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1.
Figure 4

Figure 4. From: Nonhuman Primate Models of Alzheimer-Like Cerebral Proteopathy.

Ultrastructure of a neurofibrillary tangle in a cortical neuron from a 41-year old female chimpanzee. The paired helical filaments (arrow marks an isolated PHF) are identical in size and periodicity to those in humans with AD. Bar = 200nm.

Eric Heuer, et al. Curr Pharm Des. ;18(8):1159-1169.
2.
Figure 3

Figure 3. From: Nonhuman Primate Models of Alzheimer-Like Cerebral Proteopathy.

Cortical neurons immunoreactive for abnormally phosphorylated tau in a human patient with AD (A) and in a 41 year-old female Chimpanzee (B). Note also the neuropil ‘threads’ surrounding the somata. Antibody AT8 specific for Tau doubly phosphorylated at Ser202/Thr205. Bars = 50μm.

Eric Heuer, et al. Curr Pharm Des. ;18(8):1159-1169.
3.
Figure 6

Figure 6. From: Nonhuman Primate Models of Alzheimer-Like Cerebral Proteopathy.

Abnormally distended neurites in a senile plaque from the hippocampal formation of a ~30 year old male rhesus monkey. Note the normal-appearing neuronal processes distal to the plaque. Antibody 6–17 to phosphorylated neurofilaments recognizes NF-H in axons. Bar = 50μm.

Eric Heuer, et al. Curr Pharm Des. ;18(8):1159-1169.
4.
Figure 2

Figure 2. From: Nonhuman Primate Models of Alzheimer-Like Cerebral Proteopathy.

Cerebral β-amyloid angiopathy immunostained with antibodies to Aβ in a human AD patient (A) and in a 27-year old female squirrel monkey (B). Superficial vessels are indicated by arrows, and parenchymal vessels by arrowheads. Antibody 10D5 specific to residues 3–6 of Aβ (A) and β/A4 specific to Aβ phosphorylated at threonine 743. (B), courtesy of Dale Schenk and Colin Masters, respectively. Bars = 50μm.

Eric Heuer, et al. Curr Pharm Des. ;18(8):1159-1169.
5.
Figure 1

Figure 1. From: Nonhuman Primate Models of Alzheimer-Like Cerebral Proteopathy.

Senile plaques in a human with AD (A) and in a 35 year old female rhesus macaque (B). (A) Dense core plaque (black arrow); ‘primitive’ plaque (arrowhead); diffuse plaque (gray arrow). Antibody 6E10 specific amino acids 1–17 of Aβ. Bars = 50μm.

Eric Heuer, et al. Curr Pharm Des. ;18(8):1159-1169.
6.
Figure 7

Figure 7. From: Nonhuman Primate Models of Alzheimer-Like Cerebral Proteopathy.

Maximum known lifespans and approximate ages at which Aβ deposition is present [Senile Plaques (SP), and Cerebral Amyloid Angiopathy (CAA)] in some representative nonhuman primate species. Note that there is variability in age of lesion onset (indicated by the hatched bars) among members of the same species. Some estimates are approximate, due to the relatively small numbers of aged animals studied.

Eric Heuer, et al. Curr Pharm Des. ;18(8):1159-1169.
7.
Figure 5

Figure 5. From: Nonhuman Primate Models of Alzheimer-Like Cerebral Proteopathy.

Reactive gliosis associated with senile plaques in aged rhesus monkeys. A) Activated astrocytes (red) surrounding a cortical senile plaque in a 34 year old male rhesus monkey (antibody to GFAP). B) Activated microglia (brown) in a cortical senile plaque (antibody to CD68 epitope PG-M1, which is specific for macrophages and microglia) of a 30 year old male rhesus monkey. Note that microglia tend to be spatially more centrally located; note also the relatively quiescent glia more distant from the plaques. Bars = 50μm.

Eric Heuer, et al. Curr Pharm Des. ;18(8):1159-1169.

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