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Pericellular innervation of neurons expressing abnormally hyperphosphorylated tau in the hippocampal formation of Alzheimer's disease patients.

Blazquez-Llorca L, Garcia-Marin V, Defelipe J - Front Neuroanat (2010)

Bottom Line: This neurofibrillary lesion involves the accumulation of abnormally hyperphosphorylated or abnormally phosphorylated microtubule-associated protein tau into paired helical filaments (PHF-tau) within neurons.Furthermore, the distribution of both GABAergic and glutamatergic terminals around the soma and proximal processes of PHF-tau-ir neurons does not seem to be altered as it is indistinguishable from both control cases and from adjacent neurons that did not contain PHF-tau.These observations suggest that the synaptic connectivity around the perisomatic region of these PHF-tau-ir neurons was apparently unaltered.

View Article: PubMed Central - PubMed

Affiliation: Laboratorio de Circuitos Corticales (Centro de Tecnología Biomédica), Universidad Politécnica de Madrid Madrid, Spain.

ABSTRACT
Neurofibrillary tangles (NFT) represent one of the main neuropathological features in the cerebral cortex associated with Alzheimer's disease (AD). This neurofibrillary lesion involves the accumulation of abnormally hyperphosphorylated or abnormally phosphorylated microtubule-associated protein tau into paired helical filaments (PHF-tau) within neurons. We have used immunocytochemical techniques and confocal microscopy reconstructions to examine the distribution of PHF-tau-immunoreactive (ir) cells, and their perisomatic GABAergic and glutamatergic innervations in the hippocampal formation and adjacent cortex of AD patients. Furthermore, correlative light and electron microscopy was employed to examine these neurons and the perisomatic synapses. We observed two patterns of staining in PHF-tau-ir neurons, pattern I (without NFT) and pattern II (with NFT), the distribution of which varies according to the cortical layer and area. Furthermore, the distribution of both GABAergic and glutamatergic terminals around the soma and proximal processes of PHF-tau-ir neurons does not seem to be altered as it is indistinguishable from both control cases and from adjacent neurons that did not contain PHF-tau. At the electron microscope level, a normal looking neuropil with typical symmetric and asymmetric synapses was observed around PHF-tau-ir neurons. These observations suggest that the synaptic connectivity around the perisomatic region of these PHF-tau-ir neurons was apparently unaltered.

No MeSH data available.


Related in: MedlinePlus

Drawings based on Neurolucida plots made with a 40× objective showing the distribution of diffuse, cored neuritic, and non-cored neuritic plaques (red, green, and blue circles, respectively; see Garcia-Marin et al., 2009) in the hippocampal formation and adjacent cortex from control cases. Borders between the different cortical cytoarchitectonic regions are indicated by arrowheads. Abbreviations as in Figure 5. Scale bar: 1,000 μm.
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Figure 8: Drawings based on Neurolucida plots made with a 40× objective showing the distribution of diffuse, cored neuritic, and non-cored neuritic plaques (red, green, and blue circles, respectively; see Garcia-Marin et al., 2009) in the hippocampal formation and adjacent cortex from control cases. Borders between the different cortical cytoarchitectonic regions are indicated by arrowheads. Abbreviations as in Figure 5. Scale bar: 1,000 μm.

Mentions: Human brain tissue was obtained at autopsy from two sources: from eight patients with AD [aged 80–94: 84 ± 7, mean ± standard deviation (SD)]; and from control human brain tissue from seven individuals (aged 23–69: 53 ± 17, mean ± SD) who died in an accident and were free of any neurological or known psychiatric illness (Table 1). The AD brain tissues were obtained from the Instituto de Neuropatología (Dr. I. Ferrer, Servicio de Anatomía Patológica, IDIBELL-Hospital Universitario de Bellvitge, Barcelona, Spain) and from the Banco de Tejidos Fundación CIEN (Dr. A. Rábano, área de Neuropatología, Centro Alzheimer, Fundación Reina Sofia, Madrid, Spain). The control human brains were obtained from the Servicio de Patología Forense (Dr. R. Alcaraz, Instituto Vasco de Medicina Legal, Bilbao, Spain). Following a neuropathological examination, the AD stages were defined according to Braak and Braak (1991: Table 2). Control cases (C1–C7) were associated with different scores for the amyloid and neurofibrillary pathology. While C1 and C5–C7 had a Braak score of zero for both pathologies, C2–C3 had a small number (+) of PHF-tau-ir neurons, whereas C4 had many (+++). Finally, while C2 developed numerous (+++) plaques immunostained for Aβ, there were no such plaques in cases C3–C4 (see Figures 4 and 8). In all cases, the time between death and tissue processing was between 1.5 and 3 h, and the brain samples were obtained following the guidelines and approval by the Institutional Ethical Committee. The tissue from these human brains has been used in previous studies (e.g., Arellano et al., 2004).


