bims-metalz Biomed News
on Metabolic causes of Alzheimer’s disease
Issue of 2024‒01‒21
seven papers selected by
Mikaila Chetty, Goa University



  1. Elife. 2024 Jan 15. pii: RP91775. [Epub ahead of print]12
      Visualizing synaptic connectivity has traditionally relied on time-consuming electron microscopy-based imaging approaches. To scale the analysis of synaptic connectivity, fluorescent protein-based techniques have been established, ranging from the labeling of specific pre- or post-synaptic components of chemical or electrical synapses to transsynaptic proximity labeling technology such as GRASP and iBLINC. In this paper, we describe WormPsyQi, a generalizable image analysis pipeline that automatically quantifies synaptically localized fluorescent signals in a high-throughput and robust manner, with reduced human bias. We also present a resource of 30 transgenic strains that label chemical or electrical synapses throughout the nervous system of the nematode Caenorhabditis elegans, using CLA-1, RAB-3, GRASP (chemical synapses), or innexin (electrical synapse) reporters. We show that WormPsyQi captures synaptic structures in spite of substantial heterogeneity in neurite morphology, fluorescence signal, and imaging parameters. We use these toolkits to quantify multiple obvious and subtle features of synapses - such as number, size, intensity, and spatial distribution of synapses - in datasets spanning various regions of the nervous system, developmental stages, and sexes. Although the pipeline is described in the context of synapses, it may be utilized for other 'punctate' signals, such as fluorescently tagged neurotransmitter receptors and cell adhesion molecules, as well as proteins in other subcellular contexts. By overcoming constraints on time, sample size, cell morphology, and phenotypic space, this work represents a powerful resource for further analysis of synapse biology in C. elegans.
    Keywords:  C. elegans; neuroscience; synaptic connectivity; synaptic development; synaptic dimorphisms
    DOI:  https://doi.org/10.7554/eLife.91775
  2. Gerontology. 2024 Jan 16.
      INTRODUCTION: While several antidepressants have been identified as potential geroprotectors, the effect and mechanism of sertraline on healthspan remain to be elucidated. Here, we explored the role of sertraline in lifespan and healthspan of Caenorhabditis elegans (C. elegans).METHODS: The optimal effect concentration of sertraline was first screened in wild-type N2 worms under heat stress conditions. Then, we examined the effects of sertraline on lifespan, reproduction, lipofuscin accumulation, mobility, and stress resistance. Finally, the expression of the 5-HT signaling and aging-related genes was investigated to explore the underlying mechanism, and the lifespan assays were performed in ser-7 RNAi strain, daf-2, daf-16, and aak-2 mutants.
    RESULTS: Sertraline extended lifespan in C. elegans with concomitant extension of healthspan as indicated by increasing mobility and reducing fertility and lipofuscin accumulation, as well as enhanced resistance to different abiotic stresses. Mechanistically, ser-7 orchestrated sertraline-induced longevity via the regulation of insulin and AMPK pathways, and sertraline-induced lifespan extension in nematodes was abolished in ser-7 RNAi strain, daf-2, daf-16, and aak-2 mutants.
    CONCLUSION: Sertraline promotes health and longevity in C. elegans through ser-7-insulin/AMPK pathways.
    DOI:  https://doi.org/10.1159/000536227
  3. Neurotherapeutics. 2023 Dec 19. pii: S1878-7479(23)01900-1. [Epub ahead of print]21(1): e00292
      Recent advances in understanding the role of mitochondrial dysfunction in neurodegenerative diseases have expanded the opportunities for neurotherapeutics targeting mitochondria to alleviate symptoms and slow disease progression. In this review, we offer a historical account of advances in mitochondrial biology and neurodegenerative disease. Additionally, we summarize current knowledge of the normal physiology of mitochondria and the pathogenesis of mitochondrial dysfunction, the role of mitochondrial dysfunction in neurodegenerative disease, current therapeutics and recent therapeutic advances, as well as future directions for neurotherapeutics targeting mitochondrial function. A focus is placed on reactive oxygen species and their role in the disruption of telomeres and their effects on the epigenome. The effects of mitochondrial dysfunction in the etiology and progression of Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and Huntington's disease are discussed in depth. Current clinical trials for mitochondria-targeting neurotherapeutics are discussed.
    Keywords:  Aging; Bioenergetics; Mitochondria; Neurodegeneration; Reactive oxygen species (ROS)
    DOI:  https://doi.org/10.1016/j.neurot.2023.10.002
  4. bioRxiv. 2023 Dec 26. pii: 2023.12.26.573316. [Epub ahead of print]
      In C. elegans , divergent Hedgehog-related (Hh-r) and Patched-related (PTR) proteins promote numerous processes ranging from epithelial and sense organ development to pathogen responses to cuticle shedding during the molt cycle. Here we show that Hh-r proteins are actual components of the cuticle and pre-cuticle apical extracellular matrices (aECMs) that coat, shape, and protect external epithelia. Different Hh-r proteins stably associate with the aECMs of specific tissues and with specific substructures such as furrows and alae. Hh-r mutations can disrupt matrix structure. These results provide a unifying model for the function of nematode Hh-r proteins and highlight ancient connections between Hh proteins and the extracellular matrix.
