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Table 1 Summary of cases.

From: Severe Alterations in Lipid Composition of Frontal Cortex Lipid Rafts from Parkinson’s Disease and Incidental Parkinson’s Disease

Case Age Sex Postmortem delay Neuropathology
NSL     
1 78 M 2 h 15 min No lesions
2 79 M 7 h No lesions
3 85 M 5 h 45 min ADII/A, status cribosus
4 70 M 13 h ADI/A
5 71 M 12 h Lacunes
6 73 F 5 h 30 min ADI/0
7 82 F 11 h ADI/A
8 75 F 3 h ADI/A, status cribosus
9 69 F 2 h 30 min ADI/0
10 66 F 8 h No lesions
11 65 F 4 h No lesions
PD     
12 70 M 9 h PD4, ADII/B, lacunes
13 68 M 4 h 45 min PD4, ADIII/A, lacune
14 76 M 4 h 30 min PD4
15 85 M 3 h 15 min PD4, ADIII/A, status cribosus
16 69 M 5 h 55 min PD4, ADI/A
17 74 F 10 h 15 min PD3, ADII/0, AGD1, status cribosus
18 70 F 10 h 50 min PD3, ADII/A
19 70 F 5 h 15 min PD4, ADII/A
iPD     
20 72 M 8 h 55 min PD1, ADII/A
21 74 M 10 h 50 min PD1, ADII/0, AGD3
22 83 M 3 h 30 min PD2, ADIII/A, AGD3
23 83 M 4 h 30 min PD2, ADII/A, AGD1
24 67 M 2 h 30 min PD3, ADI/0
25 78 M 10 h 45 min PD3, ADI/0
26 77 F 3 h 15 min PD1, ADII/A, lacunes
27 70 F 10 h 50 min PD3, ADI/A, lacunes
  1. NL, no lesions; 1–4 refer to Braak stages of PD-related pathology. ADI, ADII and ADIII refer to Braak stages of neurofibrillary tangle pathology; 0, A and B refer to Braak stages of β amyloid plaques; AGD, argyrophilic grain disease; 1, 2 and 3 refers to AGD stages. Cases 1–11 had not suffered from neurological deficits, and the neuropathological examination did not reveal brain lesions. Cases 12–19 had suffered from PD, and the neuropathological examination revealed the presence of LB in selected brain stem nuclei and the limbic system but not in the cerebral neocortex. Cases 20–27 did not refer neurological deficits but showed LB in the medulla oblongata, pons and substantia nigra (depending on the stage), but neuron loss in the substantia nigra did not exceed the 50% of the total number of neurons in the pars compacta. Cases 1–11 were considered as controls cases 12–19 as PD with Parkinsonism and cases 20–27 as incidental PD.