The Experts below are selected from a list of 93 Experts worldwide ranked by ideXlab platform
Joseph G. Rogers - One of the best experts on this subject based on the ideXlab platform.
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Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer’s Disease
American Journal of Pathology, 1999Co-Authors: Alex E. Roher, Libuse Brachova, Yong Shen, Thomas G. Beach, Janice H. Kurth, Russel E. Rydel, Joseph G. RogersAbstract:We have characterized amyloid β peptide (Aβ. concentration, Aβ deposition, paired helical filament formation, cerebrovascular amyloid angiopathy, apolipoprotein E (ApoE) allotype, and synaptophysin concentration in entorhinal cortex and superior frontal gyrus of normal elderly control (ND) patients, Alzheimer's disease (AD. patients, and high pathology control (HPC) patients who meet pathological criteria for AD but show no synapse loss or overt antemortem symptoms of dementia. The measures of Aβ deposition, Aβ-immunoreactive plaques with and without cores, thioflavin histofluorescent plaques, and concentrations of insoluble Aβ, failed to distinguish HPC from AD patients and were poor correlates of Synaptic Change. By contrast, concentrations of soluble Aβ clearly distinguished HPC from AD patients and were a strong inverse correlate of synapse loss. Further investigation revealed that Aβ40, whether in soluble or insoluble form, was a particularly useful measure for classifying ND, HPC, and AD patients compared with Aβ42. Aβ40 is known to be elevated in cerebrovascular amyloid deposits, and Aβ40 (but not Aβ42) levels, cerebrovascular amyloid angiopathy, and ApoE4 allele frequency were all highly correlated with each other. Although paired helical filaments in the form of neurofibrillary tangles or a penumbra of neurites surrounding amyloid cores also distinguished HPC from AD patients, they were less robust predictors of synapse Change compared with soluble Aβ, particularly soluble Aβ40. Previous experiments attempting to relate Aβ deposition to the neurodegeneration that underlies AD dementia may have failed because they assayed the classical, visible forms of the molecule, insoluble neuropil plaques, rather than the soluble, unseen forms of the molecule.
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soluble amyloid β peptide concentration as a predictor of Synaptic Change in alzheimer s disease
American Journal of Pathology, 1999Co-Authors: Alex E. Roher, Libuse Brachova, Yong Shen, Thomas G. Beach, Janice H. Kurth, Russel E. Rydel, Joseph G. RogersAbstract:We have characterized amyloid β peptide (Aβ. concentration, Aβ deposition, paired helical filament formation, cerebrovascular amyloid angiopathy, apolipoprotein E (ApoE) allotype, and synaptophysin concentration in entorhinal cortex and superior frontal gyrus of normal elderly control (ND) patients, Alzheimer's disease (AD. patients, and high pathology control (HPC) patients who meet pathological criteria for AD but show no synapse loss or overt antemortem symptoms of dementia. The measures of Aβ deposition, Aβ-immunoreactive plaques with and without cores, thioflavin histofluorescent plaques, and concentrations of insoluble Aβ, failed to distinguish HPC from AD patients and were poor correlates of Synaptic Change. By contrast, concentrations of soluble Aβ clearly distinguished HPC from AD patients and were a strong inverse correlate of synapse loss. Further investigation revealed that Aβ40, whether in soluble or insoluble form, was a particularly useful measure for classifying ND, HPC, and AD patients compared with Aβ42. Aβ40 is known to be elevated in cerebrovascular amyloid deposits, and Aβ40 (but not Aβ42) levels, cerebrovascular amyloid angiopathy, and ApoE4 allele frequency were all highly correlated with each other. Although paired helical filaments in the form of neurofibrillary tangles or a penumbra of neurites surrounding amyloid cores also distinguished HPC from AD patients, they were less robust predictors of synapse Change compared with soluble Aβ, particularly soluble Aβ40. Previous experiments attempting to relate Aβ deposition to the neurodegeneration that underlies AD dementia may have failed because they assayed the classical, visible forms of the molecule, insoluble neuropil plaques, rather than the soluble, unseen forms of the molecule.
Alex E. Roher - One of the best experts on this subject based on the ideXlab platform.
