TABLE 1.
Lipid droplet-related literature pertaining to the brain.
| Model organism | Area of interest | Cell type | Author and year of publication | Summary of findings |
| Human | Frontal cortex | Neuron | Paula-Barbosa et al., 1980 | LD-like vesicles visible in cortical dendrites that had abundant degeneration. |
| Frontal lobe | Astrocyte | Miyazu et al., 1991 | Sudanophilic LDs observed in the thalamus of a patient with Nasu-Hakola disease. | |
| Medial temporal | Various | Derk et al., 2018 | DIAPH1 colocalize with LD accumulation in myeloid cells. | |
| Choroid plexus | Adrenal Cortical | Eriksson and Westermark, 1990 | Amyloid inclusions associated with LDs in close contact to fibril bundles. | |
| Whole brain | Neuron | Hulette et al., 1992 | Brain biopsy found ballooned neurons filled with oligolamellar cytosomes and LDs. | |
| Ozsvar et al., 2018 | Demyelination debris contribute to LD formation; volume highest in corpus callosum | |||
| Rat | Cerebral cortex | Neuron | Smialek et al., 1997 | Injection of squalene led to LD accumulation in myelin sheaths of neurons. |
| Hippo-campus | Neuron | Ahdab-Barmada et al., 1986 | Excess oxygen caused neuronal necrosis. Neurons accumulate electron dense LD. | |
| Cole et al., 2002 | The protein α-synuclein was less effective at regulating TAG turnover and showed variable distribution on LDs. | |||
| Median eminence | Tanycyte | Brawer and Walsh, 1982 | The number and size of LDs increased with age. | |
| Olfactory bulbs | Neurons | de Estable-Puig and Estable-Puig, 1973 | LDs are manifestations of cell response to injury. | |
| Perineurium | Perineurial glia | Benstead et al., 1989 | LD formation was found to be an early reactive change to ischemia in perineurial, endothelial, and Schwann cells. | |
| Pineal gland | Pinealocyte | Johnson, 1980 | Removal of the hypophysis led to significant loss of LDs in the pineal gland. | |
| Pituitary gland | Folliculostellate | Stokreef et al., 1986 | Folliculostellate cells became packed with LDs after estrogen withdrawal. | |
| Neuron | Gajkowska and Zareba-Kowalska, 1989 | Supraopticus and paraventricularis neurons show increased LDs post-ischemia. | ||
| Striatum | Neuron | Marasigan et al., 1986 | LDs formed in neurons of rats injected with kainic acid. | |
| Whole brain | Glia | Kamada et al., 2003 | Macrophages and astrocytes play roles in lipid metabolism. | |
| Kamada et al., 2002 | LDs localized w/in microglia in ischemic core and astrocytes in penumbra. | |||
| Choroid plexus | Astrocyte | Ueno et al., 2001 | LD frequently found in several brain regions of senescence-accelerated mice. | |
| Mouse | Frontal lobe | Macrophage | Sturrock, 1983 | About half of macrophages in the brains studied were distended due to excess LDs or foamy aggregations. |
| Medial temporal | Various | Sturrock, 1988 | LDs appeared in the choroid plexus with increased age. | |
| Cortex | Astrocyte | Nakajima et al., 2019 | Inhibition of DAG acyltransferase blocks LD formation and lipotoxic cell death | |
| Autolysosome | Yang et al., 2014 | Lipids impeded macroautophagy and clearance in an AD mouse model. | ||
| Hippo-campus | Neuron, glia | Chali et al., 2019 | Neuronal loss and glial cell proliferation associated with changes in lipid related transcripts. | |
| Ioannou et al., 2019 | Neurons expelled fatty and nearby astrocytes engulfed and stored them as LDs. | |||
| Microglia | Marschallinger et al., 2020 | LD-accumulating microglia were defective in phagocytosis, produced high levels of ROS, and secreted pro-inflammatory cytokines. | ||
