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1.
Figure 1

Figure 1. From: Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation.

(a) Location and sequence of antigen used to generate an antibody targeting acetylated tau at lysine 274. (b) MAb 359 recognizes both 4R and 3R tau. HEK293 cells were transfected with either 4R or 3R tau in the presence or absence of p300 overexpression. MAb 359 selectively recognized p300-induced acetylation in both 4R and 3R tau. Total tau level was detected with Tau5 antibody. (c) MAb 359 is specific for ac-K274. HEK293 cells were transfected with WT or K274R tau in the presence or absence of p300 overexpression. Mutation of K274 abolished p300-induced immunoreactivity of MAb 359.

Lea Tenenholz Grinberg, et al. Acta Neuropathol. ;125(4):581-593.
2.
Figure 5

Figure 5. From: Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation.

Hippocampal sections of a case of argyrophilic grain disease (case 5) after immunostaining with CP-13 (a, c, e) and MAb 359 (b, d, f) antibodies. a– b dentate gyrus. Only phosphorylated tau immunoreactivity (CP-13) is seen (arrowheads). c – d CA1 sector. Grains are observed only in the section immunostained with CP-13 (ph-tau). Almost all AGD cases have overlapping AD and AGD pathology to varying degrees. The arrowhead shows an Alzheimer’s disease type neurofibrillary tangle. e –f CA2 sector. AGD is characterized by pre-neurofibrillary tangles with a perinuclear halo as seen in e. These pretangles are not acetylated at position 274. Scale bars represent 100 µm.

Lea Tenenholz Grinberg, et al. Acta Neuropathol. ;125(4):581-593.
3.
Figure 3

Figure 3. From: Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation.

Abnormal tau pathology in brain sections of tauopathy cases immunostained with CP-13 (a, c, e, g, i, k) or MAb 359 (b ,d ,f, h, j, l). a– d Corticobasal degeneration (case 10) – inferior temporal cortex. Star symbols indicate the white matter. c, d show the white matter at high magnification. e – h Progressive supranuclear palsy (case 20) –midbrain. Arrowheads show globose tangles in the periaqueductal gray matter. i – l Pick’s disease (case 18) – inferior temporal cortex. Arrowheads show Pick bodies in layer II. Scale bars represent 1 mm in a, b, e, f, i, j and 100 µm in c, d, g, h, k, l.

Lea Tenenholz Grinberg, et al. Acta Neuropathol. ;125(4):581-593.
4.
Figure 2

Figure 2. From: Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation.

Abnormal tau pathology in inferior temporal cortex sections of tauopathy cases immunostained with CP-13 (a, c, e, g, i, k, m, o) or MAb 359 (b ,d ,f, h, j, l, n, p). a–d Alzheimer’s disease (case 3). Arrowheads and arrows show neuritic plaques and neurofibrillary tangles, respectively. e–h White matter tauopathy with globular glial inclusions (case 22). g, h show the white matter of case 22 at high magnification. Note that the glial globolar inclusions are positive for phospho-tau and acetylated tau. i–l Atypical 4R tauopathy (case 7), and m–p chronic traumatic encephalopathy (case 8). In both cases, the tau inclusions are phosphorylated and acetylated.
Scale bars represent 1 mm in a, b, e, f, i, j, m, n and 100 µm in c, d, g, h, k, l, o, p.

Lea Tenenholz Grinberg, et al. Acta Neuropathol. ;125(4):581-593.
5.
Figure 4

Figure 4. From: Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation.

High magnification of acetylated-tau inclusions located in inferior temporal cortex (a–c and e–i) and midbrain (d), after immunostaining with MAb 359. a neuritic plaque (Alzheimer’s disease - case 3). b neurofibrillary tangle (Alzheimer’s disease - case 3). c astrocytic plaque (corticobasal degeneration - case 9). d tufted astrocyte in periaqueductal gray matter (progressive supranuclear palsy – case 21 ). e Pick body (Pick’s disease – case 18). f neuronal cytoplasmicinclusion (chronic traumatic encephalopathy- case 8). g neuronal cytoplasmicinclusion (FTLP-17 – case 11). h globular glial inclusions (white matter tauopathy with globular glial inclusion - case 22). i glial inclusion (atypical tauopathy- case 7). Scale bars represent 10 µm

Lea Tenenholz Grinberg, et al. Acta Neuropathol. ;125(4):581-593.
6.
Figure 6

Figure 6. From: Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation.

Hippocampal formation sections of a case of argyrophilic grain disease (case 5) after immunofluorescence staining with CP-13 (a, d, g, j) and MAb 359 (b, e,h,k) antibodies. a– c dentate gyrus. Only phosphorylated tau immunoreactivity (CP-13) is seen (arrowheads and green fluorescent signal). d – f CA1 sector. Grains are observed only in the section immunostained with CP-13 (ph-tau). g – i CA2 sector. AGD is characterized by pre-neurofibrillary tangles with a perinuclear halo as seen in k and m. These pretangles are not acetylated at position 274. The arrowheads show an Alzheimer’s disease type neurofibrillary tangle. j – l white matter adjacent to entorhinal cortex. As oppose to corticobasal degeneration and other tauopathies, white matter pathology, including coiled bodies (arrows) are not tau-acetylated in AGD. Scale bars represent 100 µm.

Lea Tenenholz Grinberg, et al. Acta Neuropathol. ;125(4):581-593.
7.
Figure 7

Figure 7. From: Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation.

Western blot analyses of ac-K274 in brain lysates from brains of human patients. Frozen tissues from specific regions of human tauopathy brains were lysed with RIPA buffer containing HDAC and phosphatase inhibitors. Levels of ac-K274 were probed with MAb 359; total tau was probed with Tau-5. Anti-GAPDH was used to ensure that equal amount of protein was loaded (60 µg protein/lane). The lysates were extracted from inferior temporal cortex, unless otherwise specified.
Footnote: AD: Alzheimer’s disease; AGD: Argyrophilic grain disease; CBD: corticobasal degeneration; CTE: Chronic traumatic encephalopathy; FTDP-17: frontotemporal dementia with parkinsonism linked to chromosome 17; PSP: progressive supranuclear palsy; WMT-GGI: white matter tauopathy with globular glial inclusions/ globular glial tauopathy. a insula. b precentral gyrus. c posterior cingulate gyrus

Lea Tenenholz Grinberg, et al. Acta Neuropathol. ;125(4):581-593.

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