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Constantin Bouras - One of the best experts on this subject based on the ideXlab platform.

  • impaired processing of famous faces in alzheimer s disease is related to Neurofibrillary Tangle densities in the prefrontal and anterior cingulate cortex
    Dementia and Geriatric Cognitive Disorders, 2000
    Co-Authors: Panteleimon Giannakopoulos, Patrick R. Hof, Gabriel Gold, Myriam Duc, Jeanpierre Michel, Constantin Bouras
    Abstract:

    To examine the neuroanatomical correlates of impaired processing of famous faces in Alzheimer's disease (AD), we performed an anterograde clinicopathological study of 25 patients with clinically and neuropathologically confirmed AD. Famous face recognition, identification and naming was assessed using the Famous Face Test. The assessment of Neurofibrillary Tangle (NFT) and senile plaque (SP) densities was performed in ten cortical areas in both hemispheres, and statistical analysis was made using forward stepwise logistic regression models. A statistically significant relationship was found between NFT densities in Brodmann's areas 9 and 24 in both hemispheres and impaired famous face naming and identification. SP counts did not correlate with any of the neuropsychological parameters. These data suggest that NFT formation in prefrontal and anterior cingulate cortex, two areas involved in semantic memory processes, is a key event in famous face naming and identification deficits. In agreement with previous studies, they also indicate that SP densities are not a good pathological correlate of neuropsychological deficits in AD.

  • Neurofibrillary Tangle densities in the hippocampal formation in a non demented population define subgroups of patients with differential early pathologic changes
    Neuroscience Letters, 1993
    Co-Authors: Patrick R. Hof, Constantin Bouras, John H Morrison
    Abstract:

    Detailed analyses of the neuropathologic changes in the cerebral cortex of elderly individuals and Alzheimer's disease patients have demonstrated that certain components of the neocortical and hippocampal circuits are likely to be selectively vulnerable. In order to investigate the distribution of lesions associated with aging as well as with the earliest symptoms of Alzheimer's disease, we performed a quantitative neuropathological evaluation of sixty-one non-demented patients from a geriatric hospital. All of the cases had Neurofibrillary Tangles in layer II of the entorhinal cortex, and many cases had an involvement of the CA1 field of the hippocampus and the inferior temporal cortex. In all of the cases, amyloid deposition was not correlated with age or with the number of Neurofibrillary Tangles. In addition, eight cases showed much higher Neurofibrillary Tangle counts than the remainder of the cases. It is proposed that these cases may represent the neuropathological correlate of the earliest stage of Alzheimer's disease that could antedate the appearance of clinical signs of cognitive decline and memory impairment.

  • Quantitative immunohistochemical analysis of the distribution of Neurofibrillary Tangles and senile plaques in the cerebral cortex of nonagenarians and centenarians.
    Acta neuropathologica, 1993
    Co-Authors: Panteleimon Giannakopoulos, Patrick R. Hof, Jeanpierre Michel, Maria Surini, Constantin Bouras
    Abstract:

    To investigate the neuropathological differences between normal aging and senile dementia of the Alzheimer type (SDAT) in very old people and to see how they compare with a younger population of demented elderly people, we performed an immunohistochemical quantitative analysis of the topography of senile plaques and Neurofibrillary Tangles in a series of 31 elderly patients aged from 96 to 102 years. According to the medical records, two groups were considered: 7 patients presenting with clinically documented SDAT and 24 patients with no or very mild cognitive impairment. The densities of senile plaques were comparable in both groups. Extensive Neurofibrillary Tangle formation was restricted to the CA1 hippocampal field of demented subjects, whereas the superior frontal cortex showed rare Neurofibrillary Tangles, independently of the clinical diagnosis. These results indicate an absence of direct correlation between the number of senile plaques and the clinical manifestation of SDAT. Furthermore, they suggest that the dementing process may involve different cortical structures in nonagenarians and centenarians than in younger demented individuals where a widespread cortical involvement is generally observed. Thus, the Neurofibrillary Tangle density in the CA1 field may be critical for the neuropathological diagnosis of SDAT in this particular group of very old patients.

