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

Table 1 Summary of cases.

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

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.

ISSN: 1528-3658