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Neuron-Astrocyte Metabolic Coupling Protects against Activity-Induced Fatty Acid Toxicity
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Abstract
Metabolic coordination between neurons and astrocytes is critical for the health of the brain. However, neuron-astrocyte coupling of lipid metabolism, particularly in response to neural activity, remains largely uncharacterized. Here, we demonstrate that toxic fatty acids (FAs) produced in hyperactive neurons are transferred to astrocytic lipid droplets by ApoE-positive lipid particles. Astrocytes consume the FAs stored in lipid droplets via mitochondrial β-oxidation in response to neuronal activity and turn on a detoxification gene expression program. Our findings reveal that FA metabolism is coupled in neurons and astrocytes to protect neurons from FA toxicity during periods of enhanced activity. This coordinated mechanism for metabolizing FAs could underlie both homeostasis and a variety of disease states of the brain.
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“Reactive astrocytes can upregulate VLCFA-rich phosphatidylcholines, which drive the death of neurons and OLs, probably via lipoparticle secretion [415].”
From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [415]
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“Injured neurons and oligodendrocytes have a low capacity for consuming FFAs and sequestering them into LDs61, making them more vulnerable to lipid-induced cytotoxicity in chronic inflammation62,63.”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [63]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This neuron–astrocyte metabolic coupling, mediated by apoE, plays an essential role in preventing activity‐induced lipotoxicity in neurons. 1”
From Protective mechanisms against Alzheimer's disease in APOE3‐Christchurch homozygous astrocytes (2025) · cites this paper as [1]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Ischemia is correlated with both increased lipid peroxidation and neutral lipid accumulation in the brain (Yoshida et al., 1982; Gasparovic et al., 2001; Ioannou et al., 2019).”
From APOE traffics to astrocyte lipid droplets and modulates triglyceride saturation and droplet size (2024) · cites this paper as Ioannou et al., 2019
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“recent reports revealed a role of ApoE in transporting peroxidized FAs from neuron to astrocyte upon neuronal stimulation (Ioannou et al., 2019)”
From ApoE4 Impairs Neuron-Astrocyte Coupling of Fatty Acid Metabolism (2021) · cites this paper as Ioannou et al., 2019
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“Because LDL receptors are involved in neuron-to-astrocyte FA transfer (Ioannou et al., 2019), the lower ability of E4 astrocytes in uptaking LDL (Figure S3E) is consistent with a reduced capacity of E4 astrocytes in internalizing FAs.”
From ApoE4 Impairs Neuron-Astrocyte Coupling of Fatty Acid Metabolism (2021) · cites this paper as Ioannou et al., 2019
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“Strikingly, we observed substantial accumulation of LD-like lipid structures in neurons (Figure 1A; days in vitro 8 [DIV8]) under culture conditions without extra NMDA stimulation or oxidative challenge used previously (Ioannou et al., 2019).”
From ApoE4 Impairs Neuron-Astrocyte Coupling of Fatty Acid Metabolism (2021) · cites this paper as Ioannou et al., 2019
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“while autophagy contributes to LD formation in NMDA-stimulated neurons (Ioannou et al., 2019)”
From ApoE4 Impairs Neuron-Astrocyte Coupling of Fatty Acid Metabolism (2021) · cites this paper as Ioannou et al., 2019
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“Other studies demonstrated that lipid peroxides formed in neurons under oxidative or excitotoxic stress can be transported by APOE-lipoproteins to astrocytes; astrocytes store these neuron-derived lipids in LDs, which protect against neurotoxicity and may play a role in detoxifying these deleterious lipid species (Walker et al., 2006; Liu et al., 2015, 2017; Ioannou et al., 2019; Moulton et al., 2”
From APOE traffics to astrocyte lipid droplets and modulates triglyceride saturation and droplet size (2024) · cites this paper as Ioannou et al., 2019
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In the citing paper
“Other studies demonstrated that lipid peroxides formed in neurons under oxidative or excitotoxic stress can be transported by APOE-lipoproteins to astrocytes; astrocytes store these neuron-derived lipids in LDs, which protect against neurotoxicity and may play a role in detoxifying these deleterious lipid species (Walker et al., 2006; Liu et al., 2015, 2017; Ioannou et al., 2019; Moulton et al., 2”
From APOE traffics to astrocyte lipid droplets and modulates triglyceride saturation and droplet size (2024) · cites this paper as Ioannou et al., 2019
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“Various studies have shown that lipid droplets influence intercellular communication13,17,61.”