  • Distribution of Neurofibrillary Tangles and senile plaques in the cerebral cortex in postencephalitic parkinsonism
    Neuroscience letters, 1992
    Co-Authors: Patrick R. Hof, Alain Charpiot, André Delacourte, Luc Buée, Dushyant P. Purohit, Daniel P. Perl, Constantin Bouras
    Abstract:

    Postencephalitic parkinsonism is characterized neuropathologically by severe loss of pigmented neurons in the substantia nigra and the presence of high densities of Neurofibrillary Tangles in several brainstem structures. In 5 cases of postencephalitic parkinsonism, we observed that the Neurofibrillary Tangle distribution in the cerebral cortex predominated in the hippocampus and entorhinal cortex. In the prefrontal and inferior temporal cortex, Neurofibrillary Tangles were preferentially localized in layers II and III. This pattern contrasts with the Neurofibrillary Tangle distribution observed in neocortical areas of Alzheimer's disease cases, where Neurofibrillary Tangles are denser in layer V than in layer III. These results suggest that specific elements of the cortical circuitry might be differentially affected in postencephalitic parkinsonism as compared to Alzheimer's disease, and that cortical involvement is likely to be a common feature of this condition.

  • Distribution of cortical Neurofibrillary Tangles in progressive supranuclear palsy: a quantitative analysis of six cases.
    Acta neuropathologica, 1992
    Co-Authors: Patrick R. Hof, André Delacourte, Constantin Bouras
    Abstract:

    Progressive supranuclear palsy is characterized neuropathologically by the presence of high densities of Neurofibrillary Tangles in several subcortical structures. In some cases, Neurofibrillary Tangles have also been described in the cerebral cortex. We performed a quantitative regional and laminar analysis of the distribution of these lesions in six cases of progressive supranuclear palsy. We observed that the Neurofibrillary Tangle distribution in the cerebral cortex was largely confined to the hippocampal formation. In particular, in all the cases Neurofibrillary Tangles were observed in the granule cell layer of the dentate gyrus. In the prefrontal and inferior temporal cortex, Neurofibrillary Tangles were predominantly distributed in layers II and III. In addition, there were moderate-to-high Neurofibrillary Tangle densities in the primary motor cortex. This localization pattern contrasts with the Neurofibrillary Tangle distribution observed in the cerebral cortex of Alzheimer's disease cases, where Tangles are denser in layer V than in layer III, and where the primary motor cortex and the dentate gyrus are usually not involved. These results suggest that specific elements of the cortical circuitry might be differentially vulnerable in progressive supranuclear palsy as compared to Alzheimer's disease.

Patrick R. Hof - One of the best experts on this subject based on the ideXlab platform.

  • impaired processing of famous faces in alzheimer s disease is related to Neurofibrillary Tangle densities in the prefrontal and anterior cingulate cortex
    Dementia and Geriatric Cognitive Disorders, 2000
    Co-Authors: Panteleimon Giannakopoulos, Patrick R. Hof, Gabriel Gold, Myriam Duc, Jeanpierre Michel, Constantin Bouras
    Abstract:

    To examine the neuroanatomical correlates of impaired processing of famous faces in Alzheimer's disease (AD), we performed an anterograde clinicopathological study of 25 patients with clinically and neuropathologically confirmed AD. Famous face recognition, identification and naming was assessed using the Famous Face Test. The assessment of Neurofibrillary Tangle (NFT) and senile plaque (SP) densities was performed in ten cortical areas in both hemispheres, and statistical analysis was made using forward stepwise logistic regression models. A statistically significant relationship was found between NFT densities in Brodmann's areas 9 and 24 in both hemispheres and impaired famous face naming and identification. SP counts did not correlate with any of the neuropsychological parameters. These data suggest that NFT formation in prefrontal and anterior cingulate cortex, two areas involved in semantic memory processes, is a key event in famous face naming and identification deficits. In agreement with previous studies, they also indicate that SP densities are not a good pathological correlate of neuropsychological deficits in AD.