Pericellular innervation of neurons expressing abnormally hyperphosphorylated tau in the hippocampal formation of Alzheimer's disease patients.

Blazquez-Llorca L, Garcia-Marin V, Defelipe J - Front Neuroanat (2010)

Drawings based on Neurolucida plots made with a 40× objective showing the distribution of diffuse, cored neuritic, and non-cored neuritic plaques (red, green, and blue circles, respectively; see Garcia-Marin et al., 2009) in the hippocampal formation and adjacent cortex from control cases. Borders between the different cortical cytoarchitectonic regions are indicated by arrowheads. Abbreviations as in Figure 5. Scale bar: 1,000 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2903190&req=5

Figure 8: Drawings based on Neurolucida plots made with a 40× objective showing the distribution of diffuse, cored neuritic, and non-cored neuritic plaques (red, green, and blue circles, respectively; see Garcia-Marin et al., 2009) in the hippocampal formation and adjacent cortex from control cases. Borders between the different cortical cytoarchitectonic regions are indicated by arrowheads. Abbreviations as in Figure 5. Scale bar: 1,000 μm.
Mentions: Human brain tissue was obtained at autopsy from two sources: from eight patients with AD [aged 80–94: 84 ± 7, mean ± standard deviation (SD)]; and from control human brain tissue from seven individuals (aged 23–69: 53 ± 17, mean ± SD) who died in an accident and were free of any neurological or known psychiatric illness (Table 1). The AD brain tissues were obtained from the Instituto de Neuropatología (Dr. I. Ferrer, Servicio de Anatomía Patológica, IDIBELL-Hospital Universitario de Bellvitge, Barcelona, Spain) and from the Banco de Tejidos Fundación CIEN (Dr. A. Rábano, área de Neuropatología, Centro Alzheimer, Fundación Reina Sofia, Madrid, Spain). The control human brains were obtained from the Servicio de Patología Forense (Dr. R. Alcaraz, Instituto Vasco de Medicina Legal, Bilbao, Spain). Following a neuropathological examination, the AD stages were defined according to Braak and Braak (1991: Table 2). Control cases (C1–C7) were associated with different scores for the amyloid and neurofibrillary pathology. While C1 and C5–C7 had a Braak score of zero for both pathologies, C2–C3 had a small number (+) of PHF-tau-ir neurons, whereas C4 had many (+++). Finally, while C2 developed numerous (+++) plaques immunostained for Aβ, there were no such plaques in cases C3–C4 (see Figures 4 and 8). In all cases, the time between death and tissue processing was between 1.5 and 3 h, and the brain samples were obtained following the guidelines and approval by the Institutional Ethical Committee. The tissue from these human brains has been used in previous studies (e.g., Arellano et al., 2004).

Bottom Line: This neurofibrillary lesion involves the accumulation of abnormally hyperphosphorylated or abnormally phosphorylated microtubule-associated protein tau into paired helical filaments (PHF-tau) within neurons.Furthermore, the distribution of both GABAergic and glutamatergic terminals around the soma and proximal processes of PHF-tau-ir neurons does not seem to be altered as it is indistinguishable from both control cases and from adjacent neurons that did not contain PHF-tau.These observations suggest that the synaptic connectivity around the perisomatic region of these PHF-tau-ir neurons was apparently unaltered.

View Article: PubMed Central - PubMed

Affiliation: Laboratorio de Circuitos Corticales (Centro de Tecnología Biomédica), Universidad Politécnica de Madrid Madrid, Spain.

ABSTRACT
Neurofibrillary tangles (NFT) represent one of the main neuropathological features in the cerebral cortex associated with Alzheimer's disease (AD). This neurofibrillary lesion involves the accumulation of abnormally hyperphosphorylated or abnormally phosphorylated microtubule-associated protein tau into paired helical filaments (PHF-tau) within neurons. We have used immunocytochemical techniques and confocal microscopy reconstructions to examine the distribution of PHF-tau-immunoreactive (ir) cells, and their perisomatic GABAergic and glutamatergic innervations in the hippocampal formation and adjacent cortex of AD patients. Furthermore, correlative light and electron microscopy was employed to examine these neurons and the perisomatic synapses. We observed two patterns of staining in PHF-tau-ir neurons, pattern I (without NFT) and pattern II (with NFT), the distribution of which varies according to the cortical layer and area. Furthermore, the distribution of both GABAergic and glutamatergic terminals around the soma and proximal processes of PHF-tau-ir neurons does not seem to be altered as it is indistinguishable from both control cases and from adjacent neurons that did not contain PHF-tau. At the electron microscope level, a normal looking neuropil with typical symmetric and asymmetric synapses was observed around PHF-tau-ir neurons. These observations suggest that the synaptic connectivity around the perisomatic region of these PHF-tau-ir neurons was apparently unaltered.

No MeSH data available.


Related in: MedlinePlus