The Experts below are selected from a list of 99 Experts worldwide ranked by ideXlab platform

Nigel S Bamford - One of the best experts on this subject based on the ideXlab platform.

  • loss of glutamate signaling from the thalamus to dorsal striatum impairs motor function and slows the execution of learned behaviors
    npj Parkinson's disease, 2018
    Co-Authors: Erica J Melief, Jonathan W Mckinley, Nicole M Whiteley, Alec W Gibson, John F Neumaier, Charles W Henschen, Richard D Palmiter, Nigel S Bamford
    Abstract:

    Parkinson’s disease (PD) is primarily associated with the degeneration of midbrain dopamine neurons, but it is now appreciated that pathological processes like Lewy-body inclusions and cell loss affect several other brain regions, including the central lateral (CL) and centromedian/parafascicular (CM/PF) thalamic regions. These thalamic glutamatergic neurons provide a non-cortical excitatory input to the dorsal striatum, a major projection field of dopamine neurons. To determine how thalamostriatal signaling may contribute to cognitive and motor abnormalities found in PD, we used a viral vector approach to generate mice with loss of thalamostriatal glutamate signaling specifically restricted to the dorsal striatum (CAV2Cre-Slc17a6lox/lox mice). We measured motor function and behaviors corresponding to cognitive domains (visuospatial function, attention, executive function, and working memory) affected in PD. CAV2Cre-Slc17a6lox/lox mice were impaired in motor coordination tasks such as the rotarod and beam-walk tests compared with controls (CAV2Cre-Slc17a6+/+ mice). They did not demonstrate much cognitive impairment in the Morris water maze or a water U-maze, but had slower processing reaction times in those tests and in a two-way active avoidance task. These mice could model an aspect of Bradyphrenia, the slowness of thought that is often seen in patients with PD and other neurological disorders.

  • loss of glutamate signaling from the thalamus to dorsal striatum impairs motor function and slows the execution of learned behaviors
    npj Parkinson's disease, 2018
    Co-Authors: Erica J Melief, Jonathan W Mckinley, Nicole M Whiteley, Alec W Gibson, John F Neumaier, Charles W Henschen, Richard D Palmiter, Jonathan Y Lam, Nigel S Bamford
    Abstract:

    Parkinson’s disease (PD) is primarily associated with the degeneration of midbrain dopamine neurons, but it is now appreciated that pathological processes like Lewy-body inclusions and cell loss affect several other brain regions, including the central lateral (CL) and centromedian/parafascicular (CM/PF) thalamic regions. These thalamic glutamatergic neurons provide a non-cortical excitatory input to the dorsal striatum, a major projection field of dopamine neurons. To determine how thalamostriatal signaling may contribute to cognitive and motor abnormalities found in PD, we used a viral vector approach to generate mice with loss of thalamostriatal glutamate signaling specifically restricted to the dorsal striatum (CAV2Cre-Slc17a6lox/lox mice). We measured motor function and behaviors corresponding to cognitive domains (visuospatial function, attention, executive function, and working memory) affected in PD. CAV2Cre-Slc17a6lox/lox mice were impaired in motor coordination tasks such as the rotarod and beam-walk tests compared with controls (CAV2Cre-Slc17a6+/+ mice). They did not demonstrate much cognitive impairment in the Morris water maze or a water U-maze, but had slower processing reaction times in those tests and in a two-way active avoidance task. These mice could model an aspect of Bradyphrenia, the slowness of thought that is often seen in patients with PD and other neurological disorders. Mice in which glutamate signaling from the thalamus to dorsal striatum has been genetically inactivated mimic the slowness of thought that is often observed in patients with Parkinson’s disease (PD). The midbrain and striatum are the brain regions that are most affected in PD, however, it is increasingly recognized that cell loss in other areas of the brain also contribute to disease symptoms. Martin Darvas at the University of Washington, Seattle, USA, and colleagues found that disrupting the excitatory input from thalamic projection neurons into the dorsal striatum affected motor coordination and balance in mice. Although these mice did not have significant impairments in spatial learning and memory, they were slower at reacting to cues and executing learned behaviors suggesting that they could be used to test new approaches for treating this specific cognitive symptom of PD.

Jonathan W Mckinley - One of the best experts on this subject based on the ideXlab platform.