  • amyotrophic lateral sclerosis and parkinsonism dementia from guam differences in Neurofibrillary Tangle distribution and density in the hippocampal formation and neocortex
    Brain Research, 1994
    Co-Authors: Patrick R. Hof, Daniel P. Perl, John H Morrison, Arthur J Loerzel, John C Steele
    Abstract:

    Amyotrophic lateral sclerosis/parkinsonism-dementia complex is a highly prevalent neurodegenerative disorder among the native Chamorro population of Guam, and is characterized by widespread formation of Neurofibrillary Tangles. In the present study, the distribution of Neurofibrillary Tangles was quantitatively assessed in the cerebral cortex of cases presenting with either predominant amyotrophic lateral sclerosis or parkinsonism-dementia symptomatology. Results show that although the regional and laminar lesion distribution is qualitatively similar in both groups, cases with predominant parkinsonism-dementia generally have higher lesion densities than cases with amyotrophic lateral sclerosis. Interestingly, layer II of the entorhinal cortex was affected to the same degree in both conditions. In both groups, the CA1 field of the hippocampus, subiculum, and entorhinal cortex were the most affected areas. In the neocortex, the perirhinal and inferior temporal cortex consistently had higher lesion densities than the frontal, parietal, and cingulate cortex, whereas the visual cortex was practically devoid of lesions. Also, most of the Neurofibrillary Tangles were located in the supragranular layers of the neocortex, with relatively low densities in the infragranular layers, in both brain groups. Interestingly, the primary motor cortex contained more Neurofibrillary Tangles in parkinsonism-dementia than in amyotrophic lateral sclerosis cases. It is possible that the differences in regional Neurofibrillary Tangle densities reflect the variable severity of the dementing process observed between the two groups of patients. Several studies on Alzheimer's disease and related disorders indicate that the regional and laminar cortical localization of Neurofibrillary Tangles may parallel the degeneration of specific corticocortical projections. The present data suggest that the population of corticocortical projections involved in Guamanian cases differs substantially from that affected in Alzheimer's disease. The differential distribution and densities of the lesions may contribute to the differences in symptomatology and severity of dementia among Alzheimer's disease and Guamanian cases, although these neurodegenerative disorders as well as related illnesses may share certain etiopathogenetic mechanisms.

  • Neurofibrillary Tangle densities in the hippocampal formation in a non demented population define subgroups of patients with differential early pathologic changes
    Neuroscience Letters, 1993
    Co-Authors: Patrick R. Hof, Constantin Bouras, John H Morrison
    Abstract:

    Detailed analyses of the neuropathologic changes in the cerebral cortex of elderly individuals and Alzheimer's disease patients have demonstrated that certain components of the neocortical and hippocampal circuits are likely to be selectively vulnerable. In order to investigate the distribution of lesions associated with aging as well as with the earliest symptoms of Alzheimer's disease, we performed a quantitative neuropathological evaluation of sixty-one non-demented patients from a geriatric hospital. All of the cases had Neurofibrillary Tangles in layer II of the entorhinal cortex, and many cases had an involvement of the CA1 field of the hippocampus and the inferior temporal cortex. In all of the cases, amyloid deposition was not correlated with age or with the number of Neurofibrillary Tangles. In addition, eight cases showed much higher Neurofibrillary Tangle counts than the remainder of the cases. It is proposed that these cases may represent the neuropathological correlate of the earliest stage of Alzheimer's disease that could antedate the appearance of clinical signs of cognitive decline and memory impairment.

