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APOE4 Causes Widespread Molecular and Cellular Alterations Associated with Alzheimer’s Disease Phenotypes in Human iPSC-Derived Brain Cell Types
Open accessAbstract
The apolipoprotein E4 (APOE4) variant is the single greatest genetic risk factor for sporadic Alzheimer's disease (sAD). However, the cell-type-specific functions of APOE4 in relation to AD pathology remain understudied. Here, we utilize CRISPR/Cas9 and induced pluripotent stem cells (iPSCs) to examine APOE4 effects on human brain cell types. Transcriptional profiling identified hundreds of differentially expressed genes in each cell type, with the most affected involving synaptic function (neurons), lipid metabolism (astrocytes), and immune response (microglia-like cells). APOE4 neurons exhibited increased synapse number and elevated Aβ 42 secretion relative to isogenic APOE3 cells while APOE4 astrocytes displayed impaired Aβ uptake and cholesterol accumulation. Notably, APOE4 microglia-like cells exhibited altered morphologies, which correlated with reduced Aβ phagocytosis. Consistently, converting APOE4 to APOE3 in brain cell types from sAD iPSCs was sufficient to attenuate multiple AD-related pathologies. Our study establishes a reference for human cell-type-specific changes associated with the APOE4 variant. VIDEO ABSTRACT.
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“induced pluripotent stem cells (iPSC)-derived neurons from LOAD patients expressing ApoE4 secrete higher levels of Aβ, when compared to ApoE3-expressing neurons”
From Apoe4 and Alzheimer’s Disease Pathogenesis—Mitochondrial Deregulation and Targeted Therapeutic Strategies (2023) · cites this paper as [39]
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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
“In addition, APOE4 was found to reduce the phagocytosis ability of glial cells, enhance microglia proinflammatory activation by Aβ plaques or tau aggregates and promote neurodegeneration in the mouse models.176,177”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [177]
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
“Studies that have successfully targeted APOE using gene editing in induced pluripotent stem cells (iPSCs) provide strong proof of concept that in vitro editing of ε4 to ε3 or ε2 simultaneously ‘corrects’ several phenotypes, including glial transcriptomic profiles, lipid metabolism and other functional measures7,8.”
From APOE4 to APOE2 allelic switching in mice improves Alzheimer’s disease-related metabolic signatures, neuropathology and cognition (2025) · cites this paper as [8]
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
“In disease models, ApoE4 perturbs cholesterol regulation, including expression of cholesterol metabolism-related genes, cholesterol transport and esterification10–13.”
From Decreased lipidated ApoE‐receptor interactions confer protection against pathogenicity of ApoE and its lipid cargoes in lysosomes (2025) · cites this paper as [11]
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
“The characterization of hIPSC-derived neurons indicates that neuronal APOE4 is associated with altered synaptic function, fatty acid accumulation and hyperexcitability143.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [143]
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In the citing paper
“Astrocytes derived from APOE4 human-inducible pluripotent stem cells (hiPSCs) are less efficient at secreting lipidated APOE particles and exhibit impaired cholesterol metabolism relative to APOE3 hiPSC-derived astrocytes143,144.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [143]
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.
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“APOE4 astrocytes have an increased number of lipid droplets and impaired glucose utilization and mitochondrial function, lending further support to this hypothesis143,146,147 (Fig. 2b).”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [143]
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
“Studies with human iPSC-derived neurons and organoids confirm that apoE4 increases Aβ production and aggregation as well as decreases Aβ clearance”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Lin et al 2018
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
“Studies with human iPSC-derived neurons and cerebral organoids demonstrate that apoE4 enhances tau phosphorylation and exacerbates synapse loss and neurodegeneration”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Lin et al 2018
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
“Recent studies on human induced pluripotent stem cells (iPSCs) with the APOE4 variant showed altered transcriptomic and metabolomic profiles toward the accumulation of cholesterol in glia, such as astrocytes and oligodendrocytes.5”
From ApoE4-dependent lysosomal cholesterol accumulation impairs mitochondrial homeostasis and oxidative phosphorylation in human astrocytes (2023) · cites this paper as [5]
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
“Three ApoE3 and ApoE4 isogenic iPSCs pairs were used to determine the effect of APOE4 genotype without inter-donor variability.5”
From ApoE4-dependent lysosomal cholesterol accumulation impairs mitochondrial homeostasis and oxidative phosphorylation in human astrocytes (2023) · cites this paper as [5]
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
“Multiple transcriptomic studies of APOE4-expressing iPSC-derived astrocytes and microglia demonstrate alterations in the expression of lipid metabolic genes as well as defects in cholesterol trafficking and metabolism (Lin et al., 2018; de Leeuw et al., 2022; Tcw et al., 2022).”