From APOE genotypes differentially remodel the astrocytic lipid droplet proteome to shape lipid droplet dynamics (2026) · cites this paper as [61]
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“In the brain, ApoE contributes to a bidirectional metabolic network that couples astrocytes and neurons (Ioannou et al., 2019;Liu et al., 2017;Qi et al., 2021).”
From Isoform- and cell-state-specific lipidation of ApoE in astrocytes (2022) · cites this paper as Ioannou et al., 2019
In the citing paper
“cell culture models have demonstrated that hyperactive neurons can release APOE-associated fatty acids which are taken up by astrocytes and buffer lipotoxic stress35.”
From APOE4/4 is linked to damaging lipid droplets in Alzheimer’s disease microglia (2024) · cites this paper as [35]
In the citing paper
“ApoE-mediated transport of lipids from neurons to glia in flies61 and mammalian cells is neuroprotective62.”
From Decreased lipidated ApoE‐receptor interactions confer protection against pathogenicity of ApoE and its lipid cargoes in lysosomes (2025) · cites this paper as [62]
In the citing paper
“In the CNS, apoE facilitates the transport of cholesterol and FAs between cells, maintaining lipid homeostasis.”
From Protective mechanisms against Alzheimer's disease in APOE3‐Christchurch homozygous astrocytes (2025) · cites this paper as [1]
In the citing paper
“Astrocytes are critical for maintaining central nervous system (CNS) homeostasis, playing essential roles in lipid metabolism and the clearance of toxic protein aggregates.”
From Protective mechanisms against Alzheimer's disease in APOE3‐Christchurch homozygous astrocytes (2025) · cites this paper as [1]
In the citing paper
“Upon oxidative stress or hyperactivity, neurons transfer peroxidized FAs to glia via ApoE-positive lipid particles (Ioannou et al., 2019).”
From ApoE4 Impairs Neuron-Astrocyte Coupling of Fatty Acid Metabolism (2021) · cites this paper as Ioannou et al., 2019
In the citing paper
“Collectively, these genes have been implicated in the coordination of lipid and oxidative metabolism between neurons and astrocytes30.”
From Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and TREM2-independent cellular responses in Alzheimer’s disease (2020) · cites this paper as [30]
In the citing paper
“these results and those of others demonstrate that astrocytes and microglia secrete and degrade a huge array and quantity of lipids”
From Neurotoxic reactive astrocytes induce cell death via saturated lipids (2021) · cites this paper as [21]
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Ju, Y., Li, S., Kong, X., & Zhao, Q. S. (2024) · Scientific Reports · doi:10.1038/s41598-024-82999-z · Cited by 18
“These results suggested the primary role of astrocytes for fatty acid β-oxidation and were consistent with the results of several studies 6,25 .”
Mao, S., Qiao, R., Wang, Q., Shen, L., Li, D., Huo, X., Wang, J., Liu, K., Chen, W., Zhu, T., et al. (2025) · MedComm · doi:10.1002/mco2.70329 · Cited by 17
“Neurological degenerative diseases rank among the primary causes of mortality and disability [10].”
Roles of lactylation in lipid metabolism and related diseases
Zhao, B. T., Lan, Z., Li, C., & Wang, H. (2025) · Cell Death Discovery · doi:10.1038/s41420-025-02705-4 · Cited by 15
“Alterations in neuronal phosphatidylcholine remodeling and FFA – LD coupling between neurons and astrocytes are implicated in its pathogenesis [141, 142].”
Signaling roles for astrocytic lipid metabolism in brain function
Bolaños, J. P., & Almeida, Á. (2026) · EMBO Reports · doi:10.1038/s44319-025-00683-3 · Cited by 16
“This lipid metabolism, particularly mitochondrial fatty acid ß-oxidation (FAO), is not merely an alternative energy source but serves as a crucial regulator of mitochondrial function, reactive oxygen species (ROS) signaling, and neuronal activity (Ioannou et al, 2019; Morant-Ferrando et al, 2023).”