  • loss of glutamate signaling from the thalamus to dorsal striatum impairs motor function and slows the execution of learned behaviors
    npj Parkinson's disease, 2018
    Co-Authors: Erica J Melief, Jonathan W Mckinley, Nicole M Whiteley, Alec W Gibson, John F Neumaier, Charles W Henschen, Richard D Palmiter, Nigel S Bamford
    Abstract:

    Parkinson’s disease (PD) is primarily associated with the degeneration of midbrain dopamine neurons, but it is now appreciated that pathological processes like Lewy-body inclusions and cell loss affect several other brain regions, including the central lateral (CL) and centromedian/parafascicular (CM/PF) thalamic regions. These thalamic glutamatergic neurons provide a non-cortical excitatory input to the dorsal striatum, a major projection field of dopamine neurons. To determine how thalamostriatal signaling may contribute to cognitive and motor abnormalities found in PD, we used a viral vector approach to generate mice with loss of thalamostriatal glutamate signaling specifically restricted to the dorsal striatum (CAV2Cre-Slc17a6lox/lox mice). We measured motor function and behaviors corresponding to cognitive domains (visuospatial function, attention, executive function, and working memory) affected in PD. CAV2Cre-Slc17a6lox/lox mice were impaired in motor coordination tasks such as the rotarod and beam-walk tests compared with controls (CAV2Cre-Slc17a6+/+ mice). They did not demonstrate much cognitive impairment in the Morris water maze or a water U-maze, but had slower processing reaction times in those tests and in a two-way active avoidance task. These mice could model an aspect of Bradyphrenia, the slowness of thought that is often seen in patients with PD and other neurological disorders.

  • loss of glutamate signaling from the thalamus to dorsal striatum impairs motor function and slows the execution of learned behaviors
    npj Parkinson's disease, 2018
    Co-Authors: Erica J Melief, Jonathan W Mckinley, Nicole M Whiteley, Alec W Gibson, John F Neumaier, Charles W Henschen, Richard D Palmiter, Jonathan Y Lam, Nigel S Bamford
    Abstract:

    Parkinson’s disease (PD) is primarily associated with the degeneration of midbrain dopamine neurons, but it is now appreciated that pathological processes like Lewy-body inclusions and cell loss affect several other brain regions, including the central lateral (CL) and centromedian/parafascicular (CM/PF) thalamic regions. These thalamic glutamatergic neurons provide a non-cortical excitatory input to the dorsal striatum, a major projection field of dopamine neurons. To determine how thalamostriatal signaling may contribute to cognitive and motor abnormalities found in PD, we used a viral vector approach to generate mice with loss of thalamostriatal glutamate signaling specifically restricted to the dorsal striatum (CAV2Cre-Slc17a6lox/lox mice). We measured motor function and behaviors corresponding to cognitive domains (visuospatial function, attention, executive function, and working memory) affected in PD. CAV2Cre-Slc17a6lox/lox mice were impaired in motor coordination tasks such as the rotarod and beam-walk tests compared with controls (CAV2Cre-Slc17a6+/+ mice). They did not demonstrate much cognitive impairment in the Morris water maze or a water U-maze, but had slower processing reaction times in those tests and in a two-way active avoidance task. These mice could model an aspect of Bradyphrenia, the slowness of thought that is often seen in patients with PD and other neurological disorders. Mice in which glutamate signaling from the thalamus to dorsal striatum has been genetically inactivated mimic the slowness of thought that is often observed in patients with Parkinson’s disease (PD). The midbrain and striatum are the brain regions that are most affected in PD, however, it is increasingly recognized that cell loss in other areas of the brain also contribute to disease symptoms. Martin Darvas at the University of Washington, Seattle, USA, and colleagues found that disrupting the excitatory input from thalamic projection neurons into the dorsal striatum affected motor coordination and balance in mice. Although these mice did not have significant impairments in spatial learning and memory, they were slower at reacting to cues and executing learned behaviors suggesting that they could be used to test new approaches for treating this specific cognitive symptom of PD.

Erica J Melief - One of the best experts on this subject based on the ideXlab platform.