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Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer’s Disease
American Journal of Pathology, 1999Co-Authors: Alex E. Roher, Libuse Brachova, Yong Shen, Thomas G. Beach, Janice H. Kurth, Russel E. Rydel, Joseph G. RogersAbstract:We have characterized amyloid β peptide (Aβ. concentration, Aβ deposition, paired helical filament formation, cerebrovascular amyloid angiopathy, apolipoprotein E (ApoE) allotype, and synaptophysin concentration in entorhinal cortex and superior frontal gyrus of normal elderly control (ND) patients, Alzheimer's disease (AD. patients, and high pathology control (HPC) patients who meet pathological criteria for AD but show no synapse loss or overt antemortem symptoms of dementia. The measures of Aβ deposition, Aβ-immunoreactive plaques with and without cores, thioflavin histofluorescent plaques, and concentrations of insoluble Aβ, failed to distinguish HPC from AD patients and were poor correlates of Synaptic Change. By contrast, concentrations of soluble Aβ clearly distinguished HPC from AD patients and were a strong inverse correlate of synapse loss. Further investigation revealed that Aβ40, whether in soluble or insoluble form, was a particularly useful measure for classifying ND, HPC, and AD patients compared with Aβ42. Aβ40 is known to be elevated in cerebrovascular amyloid deposits, and Aβ40 (but not Aβ42) levels, cerebrovascular amyloid angiopathy, and ApoE4 allele frequency were all highly correlated with each other. Although paired helical filaments in the form of neurofibrillary tangles or a penumbra of neurites surrounding amyloid cores also distinguished HPC from AD patients, they were less robust predictors of synapse Change compared with soluble Aβ, particularly soluble Aβ40. Previous experiments attempting to relate Aβ deposition to the neurodegeneration that underlies AD dementia may have failed because they assayed the classical, visible forms of the molecule, insoluble neuropil plaques, rather than the soluble, unseen forms of the molecule.
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soluble amyloid β peptide concentration as a predictor of Synaptic Change in alzheimer s disease
American Journal of Pathology, 1999Co-Authors: Alex E. Roher, Libuse Brachova, Yong Shen, Thomas G. Beach, Janice H. Kurth, Russel E. Rydel, Joseph G. RogersAbstract:We have characterized amyloid β peptide (Aβ. concentration, Aβ deposition, paired helical filament formation, cerebrovascular amyloid angiopathy, apolipoprotein E (ApoE) allotype, and synaptophysin concentration in entorhinal cortex and superior frontal gyrus of normal elderly control (ND) patients, Alzheimer's disease (AD. patients, and high pathology control (HPC) patients who meet pathological criteria for AD but show no synapse loss or overt antemortem symptoms of dementia. The measures of Aβ deposition, Aβ-immunoreactive plaques with and without cores, thioflavin histofluorescent plaques, and concentrations of insoluble Aβ, failed to distinguish HPC from AD patients and were poor correlates of Synaptic Change. By contrast, concentrations of soluble Aβ clearly distinguished HPC from AD patients and were a strong inverse correlate of synapse loss. Further investigation revealed that Aβ40, whether in soluble or insoluble form, was a particularly useful measure for classifying ND, HPC, and AD patients compared with Aβ42. Aβ40 is known to be elevated in cerebrovascular amyloid deposits, and Aβ40 (but not Aβ42) levels, cerebrovascular amyloid angiopathy, and ApoE4 allele frequency were all highly correlated with each other. Although paired helical filaments in the form of neurofibrillary tangles or a penumbra of neurites surrounding amyloid cores also distinguished HPC from AD patients, they were less robust predictors of synapse Change compared with soluble Aβ, particularly soluble Aβ40. Previous experiments attempting to relate Aβ deposition to the neurodegeneration that underlies AD dementia may have failed because they assayed the classical, visible forms of the molecule, insoluble neuropil plaques, rather than the soluble, unseen forms of the molecule.
Bryan Kolb - One of the best experts on this subject based on the ideXlab platform.
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Tactile stimulation after frontal or parietal cortical injury in infant rats facilitates functional recovery and produces Synaptic Changes in adjacent cortex.
Behavioural Brain Research, 2010Co-Authors: Bryan Kolb, Robbin GibbAbstract:Abstract Rats with bilateral lesions (and sham controls) of the medial frontal or posterior parietal cortex on postnatal days 2–4 were treated with tactile stimulation for 15 min three times daily for two weeks following injury. In adulthood they were trained in a spatial navigation task and a skilled reaching task, their brains were removed, and dendritic length and spine density were analyzed in layer III pyramidal neurons in area Par 1. Tactile stimulation significantly reduced the behavioral impairments after early cortical injury. Neonatal lesions decreased dendritic length and this was reversed by stimulation in rats with parietal, but not frontal, lesions. Both lesions decreased spine density and tactile stimulation reversed this loss in frontal but not parietal lesion animals. In addition, tactile stimulation decreased spine density in control animals. The results suggest that early intervention with tactile stimulation after cortical injury may be important for stimulating plastic Changes in the cortex that can underlie functional recovery and that different mechanisms of Synaptic Change may occur after different injuries.