Guoji, E., Sun, B., Liu, B., Xu, G., He, S., Wang, Y., Feng, L., Wei, H., Zhang, J., Chen, J., et al. (2022) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2022.11.002 · Cited by 15
“Among these signaling pathways, the metabolic connection between neurons and astrocytes has been recognized critically for the health of the brain (Bolanos, 2016; Ioannou et al., 2019).”
Cohen, L. D., Ziv, T., & Ziv, N. E. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.1038614 · Cited by 15
“, 2020), serving as a key player in fatty acid (FA) metabolism, by shuttling FA from neurons to astrocyte mitochondria where FAs are processed to produce ATP; the ATP produced in astrocytes then activates interneurons, driving increases in inhibitory transmission (Bowser and Khakh, 2004; Ioannou et al., 2019; Qi et al…”
BackgroundWeng, H., Song, W., Fu, K., Guan, Y., Cai, G., Huang, E., Chen, X., Zou, H., & Ye, Q. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.1035444 · Cited by 13
“Lipid accumulation in glial cells due to reactive oxygen species production and mitochondrial damage leads to further neuronal damage and degeneration (Ioannou et al., 2019).”
BackgroundLópez-López, A., Valenzuela, R., Rodriguez-Perez, A. I., Guerra, M. J., Labandeira-García, J. L., & Muñoz, A. (2023) · Antioxidants · doi:10.3390/antiox12071454 · Cited by 14
Role of Ferroptosis in Glial Cells after Ischemic Stroke
Xu, S., Ni, S.-M., Zeng, C.-L., & Peng, Y. (2023) · Frontiers in Bioscience-Landmark · doi:10.31083/j.fbl2809208 · Cited by 15
“Lipid particle-mediated FA transfer is involved in the deposition of astrocytic LDs after acute stroke and protects neurons from lipid peroxidation [137].”
BackgroundJanda, E., Parafati, M., Martino, C., Crupi, F., William, J. N. G., Reybier, K., Arbitrio, M., Mollace, V., & Boutin, J. A. (2023) · Scientific Reports · doi:10.1038/s41598-023-44666-7 · Cited by 14
Harders, A. R., Spellerberg, P., & Dringen, R. (2024) · Neurochemical Research · doi:10.1007/s11064-024-04104-0 · Cited by 14
“In addition, astrocytes have been shown to contribute to the removal of neuron-derived toxic fatty acids [22, 23].”
BackgroundLee, E. J., Bae, S., Suh, M., Choi, Y., Choi, Y., Hwang, D. W., & Lee, D. S. (2024) · BMC Genomics · doi:10.1186/s12864-024-10434-8 · Cited by 15
“Oligodendrocytes and their associated cell types were designated by following an initial report by Marques et al. [66] and were verified by other investigators’ suggestions [86, 87].”
BackgroundDobolyi, Á., Cservenák, M., Bagó, A. G., Chen, C., Степанова, А., Paál, K., Lee, J., Palkovits, M., Hudson, G., & Chinopoulos, C. (2024) · Communications Biology · doi:10.1038/s42003-024-06751-z · Cited by 14
“The concept of astrocytic mitochondria catabolizing fatty acids has also been demonstrated in murine brain or cultures by the groups of Misgeld 44 , Liu 45 , Johnson 46 and Yin 47 .”
Glia: the cellular glue that binds circadian rhythms and sleep
Carvalhas-Almeida, C., & Sehgal, A. (2025) · SLEEP · doi:10.1093/sleep/zsae314 · Cited by 15
“Under stress conditions, neurons transfer fatty acids to glial cells for temporary storage in lipid droplets and catabolism in the mitochondria, promoting detoxification and energy regulation [125, 126].”
Colas, K., Holmberg, K. O., Chiang, L., Doloczki, S., Swartling, F. J., & Dyrager, C. (2021) · RSC Advances · doi:10.1039/d1ra04419b · Cited by 14
Parkinson disease is a fatty acidopathy
Fanning, S., & Selkoe, D. J. (2025) · Nature Reviews Neurology · doi:10.1038/s41582-025-01142-2 · Cited by 18
Immunometabolism Reframes Alzheimer’s Disease: From Systemic Dysmetabolism to Glial Rewiring
Bach, D., & Nguyen, L. L. (2026) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-026-01691-0 · Cited by 15
“Together, microglia and astrocytes implement a coupled “fuel–inflammation” circuit in which immune activation and metabolic support cannot be analytically separated (Shen et al. 2023 ; Suzuki et al. 2011; Ioannou et al. 2019b).”