  • loss of glutamate signaling from the thalamus to dorsal striatum impairs motor function and slows the execution of learned behaviors
    npj Parkinson's disease, 2018
    Co-Authors: Erica J Melief, Jonathan W Mckinley, Nicole M Whiteley, Alec W Gibson, John F Neumaier, Charles W Henschen, Richard D Palmiter, Nigel S Bamford
    Abstract:

    Parkinson’s disease (PD) is primarily associated with the degeneration of midbrain dopamine neurons, but it is now appreciated that pathological processes like Lewy-body inclusions and cell loss affect several other brain regions, including the central lateral (CL) and centromedian/parafascicular (CM/PF) thalamic regions. These thalamic glutamatergic neurons provide a non-cortical excitatory input to the dorsal striatum, a major projection field of dopamine neurons. To determine how thalamostriatal signaling may contribute to cognitive and motor abnormalities found in PD, we used a viral vector approach to generate mice with loss of thalamostriatal glutamate signaling specifically restricted to the dorsal striatum (CAV2Cre-Slc17a6lox/lox mice). We measured motor function and behaviors corresponding to cognitive domains (visuospatial function, attention, executive function, and working memory) affected in PD. CAV2Cre-Slc17a6lox/lox mice were impaired in motor coordination tasks such as the rotarod and beam-walk tests compared with controls (CAV2Cre-Slc17a6+/+ mice). They did not demonstrate much cognitive impairment in the Morris water maze or a water U-maze, but had slower processing reaction times in those tests and in a two-way active avoidance task. These mice could model an aspect of Bradyphrenia, the slowness of thought that is often seen in patients with PD and other neurological disorders.

  • loss of glutamate signaling from the thalamus to dorsal striatum impairs motor function and slows the execution of learned behaviors
    npj Parkinson's disease, 2018
    Co-Authors: Erica J Melief, Jonathan W Mckinley, Nicole M Whiteley, Alec W Gibson, John F Neumaier, Charles W Henschen, Richard D Palmiter, Jonathan Y Lam, Nigel S Bamford
    Abstract:

    Parkinson’s disease (PD) is primarily associated with the degeneration of midbrain dopamine neurons, but it is now appreciated that pathological processes like Lewy-body inclusions and cell loss affect several other brain regions, including the central lateral (CL) and centromedian/parafascicular (CM/PF) thalamic regions. These thalamic glutamatergic neurons provide a non-cortical excitatory input to the dorsal striatum, a major projection field of dopamine neurons. To determine how thalamostriatal signaling may contribute to cognitive and motor abnormalities found in PD, we used a viral vector approach to generate mice with loss of thalamostriatal glutamate signaling specifically restricted to the dorsal striatum (CAV2Cre-Slc17a6lox/lox mice). We measured motor function and behaviors corresponding to cognitive domains (visuospatial function, attention, executive function, and working memory) affected in PD. CAV2Cre-Slc17a6lox/lox mice were impaired in motor coordination tasks such as the rotarod and beam-walk tests compared with controls (CAV2Cre-Slc17a6+/+ mice). They did not demonstrate much cognitive impairment in the Morris water maze or a water U-maze, but had slower processing reaction times in those tests and in a two-way active avoidance task. These mice could model an aspect of Bradyphrenia, the slowness of thought that is often seen in patients with PD and other neurological disorders. Mice in which glutamate signaling from the thalamus to dorsal striatum has been genetically inactivated mimic the slowness of thought that is often observed in patients with Parkinson’s disease (PD). The midbrain and striatum are the brain regions that are most affected in PD, however, it is increasingly recognized that cell loss in other areas of the brain also contribute to disease symptoms. Martin Darvas at the University of Washington, Seattle, USA, and colleagues found that disrupting the excitatory input from thalamic projection neurons into the dorsal striatum affected motor coordination and balance in mice. Although these mice did not have significant impairments in spatial learning and memory, they were slower at reacting to cues and executing learned behaviors suggesting that they could be used to test new approaches for treating this specific cognitive symptom of PD.

Paul Mcmonagle - One of the best experts on this subject based on the ideXlab platform.

  • behavior and cognition in corticobasal degeneration and progressive supranuclear palsy
    Journal of the Neurological Sciences, 2010
    Co-Authors: Andrew Kertesz, Paul Mcmonagle
    Abstract:

    Abstract Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD), previously described as Parkinsonian syndromes are also cognitive disorders, and biologically related to the frontotemporal dementia or Pick's disease. PSP and CBD overlap clinically, pathologically and genetically, sharing tau haplotypes and mutations. In our series of CBD/PSP patients with cognitive presentation (n = 36), primary progressive aphasia (PPA) was particularly common, but behavioral onset occurred also. CBD or PSP as motor presentations developed significant language disorder in 17/19. The underlying pathology is predictably tau positive in these clinical combinations, regardless of the presentation. Other cognitive features of CBDS include apraxia, alien hand and apathy, but often frontal lobe dementia with disinhibition develops also. CBDS also has visuospatial deficit, because of the parietal involvement. PSP was considered the prototype of subcortical dementia, with Bradyphrenia, poor recall and executive deficit, but cortical features were recognized to be important also. Language testing and a behavioral inventory should be part of neuropsychological tests to facilitate diagnosis and to quantify the deficit. The clinical, genetic and pathological relationship is strong between CBD /PSP and the aphasic and behavioral components of the Pick complex.