  • Quantitative immunohistochemical analysis of the distribution of Neurofibrillary Tangles and senile plaques in the cerebral cortex of nonagenarians and centenarians.
    Acta neuropathologica, 1993
    Co-Authors: Panteleimon Giannakopoulos, Patrick R. Hof, Jeanpierre Michel, Maria Surini, Constantin Bouras
    Abstract:

    To investigate the neuropathological differences between normal aging and senile dementia of the Alzheimer type (SDAT) in very old people and to see how they compare with a younger population of demented elderly people, we performed an immunohistochemical quantitative analysis of the topography of senile plaques and Neurofibrillary Tangles in a series of 31 elderly patients aged from 96 to 102 years. According to the medical records, two groups were considered: 7 patients presenting with clinically documented SDAT and 24 patients with no or very mild cognitive impairment. The densities of senile plaques were comparable in both groups. Extensive Neurofibrillary Tangle formation was restricted to the CA1 hippocampal field of demented subjects, whereas the superior frontal cortex showed rare Neurofibrillary Tangles, independently of the clinical diagnosis. These results indicate an absence of direct correlation between the number of senile plaques and the clinical manifestation of SDAT. Furthermore, they suggest that the dementing process may involve different cortical structures in nonagenarians and centenarians than in younger demented individuals where a widespread cortical involvement is generally observed. Thus, the Neurofibrillary Tangle density in the CA1 field may be critical for the neuropathological diagnosis of SDAT in this particular group of very old patients.

  • Distribution of Neurofibrillary Tangles and senile plaques in the cerebral cortex in postencephalitic parkinsonism
    Neuroscience letters, 1992
    Co-Authors: Patrick R. Hof, Alain Charpiot, André Delacourte, Luc Buée, Dushyant P. Purohit, Daniel P. Perl, Constantin Bouras
    Abstract:

    Postencephalitic parkinsonism is characterized neuropathologically by severe loss of pigmented neurons in the substantia nigra and the presence of high densities of Neurofibrillary Tangles in several brainstem structures. In 5 cases of postencephalitic parkinsonism, we observed that the Neurofibrillary Tangle distribution in the cerebral cortex predominated in the hippocampus and entorhinal cortex. In the prefrontal and inferior temporal cortex, Neurofibrillary Tangles were preferentially localized in layers II and III. This pattern contrasts with the Neurofibrillary Tangle distribution observed in neocortical areas of Alzheimer's disease cases, where Neurofibrillary Tangles are denser in layer V than in layer III. These results suggest that specific elements of the cortical circuitry might be differentially affected in postencephalitic parkinsonism as compared to Alzheimer's disease, and that cortical involvement is likely to be a common feature of this condition.

Gil D Rabinovici - One of the best experts on this subject based on the ideXlab platform.

  • Alzheimer’s disease clinical variants show distinct regional patterns of Neurofibrillary Tangle accumulation
    Acta Neuropathologica, 2019
    Co-Authors: Cathrine Petersen, Amber L. Nolan, Elisa Paula França Resende, Zachary Miller, Alexander J. Ehrenberg, Maria Luisa Gorno-tempini, Howard J. Rosen, Joel H. Kramer, Salvatore Spina, Gil D Rabinovici
    Abstract:

    The clinical spectrum of Alzheimer’s disease (AD) extends well beyond the classic amnestic–predominant syndrome. The previous studies have suggested differential Neurofibrillary Tangle (NFT) burden between amnestic and logopenic primary progressive aphasia presentations of AD. In this study, we explored the regional distribution of NFT pathology and its relationship to AD presentation across five different clinical syndromes. We assessed NFT density throughout six selected neocortical and hippocampal regions using thioflavin-S fluorescent microscopy in a well-characterized clinicopathological cohort of pure AD cases enriched for atypical clinical presentations. Subjects underwent apolipoprotein E genotyping and neuropsychological testing. Main cognitive domains (executive, visuospatial, language, and memory function) were assessed using an established composite z score. Our results showed that NFT regional burden aligns with the clinical presentation and region-specific cognitive scores. Cortical, but not hippocampal, NFT burden was higher among atypical clinical variants relative to the amnestic syndrome. In analyses of specific clinical variants, logopenic primary progressive aphasia showed higher NFT density in the superior temporal gyrus ( p  = 0.0091), and corticobasal syndrome showed higher NFT density in the primary motor cortex ( p  = 0.0205) relative to the amnestic syndrome. Higher NFT burden in the angular gyrus and CA1 sector of the hippocampus were independently associated with worsening visuospatial dysfunction. In addition, unbiased hierarchical clustering based on regional NFT densities identified three groups characterized by a low overall NFT burden, high overall burden, and cortical-predominant burden, respectively, which were found to differ in sex ratio, age, disease duration, and clinical presentation. In comparison, the typical, hippocampal sparing, and limbic-predominant subtypes derived from a previously proposed algorithm did not reproduce the same degree of clinical relevance in this sample. Overall, our results suggest domain-specific functional consequences of regional NFT accumulation. Mapping these consequences presents an opportunity to increase understanding of the neuropathological framework underlying atypical clinical manifestations.

