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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

Graphs showing the percentage of PHF-tau-ir neurons displaying type I and II staining in the hippocampal formation and adjacent cortex of control and AD patients. Dentate gyrus (DG); CA3/4, CA2, CA1 proximal (CA1 Prox), CA1 medial (CA1 Med), CA1 Distal (CA1 Dist), subiculum (S), presubiculum (preS), parasubiculum (paraS) and parahippocampal gyrus (PHG) that includes the entorhinal cortex, perirhinal cortex, or posterior parahippocampal cortex.
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Figure 7: Graphs showing the percentage of PHF-tau-ir neurons displaying type I and II staining in the hippocampal formation and adjacent cortex of control and AD patients. Dentate gyrus (DG); CA3/4, CA2, CA1 proximal (CA1 Prox), CA1 medial (CA1 Med), CA1 Distal (CA1 Dist), subiculum (S), presubiculum (preS), parasubiculum (paraS) and parahippocampal gyrus (PHG) that includes the entorhinal cortex, perirhinal cortex, or posterior parahippocampal cortex.

Mentions: The percentage of neurons displaying type I staining increased from the adjacent cortex of the hippocampal formation (PPC or PRC and EC) towards the DG, with the highest proportion of these neurons found in the field CA3/4 (Figure 7). The widest variability of these neurons was observed in the DG: 76% of neurons in case P3 and 78% of neurons in case P6 displayed type I staining, whereas in P7 and C4 (control case) this figure was 41 and 24%, respectively (Figure 7).


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)

Graphs showing the percentage of PHF-tau-ir neurons displaying type I and II staining in the hippocampal formation and adjacent cortex of control and AD patients. Dentate gyrus (DG); CA3/4, CA2, CA1 proximal (CA1 Prox), CA1 medial (CA1 Med), CA1 Distal (CA1 Dist), subiculum (S), presubiculum (preS), parasubiculum (paraS) and parahippocampal gyrus (PHG) that includes the entorhinal cortex, perirhinal cortex, or posterior parahippocampal cortex.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 7: Graphs showing the percentage of PHF-tau-ir neurons displaying type I and II staining in the hippocampal formation and adjacent cortex of control and AD patients. Dentate gyrus (DG); CA3/4, CA2, CA1 proximal (CA1 Prox), CA1 medial (CA1 Med), CA1 Distal (CA1 Dist), subiculum (S), presubiculum (preS), parasubiculum (paraS) and parahippocampal gyrus (PHG) that includes the entorhinal cortex, perirhinal cortex, or posterior parahippocampal cortex.
Mentions: The percentage of neurons displaying type I staining increased from the adjacent cortex of the hippocampal formation (PPC or PRC and EC) towards the DG, with the highest proportion of these neurons found in the field CA3/4 (Figure 7). The widest variability of these neurons was observed in the DG: 76% of neurons in case P3 and 78% of neurons in case P6 displayed type I staining, whereas in P7 and C4 (control case) this figure was 41 and 24%, respectively (Figure 7).

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