Table I.
Summary of demographic data, neuropathology, and experimental results of human subjects
Case | PMI | Brain area | Nuclear localization of AMPK-α-p | Nuclear localization of AMPK-α1 | Age | Gender | HD Vonsattel grade | Other pathology |
h | % | % | yr | |||||
HD-1a | 9 | Caudate nucleus | 71 ± 5 | 77 ± 4 | 80 | F | I | Cortical amyolid plaques |
HD-2a | <24 | Caudate nucleus | 67 ± 7 | 75 ± 5 | 70 | F | IV | Brainstem Lewy body |
HD-1a | 9 | Frontal cortex | 67 ± 8 | 85 ± 4 | 80 | F | I | Cortical amyolid plaques |
HD-2a | <24 | Frontal cortex | 69 ± 6 | 70 ± 9 | 70 | F | IV | Brainstem Lewy body |
HD-3b | 15 | Frontal cortex | 51 ± 8 | 56 ± 4 | 57 | M | I | None |
HD-4b | 17 | Frontal cortex | 60 ± 4 | 64 ± 7 | 58 | M | I | None |
Non–HD-1a | 6 | Caudate nucleus | 31 ± 7 | 22 ± 5 | 93 | M | n.a. | AD break NFT |
Non–HD-2a | 14 | Caudate nucleus | 17 ± 5 | 20 ± 6 | 88 | F | n.a. | None |
Non–HD-3a | <24 | Caudate nucleus | 24 ± 6 | 31 ± 3 | 82 | F | n.a. | None |
Non–HD-4a | 12 | Caudate nucleus | 25 ± 5 | 18 ± 5 | 78 | M | n.a. | AD break NFT |
Non–HD-5a | <24 | Caudate nucleus | 18 ± 4 | 26 ± 3 | 74 | M | n.a. | None |
Non–HD-6a | <24 | Caudate nucleus | 21 ± 5 | 22 ± 3 | 83 | M | n.a. | None |
Non–HD-1a | 6 | Frontal cortex | 22 ± 5 | 20 ± 7 | 93 | M | n.a. | AD break NFT |
Non–HD-2a | 14 | Frontal cortex | 12 ± 4 | 18 ± 6 | 88 | F | n.a. | None |
Non–HD-3a | <24 | Frontal cortex | 19 ± 7 | 22 ± 8 | 82 | F | n.a. | None |
Non–HD-4a | 12 | Frontal cortex | 27 ± 4 | 21 ± 5 | 78 | M | n.a. | AD break NFT |
Non–HD-5a | <24 | Frontal cortex | 25 ± 3 | 21 ± 7 | 74 | M | n.a. | None |
Non–HD-6a | <24 | Frontal cortex | 22 ± 5 | 17 ± 4 | 83 | M | n.a. | None |
Significant amounts of phosphorylated AMPK-α at Thr172 (AMPK-α-p) and AMPK-α1 were found in nuclei in brains of HD patients but not in those of age-matched controls. Brain sections were analyzed by immunofluorescence staining of AMPK-α-p or AMPK-α1 as shown in Fig. 1 and Fig. S1. At least 200 cells were counted in brain sections of each subject. The Alzheimer-type pathology (both senile plaques and neurofibrillary tangles [NFTs]) was assessed by thioflavin-S fluorescence microscopy. The Braak neurofibrillary tangle stage was assigned based on the counts of plaques and neurofibrillary tangles with this method. F, female; M, male; n.a., not applicable; PMI, postmortem interval.
Cases obtained from the Mayo Clinic College of Medicine, Rochester, MN.
Cases obtained from the National Institute of Child Health and Development Brain and Tissue Bank for Developmental Disorders at the University of Maryland, College Park, MD.