  • alzheimer s disease clinical variants show distinct regional patterns of Neurofibrillary Tangle accumulation
    Acta Neuropathologica, 2019
    Co-Authors: Cathrine Petersen, Elisa Paula França Resende, Alexander J. Ehrenberg, Howard J. Rosen, Joel H. Kramer, Salvatore Spina, Amber Nolan, Zachary A Miller, Maria Luisa Gornotempini, Gil D Rabinovici
    Abstract:

    The clinical spectrum of Alzheimer’s disease (AD) extends well beyond the classic amnestic–predominant syndrome. The previous studies have suggested differential Neurofibrillary Tangle (NFT) burden between amnestic and logopenic primary progressive aphasia presentations of AD. In this study, we explored the regional distribution of NFT pathology and its relationship to AD presentation across five different clinical syndromes. We assessed NFT density throughout six selected neocortical and hippocampal regions using thioflavin-S fluorescent microscopy in a well-characterized clinicopathological cohort of pure AD cases enriched for atypical clinical presentations. Subjects underwent apolipoprotein E genotyping and neuropsychological testing. Main cognitive domains (executive, visuospatial, language, and memory function) were assessed using an established composite z score. Our results showed that NFT regional burden aligns with the clinical presentation and region-specific cognitive scores. Cortical, but not hippocampal, NFT burden was higher among atypical clinical variants relative to the amnestic syndrome. In analyses of specific clinical variants, logopenic primary progressive aphasia showed higher NFT density in the superior temporal gyrus (p = 0.0091), and corticobasal syndrome showed higher NFT density in the primary motor cortex (p = 0.0205) relative to the amnestic syndrome. Higher NFT burden in the angular gyrus and CA1 sector of the hippocampus were independently associated with worsening visuospatial dysfunction. In addition, unbiased hierarchical clustering based on regional NFT densities identified three groups characterized by a low overall NFT burden, high overall burden, and cortical-predominant burden, respectively, which were found to differ in sex ratio, age, disease duration, and clinical presentation. In comparison, the typical, hippocampal sparing, and limbic-predominant subtypes derived from a previously proposed algorithm did not reproduce the same degree of clinical relevance in this sample. Overall, our results suggest domain-specific functional consequences of regional NFT accumulation. Mapping these consequences presents an opportunity to increase understanding of the neuropathological framework underlying atypical clinical manifestations.

Cathrine Petersen - One of the best experts on this subject based on the ideXlab platform.

  • Alzheimer’s disease clinical variants show distinct regional patterns of Neurofibrillary Tangle accumulation
    Acta Neuropathologica, 2019
    Co-Authors: Cathrine Petersen, Amber L. Nolan, Elisa Paula França Resende, Zachary Miller, Alexander J. Ehrenberg, Maria Luisa Gorno-tempini, Howard J. Rosen, Joel H. Kramer, Salvatore Spina, Gil D Rabinovici
    Abstract:

    The clinical spectrum of Alzheimer’s disease (AD) extends well beyond the classic amnestic–predominant syndrome. The previous studies have suggested differential Neurofibrillary Tangle (NFT) burden between amnestic and logopenic primary progressive aphasia presentations of AD. In this study, we explored the regional distribution of NFT pathology and its relationship to AD presentation across five different clinical syndromes. We assessed NFT density throughout six selected neocortical and hippocampal regions using thioflavin-S fluorescent microscopy in a well-characterized clinicopathological cohort of pure AD cases enriched for atypical clinical presentations. Subjects underwent apolipoprotein E genotyping and neuropsychological testing. Main cognitive domains (executive, visuospatial, language, and memory function) were assessed using an established composite z score. Our results showed that NFT regional burden aligns with the clinical presentation and region-specific cognitive scores. Cortical, but not hippocampal, NFT burden was higher among atypical clinical variants relative to the amnestic syndrome. In analyses of specific clinical variants, logopenic primary progressive aphasia showed higher NFT density in the superior temporal gyrus ( p  = 0.0091), and corticobasal syndrome showed higher NFT density in the primary motor cortex ( p  = 0.0205) relative to the amnestic syndrome. Higher NFT burden in the angular gyrus and CA1 sector of the hippocampus were independently associated with worsening visuospatial dysfunction. In addition, unbiased hierarchical clustering based on regional NFT densities identified three groups characterized by a low overall NFT burden, high overall burden, and cortical-predominant burden, respectively, which were found to differ in sex ratio, age, disease duration, and clinical presentation. In comparison, the typical, hippocampal sparing, and limbic-predominant subtypes derived from a previously proposed algorithm did not reproduce the same degree of clinical relevance in this sample. Overall, our results suggest domain-specific functional consequences of regional NFT accumulation. Mapping these consequences presents an opportunity to increase understanding of the neuropathological framework underlying atypical clinical manifestations.

  • alzheimer s disease clinical variants show distinct regional patterns of Neurofibrillary Tangle accumulation
    Acta Neuropathologica, 2019
    Co-Authors: Cathrine Petersen, Elisa Paula França Resende, Alexander J. Ehrenberg, Howard J. Rosen, Joel H. Kramer, Salvatore Spina, Amber Nolan, Zachary A Miller, Maria Luisa Gornotempini, Gil D Rabinovici
    Abstract:

    The clinical spectrum of Alzheimer’s disease (AD) extends well beyond the classic amnestic–predominant syndrome. The previous studies have suggested differential Neurofibrillary Tangle (NFT) burden between amnestic and logopenic primary progressive aphasia presentations of AD. In this study, we explored the regional distribution of NFT pathology and its relationship to AD presentation across five different clinical syndromes. We assessed NFT density throughout six selected neocortical and hippocampal regions using thioflavin-S fluorescent microscopy in a well-characterized clinicopathological cohort of pure AD cases enriched for atypical clinical presentations. Subjects underwent apolipoprotein E genotyping and neuropsychological testing. Main cognitive domains (executive, visuospatial, language, and memory function) were assessed using an established composite z score. Our results showed that NFT regional burden aligns with the clinical presentation and region-specific cognitive scores. Cortical, but not hippocampal, NFT burden was higher among atypical clinical variants relative to the amnestic syndrome. In analyses of specific clinical variants, logopenic primary progressive aphasia showed higher NFT density in the superior temporal gyrus (p = 0.0091), and corticobasal syndrome showed higher NFT density in the primary motor cortex (p = 0.0205) relative to the amnestic syndrome. Higher NFT burden in the angular gyrus and CA1 sector of the hippocampus were independently associated with worsening visuospatial dysfunction. In addition, unbiased hierarchical clustering based on regional NFT densities identified three groups characterized by a low overall NFT burden, high overall burden, and cortical-predominant burden, respectively, which were found to differ in sex ratio, age, disease duration, and clinical presentation. In comparison, the typical, hippocampal sparing, and limbic-predominant subtypes derived from a previously proposed algorithm did not reproduce the same degree of clinical relevance in this sample. Overall, our results suggest domain-specific functional consequences of regional NFT accumulation. Mapping these consequences presents an opportunity to increase understanding of the neuropathological framework underlying atypical clinical manifestations.