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chronic low dose administration of nicotine facilitates recovery and Synaptic Change after focal ischemia in rats
Neuropharmacology, 2006Co-Authors: Claudia L R Gonzalez, Omar A Gharbawie, Bryan KolbAbstract:Abstract The current study examines the effects of chronic administration of nicotine on motor behavior after focal stroke in rats. Animals were trained in a tray-reaching task for 2 weeks and then they were divided into: (1) control + saline (2) control + nicotine (3) stroke + saline, and (4) stroke + nicotine groups. Lesions were produced by devascularization of the surface blood vessels of the sensorimotor cortex contralateral to the forepaw used for reaching. Forty-eight hours after the lesions, and for a total of 12 days, animals received two daily injections of either nicotine (0.3 mg/kg) or saline (0.9%). Animals were tested in a motor battery 1 week after the lesions and every other week for a total of 7 weeks. Pyramidal cells in forelimb and cingulate areas were then examined for dendritic length and branching using a Golgi–Cox procedure. Behavioral results demonstrated that by the end of the testing stroke + nicotine animals showed significant behavioral improvement relative to stroke + saline animals. Stroke + nicotine animals showed an increase in dendritic length and branching in pyramidal cells of the forelimb and cingulate areas. The results suggest that the behavioral enhancement in the stroke + nicotine group might be attributable to the enhanced dendritic growth in residual cortical motor regions.
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Synaptic plasticity and the organization of behaviour after early and late brain injury.
Canadian Journal of Experimental Psychology, 1999Co-Authors: Bryan KolbAbstract:Abstract Hebb proposed that Synaptic Change underlies behavioural and cognitive plasticity. When applied to recovery from brain injury, the general hypothesis is that if there is recovery following brain injury, then there ought to be a correlated Synaptic Change, which is presumed to be responsible for recovery. In contrast, if recovery fails to occur, or expected recovery is blocked in some manner, then the Synaptic Change will likely not be present. Systematic study of functional recovery and Synaptic Change following brain injury at different ages supports these predictions. Good recovery is always correlated with enhanced connectivity whereas poor recovery is always correlated with an absence of reorganized connectivity. Furthermore, factors that stimulate recovery, such as neurotrophins or experience, stimulate Synaptic Change and functional recovery. Factors that retard recovery, such as depletion of neuromodulators, also block Synaptic Change. These results thus support Hebb's general idea that Synaptic plasticity is related to behavioural Change. Introduction Hebb proposed that Synaptic Change underlies behavioural and cognitive flexibility. There was little evidence of this in 1949, and although the concept of the "Hebb synapse" has become popular in the last decade, there is still rather little direct evidence that Synaptic plasticity is associated with processes such as learning or memory, except perhaps in the simplest model systems. Nonetheless, the concept has considerable appeal and remains a viable hypothesis for behavioural flexibility. I will present evidence from studies of the anatomical bases of recovery from brain injury that support the general hypothesis that Synaptic Change can support behavioural Change. ASSUMPTIONS As I begin, I must first admit to several biases (see also Kolb, Forgie, Gibb, Gorny, & Rowntree, 1998). First, I assume that the nervous system is conservative. Thus, general mechanisms that are used for one type of behavioural Change, such as learning and memory, may also be used for other types of behavioural Change, such as in recovery from brain injury. (This assumption does not preclude separate mechanisms too, but it provides a rationale for what to look for and where to look for it.) Studies of functional recovery have the advantage that perturbations of the brain at different times from birth through to ageing produce consistent differences in behavioural outcome ranging from almost complete recovery of function after cortical injury to truly devastating behavioural loss. This variation in behaviour is useful for it is reasonable to suppose that these behavioural differences are related to differences in anatomico-physiological response(s) as well. Second, I am a "cortex chauvinist" and assume that the Changes in the cerebral cortex form the principal mechanism for cognitive Change. This assumption comes from several lines of evidence. For instance, it is generally agreed that the relative increase in cortical volume across mammalian evolution is associated with increased cognitive capacity. It follows that Changes in cognitive functions in a particular mammal likely will involve Changes in cortical structure or organization. Furthermore, studies of decorticated rats show that although they are capable of a remarkable behavioural repertoire (e.g., Whishaw, 1990), there is virtually no recovery or sparing of function from decortication under conditions that would normally lead to marked recovery after restricted cortical removals. For example, Whishaw and I have found that whereas removal of frontal, motor, or parietal cortex at 7-10 days of age allows dramatic sparing of function relative to similar injury in adulthood, there is no sparing at all after complete neonatal neodecortication at 7 days (Kolb & Whishaw, 1981a, b). Further, there is no obvious evidence of anatomical reorganization in the neonatal decorticates (Kolb et al. …
Janice H. Kurth - One of the best experts on this subject based on the ideXlab platform.