InfluentialIsoform- and cell-state-specific APOE homeostasis and function
Lindner, K., & Gavin, A.-C. (2024) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-23-01470 · Cited by 13
“However, recent evidence suggests that in aging, an abnormal accumulation of toxic lipids like TAG and cholesteryl esters in the brain (Clark et al., 2021) changes APOE lipid cargo and its overall behavior from a feeding function to a detoxifying one (Ioannou et al., 2019; Lindner et al., 2022).”
BackgroundInfluentialTamas, C., Tămaș, F., Kövecsi, A., Cehan, A. R., & Bălașa, A. F. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25105482 · Cited by 14
“DGAT1 also prevents mitochondrial dysfunction and lipotoxicity, which can occur in the case of brain pathology [42–44 Physiologically, the formation of LDs is linked to the nutritional state of the cells.”
BackgroundThe Role of Astrocytes in Parkinson’s Disease
Garcia, R., Zarate, S. M., & Srinivasan, R. (2024) · Advances in neurobiology · doi:10.1007/978-3-031-64839-7_13 · Cited by 14
Modulating lipid droplet dynamics in neurodegeneration: an emerging area of molecular pharmacology
Verma, R., Sharma, P., Sharma, V., & Singh, T. G. (2025) · Molecular Biology Reports · doi:10.1007/s11033-025-10381-x · Cited by 14
“Astrocytes then sequester these lipids into LDs, thereby protecting both cell types from lipotoxicity [37].”
Homeostasis of Lipid Metabolism in Disorders of the Brain
Johnson, J. L., & Johnson, L. A. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-819641-0.00146-8 · Cited by 13
Long, C., Li, Z., Jiang, L., Yang, X., Deng, S., Jiang, Y., Zhang, B., & Yue, R. (2025) · Lipids in Health and Disease · doi:10.1186/s12944-025-02747-8 · Cited by 14
“LDs participate in metabolic coupling among certain cell types, such as neurons and astrocytes, where lipid transport, synthesis, and break-down cycles protect neurons from lipid toxicity [180].”
Walecha, V., & Luthra, P. M. (2025) · Neurochemical Research · doi:10.1007/s11064-025-04559-9 · Cited by 12
“This dysregulation of lipid shuttling and degradation initiates metabolic instability within astrocytes, contributing to oxidative stress and pro-inflammatory signalling, where the collapse of mitochondrial function in astrocytes disrupts neuro-glial homeostasis [101 , 100 ].”
Targeting lipid metabolism in neurodegenerative diseases: From experimental to clinical
Long, J., Liu, S., Shi, Y., Zhang, C., Li, Q., & Ai, Q. (2025) · Metabolism · doi:10.1016/j.metabol.2025.156436 · Cited by 12
Wang, Z., Feng, W., Li, X., Yun, X., Wu, S., Du, L., & Wang, H. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103035 · Cited by 15
Cibelli, A., Scemes, E., & Spray, D. C. (2022) · Cells · doi:10.3390/cells11203219 · Cited by 13
Chen, H., Zhao, S., Jian, Q., Yan, Y., Wang, S., Zhang, X., & Ji, Y. (2024) · Molecular Biology Reports · doi:10.1007/s11033-023-08921-4 · Cited by 13
“…neurons produce toxic FAs that are transferred to astrocytes for degradation by ApoE to protect neurons from lipid-mediated toxicity in a process called neuron-astrocyte lipid metabolism coupling, and this coupling mechanism is critical for the overall maintenance of brain health [6, 21–23].”
PCYT1A deficiency disturbs fatty acid metabolism and induces ferroptosis in the mouse retina
Wang, K., Xu, H., Zou, R., Zeng, G., Yuan, Y., Zhu, X., Zhao, X., Li, J., & Zhang, L. (2024) · BMC Biology · doi:10.1186/s12915-024-01932-y · Cited by 12
“Recent studies in the brain have shown that under hyper-activation conditions, neurons produce large amounts of toxic fatty acids, which astrocytes can use and consume, thus protecting neurons from damage [52].”
