Plaque biogenesis in brain aging and Alzheimer’s disease. II. Progressive transformation and developmental sequence of dystrophic neurites

No abstract is available for this paper.

• Publication year

  1998

• Venue

  Acta Neuropathologica

• Publication date

  1998-11-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1007/s004010050920PMID 9829809
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Molecular Pathology of Alzheimer's Disease

  2013cited by this paper
• Monoclonal antibodies with selective specificity for Alzheimer Tau are directed against phosphatase-sensitive epitopes

  2004cited by this paper
• β‐Amyloid‐Induced Neurotoxicity of a Hybrid Septal Cell Line Associated with Increased Tau Phosphorylation and Expression of β‐Amyloid Precursor Protein

  1997cited by this paper
• Beta-amyloid-induced neurotoxicity of a hybrid septal cell line associated with increased tau phosphorylation and expression of beta-amyloid precursor protein.

  1997cited by this paper
• Diffuse plaques contain C-terminal Aβ42 and not Aβ40: Evidence from cats and dogs

  1996cited by this paper
• Dystrophic neurite formation associated with age-related beta amyloid deposition in the neocortex: clues to the genesis of neurofibrillary pathology.

  1996cited by this paper
• Plaque biogenesis in brain aging and Alzheimer's disease. I. Progressive changes in phosphorylation states of paired helical filaments and neurofilaments.

  1996cited by this paper
• Exposure of rat hippocampal neurons to amyloid beta peptide (25-35) induces the inactivation of phosphatidyl inositol-3 kinase and the activation of tau protein kinase I/glycogen synthase kinase-3 beta.

  1996cited by this paper
• Diffuse plaques contain C-terminal A beta 42 and not A beta 40: evidence from cats and dogs.

  1996cited by this paper
• Beta-amyloid deposition and other measures of neuropathology predict cognitive status in Alzheimer's disease.

  1996cited by this paper
• The canine as an animal model of human aging and dementia.

  1996cited by this paper
• β-amyloid deposition and other measures of neuropathology predict cognitive status in Alzheimer's disease

  1996cited by this paper
• Mechanisms of neuronal degeneration in Alzheimer's disease.

  1996cited by this paper
• Exposure of rat hippocampal neurons to amyloid β peptide (25–35) induces the inactivation of phosphatidyl inositol-3 kinase and the activation of tau protein kinase I/glycogen synthase kinase-3β

  1996cited by this paper
• Correlations of synaptic and pathological markers with cognition of the elderly.

  1995cited by this paper
• β-Amyloid fibrils induce tau phosphorylation and loss of microtubule binding

  1995cited by this paper
• The toxicity in vitro of beta-amyloid protein.

  1995cited by this paper
• Visualization of Aβ42(43) and Aβ40 in senile plaques with end-specific Aβ monoclonals: Evidence that an initially deposited species is Aβ42(43)

  1994cited by this paper
• An extensive network of PHFτ‐rich dystrophic neurites permeates neocortex and nearly all neuritic and diffuse amyloid plaques in Alzheimer disease

  1994cited by this paper
• Subpopulations of dystrophic neurites [correction of neuritis] in Alzheimer's brain with distinct immunocytochemical and argentophilic characteristics.

  1994cited by this paper
• Alterations in neurofilament protein immunoreactivity in human hippocampal neurons related to normal aging and Alzheimer's disease.

  1994cited by this paper
• Non-Alzheimer neurofibrillary tangles show beta-amyloid-like immunoreactivity.

  1994cited by this paper
• Visualization of A beta 42(43) and A beta 40 in senile plaques with end-specific A beta monoclonals: evidence that an initially deposited species is A beta 42(43).

  1994cited by this paper
• Beta amyloid neurotoxicity and neuronal degeneration in Alzheimer's disease.

  1994cited by this paper
• Early phosphorylation of tau in Alzheimer's disease occurs at Ser-202 and is preferentially located within neurites.

  1994cited by this paper
• Subpopulations of dystrophic neuritis in Alzheimer's brain with distinct immunocytochemical and argentophilic characteristics

  1994cited by this paper
• Physiological production of the beta-amyloid protein and the mechanism of Alzheimer's disease.

  1993cited by this paper
• Identification and distribution of axonal dystrophic neurites in Alzheimer's disease.

  1993cited by this paper
• Physiological production of the β-amyloid protein and the mechanism of Alzheimer's disease

  1993cited by this paper
• Tau protein kinase I is essential for amyloid beta-protein-induced neurotoxicity.

  1993cited by this paper
• The abnormal phosphorylation of tau protein at Ser-202 in Alzheimer disease recapitulates phosphorylation during development.

  1993cited by this paper
• Beta-amyloid accumulation in aged canine brain: a model of early plaque formation in Alzheimer's disease.