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Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer’s Disease
American Journal of Pathology, 1999Co-Authors: Alex E. Roher, Libuse Brachova, Yong Shen, Thomas G. Beach, Janice H. Kurth, Russel E. Rydel, Joseph G. RogersAbstract:We have characterized amyloid β peptide (Aβ. concentration, Aβ deposition, paired helical filament formation, cerebrovascular amyloid angiopathy, apolipoprotein E (ApoE) allotype, and synaptophysin concentration in entorhinal cortex and superior frontal gyrus of normal elderly control (ND) patients, Alzheimer's disease (AD. patients, and high pathology control (HPC) patients who meet pathological criteria for AD but show no synapse loss or overt antemortem symptoms of dementia. The measures of Aβ deposition, Aβ-immunoreactive plaques with and without cores, thioflavin histofluorescent plaques, and concentrations of insoluble Aβ, failed to distinguish HPC from AD patients and were poor correlates of Synaptic Change. By contrast, concentrations of soluble Aβ clearly distinguished HPC from AD patients and were a strong inverse correlate of synapse loss. Further investigation revealed that Aβ40, whether in soluble or insoluble form, was a particularly useful measure for classifying ND, HPC, and AD patients compared with Aβ42. Aβ40 is known to be elevated in cerebrovascular amyloid deposits, and Aβ40 (but not Aβ42) levels, cerebrovascular amyloid angiopathy, and ApoE4 allele frequency were all highly correlated with each other. Although paired helical filaments in the form of neurofibrillary tangles or a penumbra of neurites surrounding amyloid cores also distinguished HPC from AD patients, they were less robust predictors of synapse Change compared with soluble Aβ, particularly soluble Aβ40. Previous experiments attempting to relate Aβ deposition to the neurodegeneration that underlies AD dementia may have failed because they assayed the classical, visible forms of the molecule, insoluble neuropil plaques, rather than the soluble, unseen forms of the molecule.
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soluble amyloid β peptide concentration as a predictor of Synaptic Change in alzheimer s disease
American Journal of Pathology, 1999Co-Authors: Alex E. Roher, Libuse Brachova, Yong Shen, Thomas G. Beach, Janice H. Kurth, Russel E. Rydel, Joseph G. RogersAbstract:We have characterized amyloid β peptide (Aβ. concentration, Aβ deposition, paired helical filament formation, cerebrovascular amyloid angiopathy, apolipoprotein E (ApoE) allotype, and synaptophysin concentration in entorhinal cortex and superior frontal gyrus of normal elderly control (ND) patients, Alzheimer's disease (AD. patients, and high pathology control (HPC) patients who meet pathological criteria for AD but show no synapse loss or overt antemortem symptoms of dementia. The measures of Aβ deposition, Aβ-immunoreactive plaques with and without cores, thioflavin histofluorescent plaques, and concentrations of insoluble Aβ, failed to distinguish HPC from AD patients and were poor correlates of Synaptic Change. By contrast, concentrations of soluble Aβ clearly distinguished HPC from AD patients and were a strong inverse correlate of synapse loss. Further investigation revealed that Aβ40, whether in soluble or insoluble form, was a particularly useful measure for classifying ND, HPC, and AD patients compared with Aβ42. Aβ40 is known to be elevated in cerebrovascular amyloid deposits, and Aβ40 (but not Aβ42) levels, cerebrovascular amyloid angiopathy, and ApoE4 allele frequency were all highly correlated with each other. Although paired helical filaments in the form of neurofibrillary tangles or a penumbra of neurites surrounding amyloid cores also distinguished HPC from AD patients, they were less robust predictors of synapse Change compared with soluble Aβ, particularly soluble Aβ40. Previous experiments attempting to relate Aβ deposition to the neurodegeneration that underlies AD dementia may have failed because they assayed the classical, visible forms of the molecule, insoluble neuropil plaques, rather than the soluble, unseen forms of the molecule.