    DOI:  https://doi.org/10.1101/2023.12.26.573316
  5. Development. 2024 Jan 12. pii: dev.202165. [Epub ahead of print]
      Mitochondria are the powerhouses of many biological processes. During spermatogenesis, post-transcriptional regulation of mitochondrial gene expression is mediated by nuclear-encoded mitochondrial RNA-binding proteins (mtRBPs). We identified AMG-1 as an mtRBP required for reproductive success in C. elegans. amg-1 mutation led to defects in mitochondrial structure and sperm budding, resulting in mitochondria being discarded into residual bodies (RBs), which ultimately delayed spermatogenesis in the proximal gonad. In addition, mitochondrial defects triggered the gonadal mitochondrial unfolded protein response and phagocytic clearance to ensure spermatogenesis but ultimately failed to rescue hermaphroditic fertility. These findings reveal a previously undiscovered role for AMG-1 in regulating C. elegans spermatogenesis, in which mitochondrial-damaged sperm prevented the transmission of defective mitochondria to mature sperm by budding and phagocytic clearance, which may also exist in the reproductive systems of higher organisms.
    Keywords:   Caenorhabditis elegans ; Mitochondria; Mitochondrial unfolded protein response; Phagocytic clearance; Sperm
    DOI:  https://doi.org/10.1242/dev.202165
  6. G3 (Bethesda). 2024 Jan 16. pii: jkae009. [Epub ahead of print]
      Parasitic nematodes are globally important and place a heavy disease burden on infected humans, crops and livestock, while commonly administered anthelmintics used for treatment are being rendered ineffective by increasing levels of resistance. It has recently been shown in the model nematode Caenorhabditis elegans that the sensory cilia of the amphid neurons play an important role in resistance towards macrocyclic lactones such as ivermectin (an avermectin) and moxidectin (a milbemycin) either through reduced uptake or inter-tissue signalling pathways. This study interrogated the extent to which ciliary defects relate to macrocyclic lactone resistance and dye filling defects using a combination of forward genetics and targeted resistance screening approaches and confirmed the importance of intraflagellar transport in this process. This approach also identified the protein trafficking pathways used by the downstream effectors and the components of the ciliary basal body that are required for effector entry into these non-motile structures. In total 24 novel C. elegans anthelmintic survival associated genes were identified in this study. When combined with previously known resistance genes, there are now 46 resistance associated genes which are directly involved in amphid, cilia and IFT function.
    Keywords:   Caenorhabditis elegans ; Amphids; Anthelmintic resistance; Ciliogenesis; Intraflagellar transport; Ivermectin; Macrocyclic lactone; Moxidectin; Xenobiotic resistance
    DOI:  https://doi.org/10.1093/g3journal/jkae009
  7. Cell Stress Chaperones. 2023 Nov;pii: S1355-8145(24)00027-0. [Epub ahead of print]28(6): 909-920
      Oxidative stress is implicated in numerous diseases, with benzo(α)pyrene (BaP) known for causing substantial oxidative damage. Bifidobacterium longum (B. longum) is recognized as an antioxidant bacterium for certain hosts, yet its influence on oxidative damages instigated by BaP remains undetermined. In our study, we introduced various strains of Caenorhabditis elegans (C. elegans) to BaP to trigger oxidative stress, subsequently treating them with different forms of B. longum to evaluate its protective effects. Additionally, we explored the role of daf-16 in this context. Our findings indicated that in wild-type N2 C. elegans, B. longum-even in the form of inactivated bacteria or bacterial ultrasonic lysates (BULs)-significantly extended lifespan. BaP exposure notably decreased lifespan, superoxide dismutase (SOD) activity, and motility, while simultaneously down-regulating the expression of reactive oxygen species (ROS)-associated genes (sod-3, sek-1, cat-1) and daf-16 downstream genes (sod-3, ctl-2). However, it significantly increased the ROS level, malondialdehyde (MDA) content, and lipofuscin accumulation and up-regulated another daf-16 downstream gene (clk-1) (P <0.05). Interestingly, when further treated with B. longum peptide-1 (BLP-1), opposite effects were observed, and all the aforementioned indices changed significantly. In the case of RNAi (daf-16) C. elegans, BaP exposure significantly shortened the lifespan (P <0.05), which was only slightly prolonged upon further treatment with BLP-1. Furthermore, the expression of daf-16 downstream genes showed minor alterations in RNAi C. elegans upon treatment with either BaP or BLP-1. In conclusion, our findings suggest that B. longum acts as a probiotic for C. elegans. BLP-1 was shown to safeguard C. elegans from numerous oxidative damages induced by BaP, but these protective effects were contingent upon the daf-16 gene.
    Keywords:  Benzo(α)pyrene; Bifidobacterium longum peptide-1; Caenorhabditis elegans; Oxidative stress; Probiotics; daf-16
    DOI:  https://doi.org/10.1007/s12192-023-01385-2