  1993cited by this paper
• Abnormal tau phosphorylation at Ser396 in Alzheimer's disease recapitulates development and contributes to reduced microtubule binding.

  1993cited by this paper
• Evidence that transmitter-containing dystrophic neurites precede those containing paired helical filaments within senile plaques in the entorhinal cortex of nondemented elderly and Alzheimer's disease patients.

  1993cited by this paper
• β-Amyloid accumulation in aged canine brain: A model of early plaque formation in Alzheimer's disease

  1993cited by this paper
• Hydrofluoric acid-treated tau PHF proteins display the same biochemical properties as normal tau.

  1992cited by this paper
• In vivo neurotoxicity of beta-amyloid [β(1–40)] and the β(25–35) fragment

  1992cited by this paper
• Senile plaques in cerebral amyloid angiopathy show accumulation of amyloid precursor protein without cytoskeletal abnormalities.

  1992cited by this paper
• beta-Amyloid induces neuritic dystrophy in vitro: similarities with Alzheimer pathology.

  1992cited by this paper
• Distribution of Alzheimer‐type pathologic changes in nondemented elderly individuals matches the pattern in Alzheimer's disease

  1992cited by this paper
• Progressive transformation of the cytoskeleton associated with normal aging and Alzheimer's disease.

  1992influential reference
• Alzheimer's disease: a cell biological perspective.

  1992cited by this paper
• In vivo neurotoxicity of beta-amyloid [beta(1-40)] and the beta(25-35) fragment.

  1992cited by this paper
• The switch of tau protein to an Alzheimer‐like state includes the phosphorylation of two serine‐proline motifs upstream of the microtubule binding region.

  1992cited by this paper
• Aggregation of the amyloid precursor protein within degenerating neurons and dystrophic neurites in Alzheimer's disease.

  1992cited by this paper
• Phosphorylation-dependent epitopes of neurofilament antibodies on tau protein and relationship with Alzheimer tau.

  1992cited by this paper
• The Consortium to Establish a Registry for Alzheimer's Disease (CERAD)

  1991cited by this paper
• In vitro aging of beta-amyloid protein causes peptide aggregation and neurotoxicity.

  1991cited by this paper
• In vitro aging of ß-amyloid protein causes peptide aggregation and neurotoxicity ☆

  1991cited by this paper
• The molecular pathology of Alzheimer's disease.

  1991cited by this paper
• Senile plaque neurites in Alzheimer disease accumulate amyloid precursor protein.

  1991cited by this paper
• THE IMMUNOHISTOCHEMICAL DEMONSTRATION OF SUBSEQUENCES OF THE PRECURSOR OF THE AMYLOID A4 PROTEIN IN SENILE PLAQUES IN ALZHEIMER'S DISEASE

  1989cited by this paper
• Identification of the major multiphosphorylation site in mammalian neurofilaments.

  1988cited by this paper
• The pathological association between Down syndrome and Alzheimer disease.

  1988cited by this paper
• Recognition of tau epitopes by anti-neurofilament antibodies that bind to Alzheimer neurofibrillary tangles

  1987cited by this paper
• Recognition of tau epitopes by anti-neurofilament antibodies that bind to Alzheimer neurofibrillary tangles.

  1987cited by this paper
• Axonal disruption and aberrant localization of tau protein characterize the neuropil pathology of Alzheimer's disease

  1987cited by this paper
• A COMPARATIVE STUDY OF MODIFIED BIELSCHOWSKY, BODIAN AND THIOFLAVIN S STAINS ON ALZHEIMER'S NEUROFIBRILLARY TANGLES

  1986cited by this paper
• Monoclonal antibodies distinguish phosphorylated and nonphosphorylated forms of neurofilaments in situ.

  1983cited by this paper

• Increased expression of the proapoptotic presenilin associated protein is involved in neuronal tangle formation in human brain

  2024cites this paper
• Differential Glial Response and Neurodegenerative Patterns in CA1, CA3, and DG Hippocampal Regions of 5XFAD Mice

  2024cites this paper
• Accelerating the in vitro emulation of Alzheimer’s disease-associated phenotypes using a novel 3D blood-brain barrier neurosphere co-culture model

  2023cites this paper
• Neuritic Plaques — Gateways to Understanding Alzheimer’s Disease

  2023cites this paper
• Alteration of neurofilament heavy chain and its phosphoforms reveals early subcellular damage beyond the optic nerve head in glaucoma

  2023cites this paper
• PLD3 affects axonal spheroids and network defects in Alzheimer’s disease

  2022cites this paper
• Improved modeling of human AD with an automated culturing platform for iPSC neurons, astrocytes and microglia

  2021cites this paper
• Plaque-Associated Oligomeric Amyloid-Beta Drives Early Synaptotoxicity in APP/PS1 Mice Hippocampus: Ultrastructural Pathology Analysis