BackgroundUnleashing metabolic power for axonal regeneration
Yang, X.-Y., & Zhou, B. (2024) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2024.07.001 · Cited by 12
Lutein and zeaxanthin reduce neuronal cell damage caused by lipid peroxidation
Morita, S., Sueyasu, T., Tokuda, H., Kaneda, Y., Izumo, T., & Nakao, Y. (2024) · Biochemistry and Biophysics Reports · doi:10.1016/j.bbrep.2024.101835 · Cited by 12
“Despite their important role in neural lipid metabolism, glial cells were absent from our culture system [35,36].”
BackgroundYin, K., Zhang, T., Lu, X., Shen, Q. X., Gu, K., Huang, Y., Li, C., Hou, J., Li, J., & Zhang, G. (2024) · Cell Reports · doi:10.1016/j.celrep.2024.114983 · Cited by 13
Astrocyte-neuron metabolic crosstalk in ischaemic stroke
Ren, Z., Lan, X., Zheng, Y., Zheng, Y.-X., Chen, C.-A., Liu, Y., He, Y.-H., Han, J.-H., Wang, Q.-G., Cheng, F., et al. (2025) · Neurochemistry International · doi:10.1016/j.neuint.2025.105954 · Cited by 12
Lipid metabolism in health and disease: Mechanistic and therapeutic insights for Parkinson’s disease
Qin, B., Fu, Y., Raulin, A., Kong, S., Li, H., Liu, J., Liu, C., & Zhao, J. (2025) · Chinese Medical Journal · doi:10.1097/cm9.0000000000003627 · Cited by 12
“[19] In PD, disrupted astrocytic lipid metabolism results in LD accumulation, oxidative stress, and inflammation, which amplify neurodegeneration.”
Chou, M., Lee, H., Liu, Y., Yen, P. S.-Y., Liu, C., Chen, C., Hsieh, T.-H., & Chen, S. (2022) · Cells · doi:10.3390/cells11020295 · Cited by 12
“The roles of astrocytes in the homeostasis of lipids in the brain are important, providing essential FAs to neurons and protecting neurons from the toxicity of FAs [23].”
BackgroundInfluentialAltered lipid homeostasis is associated with cerebellar neurodegeneration in SNX14 deficiency
Zhou, Y., Sánchez, V., Xu, P. J., Roulé, T., Flores‐Méndez, M., Ciesielski, B., Yoo, D., Teshome, H., Jimenez, T., Liu, S., et al. (2024) · JCI Insight · doi:10.1172/jci.insight.168594 · Cited by 12
Zhao, Z., Hu, X., Wang, J., Wang, J., Hou, Y., & Chen, S. (2021) · Bioengineered · doi:10.1080/21655979.2021.2012551 · Cited by 12
Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy
Bougnères, P., & Le Stunff, C. (2025) · Genes · doi:10.3390/genes16050590 · Cited by 11
Bhupana, J. N., Pabon, A., Leung, H. H., Asik, R. M., Kim, S., Tong, Y., Jang, M.-H., & Wong, C. (2025) · Nature Communications · doi:10.1038/s41467-025-60402-3 · Cited by 14
“Glial LD expansion observed upon neuronal stress appears to be a protective response 11,13,63,64 .”
The consequences of neurodegenerative disease on neuron-astrocyte metabolic and redox interactions
Jiwaji, Z., & Hardingham, G. E. (2023) · Neurobiology of Disease · doi:10.1016/j.nbd.2023.106255 · Cited by 11
Yang, X., Zhang, J., Wang, Z., Yao, Z., Yang, X. Y., Wang, X., Zhao, X., & Xu, S. (2024) · Neurotherapeutics · doi:10.1016/j.neurot.2024.e00447 · Cited by 11
Hu, H., Cao, B., Huang, D. A., Lin, Y., Zhou, B., Ying, B., Huang, L., & Zhang, L. (2024) · Scientific Reports · doi:10.1038/s41598-024-75284-6 · Cited by 11
Francés, R., Rabah, Y., Préat, T., & Plaçais, P.-Y. (2024) · Nature Communications · doi:10.1038/s41467-024-54778-x · Cited by 12
“…fatty acids with the triple role of fuelling neurons with ketone bodies in times of prolonged starvation 15,17 , sustaining mitochondrial β -oxidation and resulting reactive oxygen species (ROS) production 18 , and embedding per-oxidated lipids produced by neurons to avoid cellular damage 19 – 21 .”
