Basal forebrain atrophy and cortical amyloid deposition in nondemented elderly subjects

Both neurodegeneration of the cholinergic basal forebrain (BF) and deposition of β‐amyloid are early events in the course of Alzheimer's disease (AD). Associations between increased amyloid pathology and cholinergic atrophy have been described in autopsy studies.

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

[2]  H. Hanyu,et al.  MR analysis of the substantia innominata in normal aging, Alzheimer disease, and other types of dementia. , 2002, AJNR. American journal of neuroradiology.

[3]  M. Sabbagh,et al.  Pre- and post-synaptic cortical cholinergic deficits are proportional to amyloid plaque presence and density at preclinical stages of Alzheimer’s disease , 2011, Acta Neuropathologica.

[4]  T. Arendt,et al.  Amyloid deposition in the nucleus basalis of Meynert complex: a topographic marker for degenerating cell clusters in Alzheimer's disease , 2004, Acta Neuropathologica.

[5]  M. Albert,et al.  Introduction to the recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease , 2011, Alzheimer's & Dementia.

[6]  J. Morris,et al.  The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer's disease , 2011, Alzheimer's & Dementia.

[7]  Kewei Chen,et al.  Using positron emission tomography and florbetapir F18 to image cortical amyloid in patients with mild cognitive impairment or dementia due to Alzheimer disease. , 2011, Archives of neurology.

[8]  C. Geula,et al.  Chemoarchitectonics of axonal and perikaryal acetylcholinesterase along information processing systems of the human cerebral cortex , 1994, Brain Research Bulletin.

[9]  Nicola Toschi,et al.  Relevance of magnetic resonance imaging for early detection and diagnosis of Alzheimer disease. , 2013, The Medical clinics of North America.

[10]  N. Greig,et al.  Rivastigmine Lowers Aβ and Increases sAPPα Levels, Which Parallel Elevated Synaptic Markers and Metabolic Activity in Degenerating Primary Rat Neurons , 2011, PloS one.

[11]  H. Heinsen,et al.  Longitudinal measures of cholinergic forebrain atrophy in the transition from healthy aging to Alzheimer's disease , 2013, Neurobiology of Aging.

[12]  John Ashburner,et al.  A fast diffeomorphic image registration algorithm , 2007, NeuroImage.

[13]  Henrik Zetterberg,et al.  Cerebrospinal fluid levels of β-amyloid 1-42, but not of tau, are fully changed already 5 to 10 years before the onset of Alzheimer dementia. , 2012, Archives of general psychiatry.

[14]  Katrin Amunts,et al.  Stereotaxic probabilistic maps of the magnocellular cell groups in human basal forebrain , 2008, NeuroImage.

[15]  T. Arendt,et al.  The significance of the cholinergic system in the brain during aging and in Alzheimer’s disease , 2006, Journal of Neural Transmission.

[16]  Cindee M. Madison,et al.  Episodic memory loss is related to hippocampal-mediated beta-amyloid deposition in elderly subjects. , 2009, Brain : a journal of neurology.

[17]  C. Rowe,et al.  Relationship between atrophy and β‐amyloid deposition in Alzheimer disease , 2010, Annals of neurology.

[18]  N. Greig,et al.  Nicotine Reduces the Secretion of Alzheimer's β‐Amyloid Precursor Protein Containing β‐Amyloid Peptide in the Rat without Altering Synaptic Proteins , 2002 .

[19]  H. Möller,et al.  Measurement of basal forebrain atrophy in Alzheimer's disease using MRI. , 2005, Brain : a journal of neurology.

[20]  Keith A. Johnson,et al.  Neuronal dysfunction and disconnection of cortical hubs in non-demented subjects with elevated amyloid burden , 2011, Alzheimer's & Dementia.

[21]  W. Ma,et al.  Amyloid β peptide induces tau phosphorylation and loss of cholinergic neurons in rat primary septal cultures , 2002, Neuroscience.

[22]  W. Millard,et al.  Long-term neuropathological and neurochemical effects of nucleus basalis lesions in the rat. , 1987, Science.

[23]  N. Greig,et al.  Nicotine reduces the secretion of Alzheimer's beta-amyloid precursor protein containing beta-amyloid peptide in the rat without altering synaptic proteins. , 2002, Annals of the New York Academy of Sciences.