  • alzheimer s disease clinical variants show distinct regional patterns of Neurofibrillary Tangle accumulation
    bioRxiv, 2019
    Co-Authors: Cathrine Petersen, Elisa Paula França Resende, Alexander J. Ehrenberg, Howard J. Rosen, Joel H. Kramer, Amber Nolan, Zachary A Miller, Maria Luisa Gornotempini, Salvatore Spina
    Abstract:

    ABSTRACT Background Neurofibrillary Tangle (NFT) pathology in Alzheimer’s disease (AD) follows a stereotypic progression well-characterized by Braak staging. However, some AD cases show deviations from the Braak staging scheme. In this study, we tested the hypothesis that these variations in the regional distribution of tau pathology are linked to heterogeneity in the clinical phenotypes of AD. Methods We included a clinicopathological cohort of ninety-four AD cases enriched for atypical clinical presentations. Subjects underwent apolipoprotein E (APOE) genotyping and neuropsychological testing. Main cognitive domains (executive, visuospatial, language, and memory function) were assessed using an established composite z-score. We assessed NFT density and distribution from thioflavin S fluorescent microscopy throughout four neocortical and two hippocampal regions. A mathematical algorithm classifying AD cases into typical, hippocampal sparing (HpSp), and limbic predominant (LP) subtypes based on regional NFT burden was compared to unbiased hierarchical clustering for cases with Braak stage > IV. Results Patients diagnosed with logopenic primary progressive aphasia showed significantly higher NFT density in the superior temporal gyrus relative to patients diagnosed with Alzheimer-type dementia (p = 0.0091), while patients with corticobasal syndrome showed significantly higher NFT density in the primary motor cortex (p = 0.0205). Hierarchical clustering identified three discrete clusters of patients characterized respectively by low overall NFT burden (n = 18), high overall burden (n = 30), and cortical-predominant burden (n = 24). A regionally specific effect was observed for visuospatial ability; higher NFT density in the angular gyrus (β = - 0.0921, p = 0.0099) and in the CA1 sector of the hippocampus (β = −0.0735, p = 0.0380) was significantly associated with more severe visuospatial dysfunction, modulated by age of death. Conclusions Our results suggest domain-specific functional consequences of regional NFT accumulation. In particular, we observed focal aggregation of NFT density in clinically relevant regions among different clinical AD variants. Continued work to map the regionally specific clinical consequences of tau accumulation presents an opportunity to increase understanding of disease mechanisms underlying atypical clinical manifestations.

John H Morrison - One of the best experts on this subject based on the ideXlab platform.

  • amyotrophic lateral sclerosis and parkinsonism dementia from guam differences in Neurofibrillary Tangle distribution and density in the hippocampal formation and neocortex
    Brain Research, 1994
    Co-Authors: Patrick R. Hof, Daniel P. Perl, John H Morrison, Arthur J Loerzel, John C Steele
    Abstract:

    Amyotrophic lateral sclerosis/parkinsonism-dementia complex is a highly prevalent neurodegenerative disorder among the native Chamorro population of Guam, and is characterized by widespread formation of Neurofibrillary Tangles. In the present study, the distribution of Neurofibrillary Tangles was quantitatively assessed in the cerebral cortex of cases presenting with either predominant amyotrophic lateral sclerosis or parkinsonism-dementia symptomatology. Results show that although the regional and laminar lesion distribution is qualitatively similar in both groups, cases with predominant parkinsonism-dementia generally have higher lesion densities than cases with amyotrophic lateral sclerosis. Interestingly, layer II of the entorhinal cortex was affected to the same degree in both conditions. In both groups, the CA1 field of the hippocampus, subiculum, and entorhinal cortex were the most affected areas. In the neocortex, the perirhinal and inferior temporal cortex consistently had higher lesion densities than the frontal, parietal, and cingulate cortex, whereas the visual cortex was practically devoid of lesions. Also, most of the Neurofibrillary Tangles were located in the supragranular layers of the neocortex, with relatively low densities in the infragranular layers, in both brain groups. Interestingly, the primary motor cortex contained more Neurofibrillary Tangles in parkinsonism-dementia than in amyotrophic lateral sclerosis cases. It is possible that the differences in regional Neurofibrillary Tangle densities reflect the variable severity of the dementing process observed between the two groups of patients. Several studies on Alzheimer's disease and related disorders indicate that the regional and laminar cortical localization of Neurofibrillary Tangles may parallel the degeneration of specific corticocortical projections. The present data suggest that the population of corticocortical projections involved in Guamanian cases differs substantially from that affected in Alzheimer's disease. The differential distribution and densities of the lesions may contribute to the differences in symptomatology and severity of dementia among Alzheimer's disease and Guamanian cases, although these neurodegenerative disorders as well as related illnesses may share certain etiopathogenetic mechanisms.

