TY - JOUR
T1 - Alzheimer's disease, Lewy body disease and aging
T2 - A comparative study of the perforant pathway
AU - Lippa, C. F.
AU - Pulaski-Salo, D.
AU - Dickson, D. W.
AU - Smith, T. W.
N1 - Funding Information:
The authors would like to thank Dr. David A. Drachman for support and advice, Jeff Gonet and Ken Dole for helping us obtain brain tissue. The Joseph and Kathleen Bryan ADRC for contributing tissue for the study. Supported by NIA Grant AG-13623.
PY - 1997/4/15
Y1 - 1997/4/15
N2 - The relationship between Alzheimer's disease (AD) and Lewy body disease (LED) is poorly understood. In AD there is severe loss of neurons comprising the perforant pathway. To assess perforant pathway integrity in pure LED we compared neuronal counts in layer II of the entorhinal cortex (ERC) in 11 cases of pure LED that did not meet CERAD pathologic criteria for AD with ERC neuronal counts from seven AD cases with a similar disease duration and six cognitively normal individuals. We counted cell bodies/island in layer II of the ERC using formalin-fixed, paraffin-embedded, tau/cresyl violet-stained sections at the level of the rostral-most body of the hippocampus. There was marked variability in neuronal counts among cases in the LED group; LED data overlapped with data from both normal and AD groups. Overall, perforant pathway perikaryal counts in LED differed significantly from those in AD, but not from those in aged normals (mean perikarya/island = 30.09 ± 8.95, 7.57 ± 6.08, and 38.83 ± 8.98, respectively; F=26.131, P<0.001). The percent of remaining neurons bearing neurofibrillary tangles in LED also overlapped with AD and control groups (16.17 ± 13.85%, 87.86 ± 11.81%, and 24.36 ± 13.30% of remaining neurons, respectively, F=65.62, P<0.001). We conclude that although perforant pathway neuronal loss may occur in LED, it is more often milder and more variable than that seen in AD.
AB - The relationship between Alzheimer's disease (AD) and Lewy body disease (LED) is poorly understood. In AD there is severe loss of neurons comprising the perforant pathway. To assess perforant pathway integrity in pure LED we compared neuronal counts in layer II of the entorhinal cortex (ERC) in 11 cases of pure LED that did not meet CERAD pathologic criteria for AD with ERC neuronal counts from seven AD cases with a similar disease duration and six cognitively normal individuals. We counted cell bodies/island in layer II of the ERC using formalin-fixed, paraffin-embedded, tau/cresyl violet-stained sections at the level of the rostral-most body of the hippocampus. There was marked variability in neuronal counts among cases in the LED group; LED data overlapped with data from both normal and AD groups. Overall, perforant pathway perikaryal counts in LED differed significantly from those in AD, but not from those in aged normals (mean perikarya/island = 30.09 ± 8.95, 7.57 ± 6.08, and 38.83 ± 8.98, respectively; F=26.131, P<0.001). The percent of remaining neurons bearing neurofibrillary tangles in LED also overlapped with AD and control groups (16.17 ± 13.85%, 87.86 ± 11.81%, and 24.36 ± 13.30% of remaining neurons, respectively, F=65.62, P<0.001). We conclude that although perforant pathway neuronal loss may occur in LED, it is more often milder and more variable than that seen in AD.
KW - Alzheimer's disease
KW - Dementia
KW - Lewy body disease
KW - Perforant pathway
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U2 - 10.1016/S0022-510X(96)05321-X
DO - 10.1016/S0022-510X(96)05321-X
M3 - Article
C2 - 9106122
AN - SCOPUS:0031569804
SN - 0022-510X
VL - 147
SP - 161
EP - 166
JO - Journal of the neurological sciences
JF - Journal of the neurological sciences
IS - 2
ER -