Journal: Molecular Biomedicine

Article Title: Docosahexaenoic acid remodels lipid composition of lipid rafts and mitochondrial function in ApoE4/4 mouse brain: a multi-omic investigation

doi: 10.1186/s43556-026-00618-x

Figure Lengend Snippet: Growth, Behavioral Performance, and Cortical AD-Related Marker Levels in Mice. a Schematic overview of the experimental design. b - c Changes in body weight ( b ) and dietary intake ( c ) of mice in each group during the intervention period ( N ≥ 7, mean ± SEM). d - e Morris water maze performance: acquisition phase ( d ) and probe trial ( e ) ( N ≥ 7, mean ± SEM). f Cortical ApoE levels (pg/mg protein) ( N = 4). g : Cortical Aβ 1–42 , Aβ 1–40 and Aβ 1–40/Aβ1–42 ratios (pg/mg protein) ( N = 4). h – l Cortical expression of proteins related to Aβ synthesis and degradation ( h ), tau protein and phosphorylated tau( j - l ) ( N ≥ 3). ApoE, apolipoprotein E; Aβ, amyloid-beta protein; APP, amyloid precursor protein; BACE1, β-site APP cleaving enzyme 1; LRP1, low-density lipoprotein receptor-related protein 1; IDE, insulin-degrading enzyme; TAU, tau protein. Statistical significance: *** P < 0.001, ** P < 0.01, * P < 0.05, ### P < 0.001, ## P < 0.01, # P < 0.05 vs. corresponding group after 6-month intervention

Article Snippet: The levels of ApoE (RK00231, ABclonal, China), Aβ 1–40 (E-EL-M3009, Elabscience, China), and Aβ 1–42 (E-EL-M3010, Elabscience, China) were quantified following the instructions.

Techniques: Marker, Expressing, Transmission Electron Microscopy, Polymerase Chain Reaction

Journal: CNS Neuroscience & Therapeutics

Article Title: mTORC1 Activation Links Chronic Stress to Meso‐Circuit Desynchronization and Accelerated Amyloid Pathology via Autophagic Dysfunction

doi: 10.1002/cns.71174

Figure Lengend Snippet: CRS‐induced depression exacerbates Aβ deposition, axonal dystrophy, and neuroinflammation in 5xFAD mice. (a) Representative panoramic and high‐magnification confocal images of brain sections from PFC of 5xFAD and 5xFAD + CRS mice, stained with Congo red (red, amyloid plaques) and DAPI (gray, nuclei). (b) Cumulative frequency distribution of amyloid plaque size. Inset histogram quantifies the plaque size ( n = 12 mice per group, 61–235 plaques analyzed and averaged per mouse, Mann–Whitney test). (c) Quantification of amyloid plaque density in PFC, expressed as the number of plaques per square millimeter ( n = 12 mice per group, 3–5 fields of view analyzed and averaged per mouse, Mann–Whitney test). (d) ELISA quantification of Aβ40 concentrations in TBS‐, SDS‐, and FA‐soluble fractions, sequentially extracted from cortical homogenates ( n = 12 mice per group, Mann–Whitney test). (e) ELISA quantification of Aβ42 concentrations in TBS‐, SDS‐, and FA‐soluble fractions, sequentially extracted from cortical homogenates ( n = 12 mice per group, Mann–Whitney test). (f) Representative high‐resolution confocal micrographs demonstrating dystrophic neurites surrounding the periphery of amyloid plaques, co‐stained for LAMP1 (dystrophic neurites marker) and plaque cores (Congo red, white). (g) Statistical analysis of plaque‐associated dystrophic neurites size ( n = 12 mice per group, 4–8 dystrophic neurites analyzed and averaged per mouse; Mann–Whitney test). (h) Statistical analysis of plaque‐associated dystrophic neurites density ( n = 12 mice per group, 2–3 fields of view analyzed and averaged per mouse, Mann–Whitney test). (i) Representative immunostaining images of astrogliosis in the prefrontal cortex, labeled with GFAP (red) and DAPI (blue). Right panels show magnified single‐astrocyte morphology (top) and the corresponding skeletonized reconstruction used for morphometric profiling (bottom). (j) Quantitative morphometric evaluation of astrocyte complexity, indicated by the total number of intersections derived from Sholl analysis ( n = 12 mice per group, 2–4 astrocytes analyzed and averaged per mouse, Mann–Whitney test). (k) Representative immunostaining images of microglia in the prefrontal cortex, labeled with IBA1 (red) and DAPI (blue). Right panels display magnified single‐microglia morphology (top) and the corresponding skeletonized reconstruction used for morphometric profiling (bottom). (l) Quantitative analysis of microglial ramification, showing the total number of intersections from Sholl analysis ( n = 12 mice per group, 3–4 microglia analyzed and averaged per mouse, Mann–Whitney test). Each dot represents an individual animal. Error bars represent mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, ns = no significance.

