecular brain research.