Russel E. Rydel - One of the best experts on this subject based on the ideXlab platform.
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Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer’s Disease
American Journal of Pathology, 1999Co-Authors: Alex E. Roher, Libuse Brachova, Yong Shen, Thomas G. Beach, Janice H. Kurth, Russel E. Rydel, Joseph G. RogersAbstract:We have characterized amyloid β peptide (Aβ. concentration, Aβ deposition, paired helical filament formation, cerebrovascular amyloid angiopathy, apolipoprotein E (ApoE) allotype, and synaptophysin concentration in entorhinal cortex and superior frontal gyrus of normal elderly control (ND) patients, Alzheimer's disease (AD. patients, and high pathology control (HPC) patients who meet pathological criteria for AD but show no synapse loss or overt antemortem symptoms of dementia. The measures of Aβ deposition, Aβ-immunoreactive plaques with and without cores, thioflavin histofluorescent plaques, and concentrations of insoluble Aβ, failed to distinguish HPC from AD patients and were poor correlates of Synaptic Change. By contrast, concentrations of soluble Aβ clearly distinguished HPC from AD patients and were a strong inverse correlate of synapse loss. Further investigation revealed that Aβ40, whether in soluble or insoluble form, was a particularly useful measure for classifying ND, HPC, and AD patients compared with Aβ42. Aβ40 is known to be elevated in cerebrovascular amyloid deposits, and Aβ40 (but not Aβ42) levels, cerebrovascular amyloid angiopathy, and ApoE4 allele frequency were all highly correlated with each other. Although paired helical filaments in the form of neurofibrillary tangles or a penumbra of neurites surrounding amyloid cores also distinguished HPC from AD patients, they were less robust predictors of synapse Change compared with soluble Aβ, particularly soluble Aβ40. Previous experiments attempting to relate Aβ deposition to the neurodegeneration that underlies AD dementia may have failed because they assayed the classical, visible forms of the molecule, insoluble neuropil plaques, rather than the soluble, unseen forms of the molecule.
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soluble amyloid β peptide concentration as a predictor of Synaptic Change in alzheimer s disease
American Journal of Pathology, 1999Co-Authors: Alex E. Roher, Libuse Brachova, Yong Shen, Thomas G. Beach, Janice H. Kurth, Russel E. Rydel, Joseph G. RogersAbstract:We have characterized amyloid β peptide (Aβ. concentration, Aβ deposition, paired helical filament formation, cerebrovascular amyloid angiopathy, apolipoprotein E (ApoE) allotype, and synaptophysin concentration in entorhinal cortex and superior frontal gyrus of normal elderly control (ND) patients, Alzheimer's disease (AD. patients, and high pathology control (HPC) patients who meet pathological criteria for AD but show no synapse loss or overt antemortem symptoms of dementia. The measures of Aβ deposition, Aβ-immunoreactive plaques with and without cores, thioflavin histofluorescent plaques, and concentrations of insoluble Aβ, failed to distinguish HPC from AD patients and were poor correlates of Synaptic Change. By contrast, concentrations of soluble Aβ clearly distinguished HPC from AD patients and were a strong inverse correlate of synapse loss. Further investigation revealed that Aβ40, whether in soluble or insoluble form, was a particularly useful measure for classifying ND, HPC, and AD patients compared with Aβ42. Aβ40 is known to be elevated in cerebrovascular amyloid deposits, and Aβ40 (but not Aβ42) levels, cerebrovascular amyloid angiopathy, and ApoE4 allele frequency were all highly correlated with each other. Although paired helical filaments in the form of neurofibrillary tangles or a penumbra of neurites surrounding amyloid cores also distinguished HPC from AD patients, they were less robust predictors of synapse Change compared with soluble Aβ, particularly soluble Aβ40. Previous experiments attempting to relate Aβ deposition to the neurodegeneration that underlies AD dementia may have failed because they assayed the classical, visible forms of the molecule, insoluble neuropil plaques, rather than the soluble, unseen forms of the molecule.