  2021cites this paper
• Early Dendritic Dystrophy in Human Brains With Primary Age-Related Tauopathy

  2020cites this paper
• Axonal Degeneration in AD: The Contribution of Aβ and Tau

  2020cites this paper
• Correction of microtubule defects within Aβ plaque‐associated dystrophic axons results in lowered Aβ release and plaque deposition

  2020cites this paper
• Pathological Links between Traumatic Brain Injury and Dementia: Australian Pre-Clinical Research

  2020cites this paper
• BAP31 deficiency contributes to the formation of amyloid‐β plaques in Alzheimer's disease by reducing the stability of RTN3

  2018cites this paper
• Contribution of Neurons and Glial Cells to Complement-Mediated Synapse Removal during Development, Aging and in Alzheimer's Disease

  2018cites this paper
• Amyloid Plaques of Alzheimer’s Disease as Hotspots of Glutamatergic Activity

  2018cites this paper
• Microglia-Mediated Neuroprotection, TREM2, and Alzheimer's Disease: Evidence From Optical Imaging.

  2018cites this paper
• Integrative Analysis of Gene Expression Profiles in Aging and Alzheimer ’ s Disease

  2018cites this paper
• Hypoxia and alzheimer's disease: the processing of amyloid precursor protein and the role of prolyl-hydroxylase 3 in microglia.

  2018cites this paper
• High plasticity of axonal pathology in Alzheimer’s disease mouse models

  2017cites this paper
• Synaptic Plasticity, Dementia and Alzheimer Disease.

  2017cites this paper
• Cerebral hypoperfusion and glucose hypometabolism: Key pathophysiological modulators promote neurodegeneration, cognitive impairment, and Alzheimer's disease

  2017cites this paper
• Alterations in neurofilaments and the transformation of the cytoskeleton in axons may provide insight into the aberrant neuronal changes of Alzheimer's disease.

  2016cites this paper
• Defining the Earliest Pathological Changes of Alzheimer’s Disease

  2016cites this paper
• Plaque-Associated Local Toxicity Increases over the Clinical Course of Alzheimer Disease.

  2016cites this paper
• Quantitative analysis of neuropathological alterations in two transgenic mouse models of Alzheimer's disease

  2016cites this paper
• Amyloid beta 4-42 in Alzheimer’s disease: Target, Therapy, Mechanism

  2016cites this paper
• Immunolocalization of Tom1 in relation to protein degradation systems in Alzheimer's disease.

  2016cites this paper
• Ambient Glutamate Promotes Paroxysmal Hyperactivity in Cortical Pyramidal Neurons at Amyloid Plaques via Presynaptic mGluR1 Receptors

  2016cites this paper
• Invited review: Neuropathology of tauopathies: principles and practice

  2015cites this paper
• Evidence of neurodegeneration in obstructive sleep apnea: Relationship between obstructive sleep apnea and cognitive dysfunction in the elderly

  2015cites this paper
• The role of amyloid beta 4-42 in the etiology of Alzheimer's disease

  2015cites this paper
• Noradrenergic Deficits Contribute to Impairment in the TgCRND8 Mouse Model of Alzheimer's Disease

  2014cites this paper
• Neurites containing the neurofilament-triplet proteins are selectively vulnerable to cytoskeletal pathology in Alzheimer’s disease and transgenic mouse models

  2013cites this paper
• Differential relationships of reactive astrocytes and microglia to fibrillar amyloid deposits in Alzheimer disease.

  2013cites this paper
• Axonal and synaptic pathology in Alzheimer’s disease

  2013cites this paper
• α‐Secretase cleaved amyloid precursor protein (APP) accumulates in cholinergic dystrophic neurites in normal, aged hippocampus

  2013cites this paper
• The 5XFAD mouse model: a tool for genetic modulation of Alzheime's disease pathology

  2012cites this paper
• Alteration of the Cerebral Zinc Pool in a Mouse Model of Alzheimer Disease

  2012cites this paper
• Vaccination with a non-human random sequence amyloid oligomer mimic results in improved cognitive function and reduced plaque deposition and micro hemorrhage in Tg2576 mice

  2012cites this paper
• Abnormal accumulation of autophagic vesicles correlates with axonal and synaptic pathology in young Alzheimer’s mice hippocampus

  2011cites this paper
• Neuropathological alterations in Alzheimer disease.

  2011cites this paper
• Rosiglitazone Rescues Memory Impairment in Alzheimer's Transgenic Mice: Mechanisms Involving a Reduced Amyloid and Tau Pathology

  2010cites this paper
• Molecular Pathogenesis of Alzheimer’s Disease: Reductionist versus Expansionist Approaches

  2009cites this paper
• Does β-amyloid plaque formation cause structural injury to neuronal processes?

