Fig 1: β-amyloid accumulation in the dorsolateral PFC (dlPFC) and hippocampal dentate gyrus from human autopsy HIV-infected cases with HAND. (A–F) Representative images of double staining of β-amyloid with NeuN (a neuronal marker) in the dlPFC (A–C), and in the hippocampus from human autopsy (D–F). (G,H) Confocal images of amyloid precursor protein expression in the dlPFC and hippocampus. (I) Quantification of β-amyloid and amyloid precursor protein expression in the dlPFC and hippocampus.
Fig 2: IHC double staining revealed an abnormal intraneuronal accumulation of β-amyloid in the HIV-1 Tg rat. (A,B) Representative confocal images of β-amyloid expression and co-localization with NeuN (neuronal marker) in the mPFC and CA3 area of hippocampus in F344/N and HIV-1 Tg rats. The Alexa 488 green fluorescence indicates expression of β-amyloid; the Alexa 594 red fluorescence represents NeuN signals. (C) Representative images of amyloid precursor protein (APP) expression in the mPFC and hippocampal CA3 region in HIV-1 Tg and F344/N rats. APP expression is indicated by green fluorescence. (D) HIV-1 Tg rats exhibited abnormal accumulation of β-amyloid in both the mPFC and hippocampal CA3 region relative to control animals. (E) Statistical evaluation of APP in the mPFC and hippocampal CA3 areas compared to control rat. Statistically significant (p ≤ 0.05) differences between HIV-1 Tg and control animals are indicated using an *.
Fig 3: Depletion of IL-10 in microglia significantly attenuates diabetes-associated cerebral atherosclerosis in mice. (A) Atherosclerotic lesion size in the aortic arc. (B) The weight of left ventricle (LV mass). (C) Cerebral blood flow. (D) Flow cytometry analysis and sorting of GFP+ cells or NeuN+ cells from mouse brains at analysis. (E) ELISA for TGFβ1 in GFP+ microglia. (F) ELISA for Caspase 3 (Casp3) in NeuN+ neuronal cells. *p < 0.05. ns: non-significant. N = 5.
Fig 4: Reduced SOD1 aggregation in SOD1*G93A mice treated with Atp1a2 ASOs without altering motor neuron loss.(A) Overview of experimental design. ASO1 (50μg, n = 23 mice:10 females, 13 males), ASO3 (25μg) or ctrl ASO (50 and 25μg; n = 21 mice: 10 females, 11 males in ASO3 and each control group) were delivered via ICV in 5–8 weeks old SOD1*G93A mice, prior to disease onset. (B) Atp1a2 mRNA measured in spinal cords from end-stage SOD1*G93A mice treated with ASO1 (50μg), ASO3 (25μg) or ctrl ASO. Unpaired t-test with Welch’s correction, **p < 0.01, *p<0.05 (C). Representative immunoblots of detergent soluble and insoluble fractions of spinal cords from end-stage SOD1*G93A mice treated with single dose ICV injection of ASO1 (top panel) or ASO3 (bottom panel). (D) Quantification of relative aggregation propensity ‐ an index of the amount of SOD1 in the detergent-insoluble fraction (P2) compared to the detergent-soluble fraction (S1), n = 9 mice per group. Unpaired t-test with Welch’s correction, ***p<0.001, **p < 0.01. (E, F) Immunohistochemistry for motor neuron markers (NeuN, red and ChAT, cyan) and misfolded SOD1 (mfSOD1 C4F6, green) in spinal cord tissue from ctrl and ASO1- (E) or ASO3-treated (F) mice; DAPI-stained nuclei shown in blue in overlay images. (G, H) Quantification of ChAT+ motor neurons (MNs)/section in ASO1 v ctrl-treated mice in (G) and ASO3 v ctrl-treated mice in (H). Representative images at 20x magnification from n = 3 mice for ASO1 v ctrl and n = 2 mice for ASO3 v ctrl are shown in (E, F), scale bar represents 100μm and 3–4 sections per mouse were counted in a blinded manner, ns = not significant by unpaired t-test with Welch’s correction.
Fig 5: Circ_0000811 overexpression alleviated experimental CI-induced vertigo in mice.A qRT-PCR to determine the expression of circ_0000811 in the MVN of mice with CI-induced vertigo in response to circ_0000811 overexpression; B the escape latency of mice with CI-induced vertigo in response to circ_0000811 overexpression; C the decrease rate of blood flow in the MVN of mice with CI-induced vertigo in response to circ_0000811 overexpression; D H&E and Nissl staining to detect the histopathological changes of the MVN of mice with CI-induced vertigo in response to circ_0000811 overexpression; E NeuN/Annexin counterstaining to detect the apoptotic rate of neurons in the MVN of mice with CI-induced vertigo in response to circ_0000811 overexpression. ***p < 0.001 compared with the Vertigo + oe-NC group. The independent sample t test was applied for the comparison between two groups. CI cerebral ischemia, qRT-PCR quantitative reverse-transcription polymerase chain reaction, MVN medial vestibular nucleus, H&E hematoxylin and eosin; NeuN neuronal nuclei.
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