Astrocytic lipid droplets contain MHCII and may act as cogs in the antigen presentation machinery
Beretta, C., Dakhel, A., Eltom, K., Rosqvist, F., Uzoni, S., Mothes, T., Fletcher, J. S., Risérus, U., Sehlin, D., Rostami, J., et al. (2025) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03452-0 · Cited by 12
“The astrocytes support neurons with energy and store excess fatty acids in lipid droplets (LDs) [2–4].”
Neuron–Astrocyte Liaison to Maintain Lipid Metabolism of Brain
Mukherjee, S., & Suresh, S. (2019) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2019.07.018 · Cited by 11
Liu, X., Wei, Q., Yang, X., Wang, X., Zhang, J., Xu, R., Zhang, H., Wang, S., Wan, X., Jiang, L., et al. (2021) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.1c00608 · Cited by 11
Wang, Q., Lu, M., Zhu, X., Gu, X., Zhang, T., Xia, C., Li, Y., Xu, Y., & Zhou, M. (2022) · Aging and Disease · doi:10.14336/ad.2022.0221 · Cited by 11
Emerson, J., Delgado, T., Girardi, P., & Johnson, G. V. W. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076058 · Cited by 12
“In this assay, astrocytes were seeded on PDL-coated glass coverslips and sandwiched with neuron-seeded coverslips, separated only by paraffin pedestals as described previously [34].”
MethodInfluentialGrease on—Perspectives in lipid droplet biology
Beller, M., Herker, E., & Füllekrug, J. (2020) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2020.06.017 · Cited by 12
Peptide Profile of Zebrafish Brain in a 6-OHDA-Induced Parkinson Model
Fiametti, L. O., Correa, C. N., & de Castro, L. M. (2021) · Zebrafish · doi:10.1089/zeb.2020.1945 · Cited by 11
“58,59 Apolipoprotein A-II has been identified as a biomarker in cerebrospinal fluid, blood, and also in choroid plexus homogenates in patients with Parkinson’s and Alzheimer’s disease.”
Noncanonical Transmission of a Measles Virus Vaccine Strain from Neurons to Astrocytes
Poelaert, K. C. K., Williams, R. M., Matullo, C. M., & Rall, G. F. (2021) · mBio · doi:10.1128/mbio.00288-21 · Cited by 11
“The astrocytes were separated from the neurons by a small bead of paraffin wax (approximately 5mm), as previously described (33), and cocultured for 72 h.”
BackgroundMethodLipid metabolism and metabolites: emerging roles in systemic physiology and metabolic diseases
Xu, J., Lu, D., & Huang, X. (2026) · Journal of genetics and genomics/Journal of Genetics and Genomics · doi:10.1016/j.jgg.2026.01.006 · Cited by 13
Metadata
- Authors
- Ioannou, M. S., Jackson, J., Sheu, S.-H., Chang, C.-L., Weigel, A. V., Liu, H., Pasolli, H. A., Xu, C. S., Pang, S., Matthies, D., Hess, H. F., Lippincott-Schwartz, J., & Liu, Z.
- Affiliations
- Howard Hughes Medical Institute (US)
- University of Alberta (CA)
- Corresponding author
- Ioannou, Maria S.
- Liu, Zhe
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2019-05
- Volume
- 177
- Issue
- 6
- Pages
- 1522-1535.e14
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2946373463
- Cited by
- 760
- References
- 72
- Citations by year
- 2026: 129 · 2025: 150 · 2024: 133 · 2023: 117 · 2022: 74 · 2021: 92 · 2020: 47 · 2019: 15
- FWCI
- 23.82
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- fatty acid toxicity, lipid droplets, apolipoprotein E, mitochondrial beta-oxidation, fatty acid metabolism, neuronal hyperactivity, astrocytes, lipid metabolism, neuroprotection
- MeSH terms
- Animals, Apolipoproteins E, Astrocytes, Brain, Fatty Acids, Homeostasis, Male, Mice, Inbred C57BL, Mitochondria, Neurons, Oxidation-Reduction, Rats, Sprague-Dawley, Mice, Knockout, Lipid Metabolism, Mice, Rats, Lipid Droplets
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