[24]  Keith A. Johnson,et al.  Amyloid-β Associated Cortical Thinning in Clinically Normal Elderly , 2011, Annals of neurology.

[25]  Alan C. Evans,et al.  Volumetry of hippocampus and amygdala with high-resolution MRI and three-dimensional analysis software: minimizing the discrepancies between laboratories. , 2000, Cerebral cortex.

[26]  T. Cataudella,et al.  Septal grafts restore cognitive abilities and amyloid precursor protein metabolism , 2009, Neurobiology of Aging.

[27]  Olivier Salvado,et al.  Larger temporal volume in elderly with high versus low beta-amyloid deposition. , 2010, Brain : a journal of neurology.

[28]  T. Harkany,et al.  β-Amyloid(1–42) affects cholinergic but not parvalbumin-containing neurons in the septal complex of the rat , 1995, Brain Research.

[29]  D. Bennett,et al.  The amyloid pathology progresses in a neurotransmitter-specific manner , 2006, Neurobiology of Aging.

[30]  H. Braak,et al.  Phases of Aβ-deposition in the human brain and its relevance for the development of AD , 2002, Neurology.

[31]  S. Leurgans,et al.  MRI-based volumetric measurement of the substantia innominata in amnestic MCI and mild AD , 2011, Neurobiology of Aging.

[32]  C. Jack,et al.  Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade , 2010, The Lancet Neurology.

[33]  M. Mesulam,et al.  Cholinergic nucleus basalis tauopathy emerges early in the aging‐MCI‐AD continuum , 2004, Annals of neurology.

[34]  E K Perry,et al.  Correlation of cholinergic abnormalities with senile plaques and mental test scores in senile dementia. , 1978, British medical journal.

[35]  H. Heinsen,et al.  Atrophy of the Cholinergic Basal Forebrain Over the Adult Age Range and in Early Stages of Alzheimer's Disease , 2012, Biological Psychiatry.

[36]  L. H. Hughes,et al.  Cholinergic fibre loss associated with diffuse plaques in the non-demented elderly: the preclinical stage of Alzheimer’s disease? , 1997, Acta Neuropathologica.

[37]  R. Bartus,et al.  The cholinergic hypothesis of geriatric memory dysfunction. , 1982, Science.

[38]  S. DeKosky,et al.  Precuneus amyloid burden is associated with reduced cholinergic activity in Alzheimer disease , 2011, Neurology.

[39]  A. Levey,et al.  Cholinergic innervation of cortex by the basal forebrain: Cytochemistry and cortical connections of the septal area, diagonal band nuclei, nucleus basalis (Substantia innominata), and hypothalamus in the rhesus monkey , 1983, The Journal of comparative neurology.

[40]  Mark A Mintun,et al.  Cognitive decline and brain volume loss as signatures of cerebral amyloid-beta peptide deposition identified with Pittsburgh compound B: cognitive decline associated with Abeta deposition. , 2009, Archives of neurology.

[41]  D. Mann,et al.  Changes in nerve cells of the nucleus basalis of Meynert in Alzheimer's disease and their relationship to ageing and to the accumulation of lipofuscin pigment , 1984, Mechanisms of Ageing and Development.

[42]  K. Amunts,et al.  Reduction of basal forebrain cholinergic system parallels cognitive impairment in patients at high risk of developing Alzheimer's disease. , 2010, Cerebral cortex.

[43]  M. Mintun,et al.  Amyloid-β Imaging with Pittsburgh Compound B and Florbetapir: Comparing Radiotracers and Quantification Methods , 2013, The Journal of Nuclear Medicine.

[44]  J. Coyle,et al.  Alzheimer disease: Evidence for selective loss of cholinergic neurons in the nucleus basalis , 1981, Annals of neurology.

[45]  P. Kelly,et al.  Cholinergic Changes in the APP23 Transgenic Mouse Model of Cerebral Amyloidosis , 2002, The Journal of Neuroscience.

[46]  T. Arendt,et al.  Neuronal loss in different parts of the nucleus basalis is related to neuritic plaque formation in cortical target areas in alzheimer's disease , 1985, Neuroscience.

[47]  T. Beach,et al.  Senile plaques, amyloid β-protein, and acetylcholinesterase fibres: laminar distributions in Alzheimer's disease striate cortex , 2004, Acta Neuropathologica.