Tau, β-amyloid and β-amyloid precursor protein distribution in the entorhinal-hippocampal alvear and perforant pathways in the Alzheimer's brain
Tau, β-amyloid and β-amyloid precursor protein distribution in the entorhinal-hippocampal alvear and perforant pathways in the Alzheimer's brain
It has been suggested that the pathological lesions of Alzheimer's disease (AD) spread along neuronal connections. This study was designed to examine this hypothesis in the alvear and perforant pathways, two well-defined neuroanatomical pathways that project from the entorhinal cortex to the hippocampus. Paraffin-sections of hippocampal-entorhinal cortex from 25 AD cases were immunolabelled for tau, β-amyloid (Aβ) and β-amyloid precursor protein (βAPP). We used image-analysis to quantify immunolabelling at both ends of the alvear and perforant pathways. At the beginning and the end of the alvear pathway, area of immunolabelling in µm2 per area of field (72000 µm2) were as follows: tau 349 and 821 (P<0.01), Aβ 349 and 61 (P<0.05) and βAPP 18 and 73 (P<0.01). Corresponding values for the perforant pathway were tau 421 and 387, Aβ382 and 115 (P<0.05) and βAPP 55 and 83. Tau was significantly greater at the end than at the beginning of the alvear pathway, but similar at both ends of the perforant pathway. There was significantly more Aβ at the beginning than at the end of the alvear and perforant pathway. These results at least in part reinforce previous work [19] that tau-rich areas may be neuronally connected to Aβ-rich areas.
Alzheimer's disease, ?-amyloid, ?-amyloid precursor protein, tau, senile plaques, neurofibrillary tangles, neuroanatomy
193-197
Shukla, C.
e6ebea1a-77c2-4aed-bb51-becadede8663
Bridges, L.R.
4858d61d-57ff-4265-9164-745dc342ca4c
2001
Shukla, C.
e6ebea1a-77c2-4aed-bb51-becadede8663
Bridges, L.R.
4858d61d-57ff-4265-9164-745dc342ca4c
Shukla, C. and Bridges, L.R.
(2001)
Tau, β-amyloid and β-amyloid precursor protein distribution in the entorhinal-hippocampal alvear and perforant pathways in the Alzheimer's brain.
Neuroscience Letters, 303 (3), .
(doi:10.1016/S0304-3940(01)01719-0).
Abstract
It has been suggested that the pathological lesions of Alzheimer's disease (AD) spread along neuronal connections. This study was designed to examine this hypothesis in the alvear and perforant pathways, two well-defined neuroanatomical pathways that project from the entorhinal cortex to the hippocampus. Paraffin-sections of hippocampal-entorhinal cortex from 25 AD cases were immunolabelled for tau, β-amyloid (Aβ) and β-amyloid precursor protein (βAPP). We used image-analysis to quantify immunolabelling at both ends of the alvear and perforant pathways. At the beginning and the end of the alvear pathway, area of immunolabelling in µm2 per area of field (72000 µm2) were as follows: tau 349 and 821 (P<0.01), Aβ 349 and 61 (P<0.05) and βAPP 18 and 73 (P<0.01). Corresponding values for the perforant pathway were tau 421 and 387, Aβ382 and 115 (P<0.05) and βAPP 55 and 83. Tau was significantly greater at the end than at the beginning of the alvear pathway, but similar at both ends of the perforant pathway. There was significantly more Aβ at the beginning than at the end of the alvear and perforant pathway. These results at least in part reinforce previous work [19] that tau-rich areas may be neuronally connected to Aβ-rich areas.
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Published date: 2001
Keywords:
Alzheimer's disease, ?-amyloid, ?-amyloid precursor protein, tau, senile plaques, neurofibrillary tangles, neuroanatomy
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Local EPrints ID: 27712
URI: http://eprints.soton.ac.uk/id/eprint/27712
ISSN: 0304-3940
PURE UUID: 90647b2c-fdec-4da6-997d-652ad550d32e
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Date deposited: 27 Apr 2006
Last modified: 15 Mar 2024 07:20
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Author:
C. Shukla
Author:
L.R. Bridges
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