| Hypothalamus | Astrocyte | Kwon et al., 2017 | Hypothalamic astrocytes accumulated LDs and had increased cytokines. | |
| Tanycyte | Rawish et al., 2020 | There was high LD signal in mice fed a high at diet, which returned to normal under telmisartan treatment. | ||
| Kim et al., 2020 | A high fat diet increased the number and size of LDs. | |||
| Neuron | Crespo et al., 1995 | Neurons stimulated with CDP-choline displayed LDs in their cytoplasm. | ||
| Mesencephalon | Neuron | Han et al., 2018 | Lipid dysregulation in PD involved upregulated expression of Plin4, increased LD deposition, and loss of neurons. | |
| Neo-striatum | Various | Sturrock, 1980 | Pericytes contained LDs in the neostriatum, indusium griseum, and anterior commissure at various ages. | |
| SVZ | Neuronal stem | Bouab et al., 2011 | Cells with increased numbers of large LDs showed heightened signs of quiescence and metabolic disturbance. | |
| Hamilton et al., 2015 | Impaired FA metabolism suppressed neural stem cell activity | |||
| White matter | Various | Liberski et al., 1989 | Macrophages in mice with Creutzfeldt-Jakob disease were filled with LDs. | |
| Whole brain | Glia | Ogrodnik et al., 2019 | Mice fed high fat diets had increased LDs and cells with more LDs were more likely to be senescent. | |
| Neuron | Hamilton et al., 2010 | Postmortem AD brains and 3xTg mice were shown to accumulate neutral lipids in ependymal cells. | ||
| Various | Shimabukuro et al., 2016 | Lipid-loaded cells displayed a variety of distinct phenotypes based on their location and numbers increased with age. | ||
| Cortex | Glia | Cabirol-Pol et al., 2018 | ND23 knockdown in glial cells created massive LD accumulation and induced brain degeneration. | |
| Kis et al., 2015 | LDs were localized in glia and enriched in the cortex. | |||
| Fly | Whole brain | Neuronal stem | Bailey et al., 2015 | LDs played an antioxidant role in neural stem cells by reducing ROS and protecting against peroxidation. |
| Hypothalamus | Neuron | Nakai et al., 1979 | Large LDs were found in CSF contacting neurons. | |
| Various | HeLa | Papadopoulos et al., 2015 | LD targeting may contribute to HSP pathogenesis. | |
| Glia | Meng et al., 2015 | ROS and neuronal mitochondrial dysfunction contributed to LD accumulation prior to neurodegeneration onset. | ||
| Neuron | Calderon-Garciduenas et al., 2002 | Air pollution caused ApoE-positive LDs to be deposited in SMC and pericytes | ||
| Other | Zebra-fish | Embryo | Arribat et al., 2020 | Loss of spastin resulted in a higher number of smaller LDs. |
| In vitro | Glia | Lucken-Ardjomande Hasler et al., 2014 | GRAF1α was found on LDs in primary glial cells that were fed oleic acid. Overexpression of GRAF1a promoted LD clustering and perturbed lipolysis. | |
| In vitro | In vitro | Glia | Khatchadourian et al., 2012 | LPS treated microglia accumulated LDs and Plin2 colocalized with droplets. |
| Lee et al., 2017 | An increased BBB Ki induced LD formation, activated stress pathways, and increased inflammatory cytokines. | |||
| Farmer et al., 2019 | E4 astrocytes have increased lipid content compared to E3 | |||
| HeLa | Edwards et al., 2009 | Spartin may be recruited to LDs. | ||
| Hooper et al., 2010 | Lack of spartin expression contributes to Troyer syndrome. | |||
| Cole et al., 2002 | PD mutations in α-syn showed less variable LD distribution and less TG turnover. α-syn formed oligomers within cells and associated with LD. | |||
| N41 | Libby et al., 2015 | Cells treated with LPL accumulated lipid into droplets. |
These papers have been classified by the model organism that was used, area of the brain that was studied, and cell type of focus.