Nicole M Whiteley - One of the best experts on this subject based on the ideXlab platform.

  • loss of glutamate signaling from the thalamus to dorsal striatum impairs motor function and slows the execution of learned behaviors
    npj Parkinson's disease, 2018
    Co-Authors: Erica J Melief, Jonathan W Mckinley, Nicole M Whiteley, Alec W Gibson, John F Neumaier, Charles W Henschen, Richard D Palmiter, Nigel S Bamford
    Abstract:

    Parkinson’s disease (PD) is primarily associated with the degeneration of midbrain dopamine neurons, but it is now appreciated that pathological processes like Lewy-body inclusions and cell loss affect several other brain regions, including the central lateral (CL) and centromedian/parafascicular (CM/PF) thalamic regions. These thalamic glutamatergic neurons provide a non-cortical excitatory input to the dorsal striatum, a major projection field of dopamine neurons. To determine how thalamostriatal signaling may contribute to cognitive and motor abnormalities found in PD, we used a viral vector approach to generate mice with loss of thalamostriatal glutamate signaling specifically restricted to the dorsal striatum (CAV2Cre-Slc17a6lox/lox mice). We measured motor function and behaviors corresponding to cognitive domains (visuospatial function, attention, executive function, and working memory) affected in PD. CAV2Cre-Slc17a6lox/lox mice were impaired in motor coordination tasks such as the rotarod and beam-walk tests compared with controls (CAV2Cre-Slc17a6+/+ mice). They did not demonstrate much cognitive impairment in the Morris water maze or a water U-maze, but had slower processing reaction times in those tests and in a two-way active avoidance task. These mice could model an aspect of Bradyphrenia, the slowness of thought that is often seen in patients with PD and other neurological disorders.

  • loss of glutamate signaling from the thalamus to dorsal striatum impairs motor function and slows the execution of learned behaviors
    npj Parkinson's disease, 2018
    Co-Authors: Erica J Melief, Jonathan W Mckinley, Nicole M Whiteley, Alec W Gibson, John F Neumaier, Charles W Henschen, Richard D Palmiter, Jonathan Y Lam, Nigel S Bamford
    Abstract:

    Parkinson’s disease (PD) is primarily associated with the degeneration of midbrain dopamine neurons, but it is now appreciated that pathological processes like Lewy-body inclusions and cell loss affect several other brain regions, including the central lateral (CL) and centromedian/parafascicular (CM/PF) thalamic regions. These thalamic glutamatergic neurons provide a non-cortical excitatory input to the dorsal striatum, a major projection field of dopamine neurons. To determine how thalamostriatal signaling may contribute to cognitive and motor abnormalities found in PD, we used a viral vector approach to generate mice with loss of thalamostriatal glutamate signaling specifically restricted to the dorsal striatum (CAV2Cre-Slc17a6lox/lox mice). We measured motor function and behaviors corresponding to cognitive domains (visuospatial function, attention, executive function, and working memory) affected in PD. CAV2Cre-Slc17a6lox/lox mice were impaired in motor coordination tasks such as the rotarod and beam-walk tests compared with controls (CAV2Cre-Slc17a6+/+ mice). They did not demonstrate much cognitive impairment in the Morris water maze or a water U-maze, but had slower processing reaction times in those tests and in a two-way active avoidance task. These mice could model an aspect of Bradyphrenia, the slowness of thought that is often seen in patients with PD and other neurological disorders. Mice in which glutamate signaling from the thalamus to dorsal striatum has been genetically inactivated mimic the slowness of thought that is often observed in patients with Parkinson’s disease (PD). The midbrain and striatum are the brain regions that are most affected in PD, however, it is increasingly recognized that cell loss in other areas of the brain also contribute to disease symptoms. Martin Darvas at the University of Washington, Seattle, USA, and colleagues found that disrupting the excitatory input from thalamic projection neurons into the dorsal striatum affected motor coordination and balance in mice. Although these mice did not have significant impairments in spatial learning and memory, they were slower at reacting to cues and executing learned behaviors suggesting that they could be used to test new approaches for treating this specific cognitive symptom of PD.