Senile plaques in temporal lobe epilepsy - PubMed (original) (raw)
Comparative Study
doi: 10.1007/BF00294177.
Affiliations
- PMID: 8059603
- DOI: 10.1007/BF00294177
Comparative Study
Senile plaques in temporal lobe epilepsy
I R Mackenzie et al. Acta Neuropathol. 1994.
Abstract
Senile plaques (SP) are one of the characteristic pathological lesions of Alzheimer's disease (AD). They are also seen in the brains of some non-demented individuals as an age-related change. Identification of clinical conditions associated with these "incidental" SP could provide insight into AD pathogenesis. We have examined the presence of SP in lobectomy specimens (n = 101) removed in the surgical treatment of temporal lobe epilepsy (TLE). SP were present in 10 specimens from epileptic patients aged 36 to 61 years and the presence of SP correlated positively with patient age. No other significant AD-related pathology was identified and no patients showed any evidence of dementia on neuropsychological testing. When compared with temporal lobe tissue from non-demented, non-epileptic autopsy controls (n = 406), the density and distribution of SP was the same. The age-related incidence of SP however, was significantly greater in the epileptics. This suggests that some aspects of TLE has a positive influence on the formation of SP.
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References
- Nature. 1988 Feb 11;331(6156):530-2 - PubMed
- Neurology. 1992 Sep;42(9):1681-8 - PubMed
- Acta Neuropathol. 1988;77(2):113-9 - PubMed
- Science. 1987 Feb 20;235(4791):880-4 - PubMed
- N Engl J Med. 1989 Jun 1;320(22):1446-52 - PubMed
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