Article Snippet: Aβ levels were quantified via commercial ELISA kits (Elabscience, E‐UNEL‐H0256 and E‐EL‐H0543) and normalized to total protein concentration.

Techniques: Confocal, Staining, MANN-WHITNEY, Enzyme-linked Immunosorbent Assay, Marker, Analysis, Immunostaining, Labeling, Morphology, Profiling, Derivative Assay

Journal: CNS Neuroscience & Therapeutics

Article Title: mTORC1 Activation Links Chronic Stress to Meso‐Circuit Desynchronization and Accelerated Amyloid Pathology via Autophagic Dysfunction

doi: 10.1002/cns.71174

Figure Lengend Snippet: EN6 attenuates amyloid deposition by shifting the APP processing pathway in depression‐AD comorbidity. (a) Representative panoramic and high‐magnification confocal micrographs of coronal brain sections containing the PFC from 5xFAD + CRS + Vehicle and 5xFAD + CRS + EN6 mice, co‐stained with Congo red (red, amyloid plaques) and DAPI (gray, nuclei). (b) Statistical assessment of PFC amyloid plaque burden. Cumulative distribution of amyloid plaque size. Inset plot quantifies the plaque size ( n = 13 mice per group, 93–209 plaques analyzed and averaged per mouse, Mann–Whitney test). (c) Statistical assessment of PFC plaque density ( n = 13 mice per group, 3–5 fields of view analyzed and averaged per mouse, Mann–Whitney test). (d) ELISA quantification of Aβ40. Peptide concentrations (ng/g) in TBS‐, SDS‐, and FA‐soluble fractions sequentially extracted from cortical homogenates ( n = 13 mice per group, Mann–Whitney test). (e) ELISA quantification of Aβ42. Peptide concentrations (ng/g) in TBS‐, SDS‐, and FA‐soluble fractions sequentially extracted from cortical homogenates ( n = 13 mice per group, Mann–Whitney test). (f) Representative blot bands showing the protein expression levels of full‐length APP (APPfl), soluble APPα (sAPPα), and C‐terminal fragments CTFβ and CTFα in cortical tissue from the indicated groups. (g–j) Quantification of protein abundance normalized to ACTB, including: APPfl/ACTB, sAPPα/ACTB, CTFβ/ACTB, and CTFα/ACTB ( n = 6 mice per group, Mann–Whitney test). (k) Representative blot bands of APP‐cleaving secretases, including ADAM10 (α‐secretase), BACE1 (β‐secretase), and PS1 (γ‐secretase catalytic subunit) in cortical homogenates. (l–n) Densitometric analysis of secretase expression normalized to ACTB: ADAM10/ACTB, BACE1/ACTB, and PS1/ACTB ( n = 6 mice per group, Mann–Whitney test). Each dot represents an individual animal. Error bars represent mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, ns = no significance.

Article Snippet: Aβ levels were quantified via commercial ELISA kits (Elabscience, E‐UNEL‐H0256 and E‐EL‐H0543) and normalized to total protein concentration.

Techniques: Confocal, Staining, MANN-WHITNEY, Enzyme-linked Immunosorbent Assay, Expressing, Tissue, Quantitative Proteomics, Analysis