Research output: Contribution to Journal/Magazine › Journal article › peer-review
Research output: Contribution to Journal/Magazine › Journal article › peer-review
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TY - JOUR
T1 - Quantitative differences in the deposition of βA4 protein in the sulci and gyri of frontal and temporal isocortex in Alzheimer's disease
AU - Gentleman, S M
AU - Allsop, D
AU - Bruton, C J
AU - Jagoe, R
AU - Polak, J M
AU - Roberts, G W
PY - 1992/2/17
Y1 - 1992/2/17
N2 - The distribution of beta-amyloid protein (beta A4) in the frontal and temporal isocortex of 14 Alzheimer's disease brains was examined using a combination of immunohistochemistry and computer image analysis. The area of cortex covered by beta A4 deposits was determined and expressed as a percentage of the total cortical grey matter area in each field of interest. Significantly more beta A4 was found in the grey matter of the sulci as compared to that of the gyral crests in both the frontal and the temporal lobes (P less than 0.05). Furthermore, in each case, greater quantities of beta A4 were observed in the frontal rather than the temporal lobes. This apparent differential vulnerability is likely to reflect underlying anatomical connections or perhaps differences in cell packing density and appears to strengthen the case for an anatomical basis for the spread of the disease pathology.
AB - The distribution of beta-amyloid protein (beta A4) in the frontal and temporal isocortex of 14 Alzheimer's disease brains was examined using a combination of immunohistochemistry and computer image analysis. The area of cortex covered by beta A4 deposits was determined and expressed as a percentage of the total cortical grey matter area in each field of interest. Significantly more beta A4 was found in the grey matter of the sulci as compared to that of the gyral crests in both the frontal and the temporal lobes (P less than 0.05). Furthermore, in each case, greater quantities of beta A4 were observed in the frontal rather than the temporal lobes. This apparent differential vulnerability is likely to reflect underlying anatomical connections or perhaps differences in cell packing density and appears to strengthen the case for an anatomical basis for the spread of the disease pathology.
KW - Alzheimer Disease
KW - Amyloid beta-Peptides
KW - Frontal Lobe
KW - Humans
KW - Neurofibrillary Tangles
KW - Temporal Lobe
U2 - 10.1016/0304-3940(92)90639-O
DO - 10.1016/0304-3940(92)90639-O
M3 - Journal article
C2 - 1635663
VL - 136
SP - 27
EP - 30
JO - Neuroscience Letters
JF - Neuroscience Letters
SN - 0304-3940
IS - 1
ER -