  2009cites this paper
• Dystrophic neurites in TgCRND8 and Tg2576 mice mimic human pathological brain aging.

  2009cites this paper
• CD40 ligation mediates plaque-associated tau phosphorylation in beta-amyloid overproducing mice.

  2008cites this paper
• Cytoskeletal alterations differentiate presenilin-1 and sporadic Alzheimer’s disease

  2008influential citation
• Epidermal growth factor receptor in adult retinal neurons of rat, mouse, and human

  2007cites this paper
• Mechanisms of amyloid plaque pathogenesis

  2007cites this paper
• Caspase-3 cleaved spectrin colocalizes with neurofilament-immunoreactive neurons in Alzheimer's disease.

  2006cites this paper
• Cytoplasmic cytochrome c immunolabelling in dystrophic neurites in Alzheimer’s disease

  2006cites this paper
• Homocysteic acid induces intraneuronal accumulation of neurotoxic Aβ42: Implications for the pathogenesis of Alzheimer's disease

  2005cites this paper
• alpha-Internexin immunoreactivity reflects variable neuronal vulnerability in Alzheimer's disease and supports the role of the beta-amyloid plaques in inducing neuronal injury.

  2005cites this paper
• Does beta-amyloid plaque formation cause structural injury to neuronal processes?

  2005cites this paper
• α-Internexin immunoreactivity reflects variable neuronal vulnerability in Alzheimer's disease and supports the role of the β-amyloid plaques in inducing neuronal injury

  2005cites this paper
• Neurofilament phosphoforms: surrogate markers for axonal injury, degeneration and loss.

  2005cites this paper
• Selective vulnerability of dentate granule cells prior to amyloid deposition in PDAPP mice: digital morphometric analyses.

  2004cites this paper
• Exclusive association and simultaneous appearance of congophilic plaques and AT8-positive dystrophic neurites in Tg2576 mice suggest a mechanism of senile plaque formation and progression of neuritic dystrophy in Alzheimer’s disease

  2004cites this paper
• Brain–specific proteins in Multiple Sclerosis

  2003cites this paper
• Time sequence of maturation of dystrophic neurites associated with Abeta deposits in APP/PS1 transgenic mice.

  2003cites this paper
• Analysis of glial acidic fibrillary protein in the human entorhinal cortex during aging and in Alzheimer's disease.

  2003cites this paper
• Ultrastructural and behavioural changes precede amyloid deposition in a transgenic model of Alzheimer's disease.

  2003cites this paper
• Fas and Fas ligand are associated with neuritic degeneration in the AD brain and participate in beta-amyloid-induced neuronal death.

  2003cites this paper
• A Vaccine Against Alzheimer’s Disease

  2002cites this paper
• NEURONAL POPULATIONS OF RAT CEREBRAL CORTEX AND HIPPOCAMPUS EXPRESSED A HIGHER DENSITY OF L-TYPE Ca2+ CHANNEL THAN CORRESPONDING CEREBRAL VESSELS

  2002cites this paper
• EFFECT OF NICARDIPINE TREATMENT ON THE EXPRESSION OF NEUROFILAMENT 200 KDa IMMUNOREACTIVITY IN THE BRAIN OF SPONTANEOUSLY HYPERTENSIVE RATS

  2001cites this paper
• Neurofilament proteins NF-L, NF-M and NF-H in brain of patients with Down syndrome and Alzheimer's disease

  2001cites this paper
• Cotton Wool Plaques in Non‐Familial Late‐Onset Alzheimer Disease

  2001cites this paper
• Neurofibrillary Pathology in Transgenic Mice Overexpressing V717F β‐Amyloid Precursor Protein

  2001cites this paper
• The cause of neuronal degeneration in Alzheimer's disease.

  2000cites this paper
• The formation of PHF-1 and SMI-31 positive dystrophic neurites in rat hippocampus following acute injection of okadaic acid.

  2000cites this paper
• A Unifying Hypothesis of Alzheimer's Disease. IV. Causation and Sequence of Events

  2000cites this paper
• Wnt signaling function in Alzheimer's disease.

  2000cites this paper
• Anti-Aging Medicine LiteratureWatch

  1999cites this paper
• Amyloid precursor proteins in the cerebellar cortex of Alzheimer's disease patients devoid of cerebellar β-amyloid deposits: immunocytochemical study of five cases

  1999cites this paper
• A unifying hypothesis of Alzheimer's disease. II. Pathophysiological processes

  1999cites this paper
• Sequence of neurodegeneration and accumulation of phosphorylated tau in cultured neurons after okadaic acid treatment.

  1999cites this paper
• Emerging strategies for the treatment of Alzheimers disease at the Millennium

  1999cites this paper