  • Neurofibrillary Tangle densities in the hippocampal formation in a non demented population define subgroups of patients with differential early pathologic changes
    Neuroscience Letters, 1993
    Co-Authors: Patrick R. Hof, Constantin Bouras, John H Morrison
    Abstract:

    Detailed analyses of the neuropathologic changes in the cerebral cortex of elderly individuals and Alzheimer's disease patients have demonstrated that certain components of the neocortical and hippocampal circuits are likely to be selectively vulnerable. In order to investigate the distribution of lesions associated with aging as well as with the earliest symptoms of Alzheimer's disease, we performed a quantitative neuropathological evaluation of sixty-one non-demented patients from a geriatric hospital. All of the cases had Neurofibrillary Tangles in layer II of the entorhinal cortex, and many cases had an involvement of the CA1 field of the hippocampus and the inferior temporal cortex. In all of the cases, amyloid deposition was not correlated with age or with the number of Neurofibrillary Tangles. In addition, eight cases showed much higher Neurofibrillary Tangle counts than the remainder of the cases. It is proposed that these cases may represent the neuropathological correlate of the earliest stage of Alzheimer's disease that could antedate the appearance of clinical signs of cognitive decline and memory impairment.

  • Neurofibrillary Tangle distribution in the cerebral cortex of parkinsonism dementia cases from guam differences with alzheimer s disease
    Brain Research, 1991
    Co-Authors: Patrick R. Hof, Daniel P. Perl, Arthur J Loerzel, John H Morrison
    Abstract:

    Abstract Parkinsonism-dementia together with amyotrophic lateral sclerosis is a highly prevalent disorder among the native Chamorro population of Guam and is accompanied by severe widespread Neurofibrillary Tangle formation. In the present study we compared the regional and laminar distribution of Neurofibrillary Tangles in the cerebral cortex of 5 Guamanian parkinsonism-dementia cases to 9 Caucasian Alzheimer's disease cases. Although in both diseases the superior frontal and inferior temporal cortex were affected to a comparable degree, there was a striking difference in the laminar distribution of Neurofibrillary Tangles. Neurofibrillary Tangles in Alzheimer's disease are known to be more numerous in layers V–VI than in layers II–III of frontal and temporal cortex, however in the Guam cases, the opposite distribution was observed with most of the Tangles located within layer II and the superior part of layer III and relatively low Tangle density in layers V–VI. Interestingly, in both conditions, the hippocampal pyramidal layer showed a comparable degree of degeneration. Moreover no amyloid deposits and neuritic plaques were observed in the Guam brains, whereas they were frequent in the Alzheimer's disease cases. Previous studies have suggested that the clinical symptomatology observed in patients suffering from Alzheimer's disease is related to the dramatic loss of specific corticocortically projecting neurons in the neocortex. The present data on Guam parkinsonism-dementia further support this hypothesis, although the set of corticocortical connections affected in Guam cases might differ from that observed in Alzheimer's disease, which may contribute to some extent to the different clinical symptoms of the dementia observed in Guamanian patients.