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Post mortem delay of all cases was between 2 ½ and 9 hours.
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Here we report the development of a simple and highly reproducible method that enables relatively high-throughput measurement of the fatty acid composition in samples of brain tissue and using this method we have demonstrated that there is no significant change in fatty acid composition under conditions designed to model post-mortem delay of up to 3 days at 4 °C (or even at room temperature).
Post-mortem delay of the control subjects was <12 h and of ALS patients was <12 h (n = 3), <24 h (n = 4).
Tissues were collected within a maximum post-mortem delay of 6 8 h to reduce degradation.
The brain was obtained with a post-mortem delay of 17 h.
Poorly fixed and long post-mortem delay of tissue (>72 h) which may impact on the quality of subsequent immunostaining were also excluded.
The patient died aged 79 years, after being in a nursing home for 2 years, and autopsy (post-mortem delay of 16 h) confirmed AD with at least Braak stage V.
After 4 years in a nursing home, the patient died at the age of 60, and autopsy (post-mortem delay of 25 h) confirmed AD pathology, with Braak stages V-VI.
For primary human adult astrocyte cultures, we obtained freshly dissected post-mortem subcortical white matter from a 79-year-old female control with a post-mortem delay of <18 hours (h) and a pH of the cerebrospinal fluid of 6.30 from the NBB.
Importantly, the differences in 51A expression observed in control versus AD patients were not related to the time of the sampling: we observed the lack of any relationship between the post-mortem delay of brain sampling and 51A expression (data not shown).
The patient was diagnosed with AD, treated with rivastigmine (anticholinesterase inhibitor) and memantine (NMDA antagonist, and underwent three F-FDG PET examinations at 70, 72 and 75 years of age. The patient died aged 81 years after four years in a nursing home, and autopsy (post-mortem delay of 17 h) confirmed Braak stages V-VI with slight atrophy of the frontal lobe.
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