From APOE traffics to astrocyte lipid droplets and modulates triglyceride saturation and droplet size (2024) · cites this paper as Lin et al., 2018
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
“CRISPR/Cas9 technology, which allow precise genetic modifications, was used to convert APOE ε4 into APOE ε3 in neuronal, astrocytic and microglial cells types from iPSCs derived from LOAD patients, which led to the attenuation of some AD-related pathologies, namely Aβ glial uptake [39].”
From Apoe4 and Alzheimer’s Disease Pathogenesis—Mitochondrial Deregulation and Targeted Therapeutic Strategies (2023) · cites this paper as [39]
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
“The fact that human iPSC-derived APOE4/E4 astrocytes were recently reported to accumulate endolysosomal cholesterol”
From TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge (2020) · cites this paper as Lin et al., 2018
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
“ApoE4 drives the accumulation of lipids and increased inflammatory cytokine production in vitro in human induced pluripotent stem cell (iPSC)-derived astrocytes, microglia, and oligodendrocytes.”
From Amelioration of Tau and ApoE4-linked glial lipid accumulation and neurodegeneration with an LXR agonist (2024) · cites this paper as [8]
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
“Multiple studies on astrocytes, microglia, and oligodendrocytes derived from iPSCs demonstrate an important role for ApoE4 in cholesterol metabolism pathways.6”
From Amelioration of Tau and ApoE4-linked glial lipid accumulation and neurodegeneration with an LXR agonist (2024) · cites this paper as [8]
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
“Along the same lines, ApoE4 increased the number and size of early endosomes in AD patients (Cataldo et al., 2000) and in neurons derived from induced pluripotent stem cells (Lin et al., 2018).”
From Reversal of ApoE4-induced recycling block as a novel prevention approach for Alzheimer’s disease (2018) · cites this paper as Lin et al., 2018
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
“In this regard, transcriptomic studies of ApoE4 astrocytes deriving from human-induced pluripotent stem cells (hiPSCs) of AD patients demonstrated that lipid metabolism is one of main altered processes [15,16].”
From ApoE3 vs. ApoE4 Astrocytes: A Detailed Analysis Provides New Insights into Differences in Cholesterol Homeostasis (2022) · cites this paper as [16]
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
“Recently, it has been shown that cholesterol homeostasis is also impaired in ApoE4 astrocytes, although controversial data concerning intracellular and secreted cholesterol levels are present in literature depending on the different experimental model employed [15,16,24].”
From ApoE3 vs. ApoE4 Astrocytes: A Detailed Analysis Provides New Insights into Differences in Cholesterol Homeostasis (2022) · cites this paper as [16]
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
“Similarly, although both groups could perform phagocytosis, both the percentage of phagocytic cells and the phagocytic index were lower in AD than in healthy control iMGs (Fig. 2H, Supplementary Fig. 2F), as has been previously reported in human iPSC-derived microglia with altered expression of AD risk genes [60–64].”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [60]
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
“Notable shared features include reduced phagocytosis, previously reported in human iPSC-derived microglia with altered expression of AD risk genes [60–64], and increased expression of inflammatory genes (such as complement C3), consistent with findings from human AD brain and APOE4/4 iPSC-derived microglia [52, 60, 61].”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [60]
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
“Notably, iPSC-derived microglia with altered expression of the sAD risk genes APOE4 and TREM2 display pronounced phenotypic differences from control microglia, such as impaired phagocytosis, whereas mutations involved in familial AD have a more limited impact on microglial function [51, 60–63, 119–122].”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [60]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The APOE genotype has a widespread impact on cell-autonomous and non-autonomous biological processes14.”
From APOE4 impairs myelination via cholesterol dysregulation in oligodendrocytes (2022) · cites this paper as [14]
The cited source says what the claim attributes to it.
In the citing paper
“APOE ε4 is known to disrupt lipid homeostasis and immune response and to cause mitochondrial dysfunction [31–34]”
From Protective PLCG2 variants associate with a delayed onset of Alzheimer’s disease among heterozygous APOE ε4 carriers (2026) · cites this paper as [32]
The cited source says what the claim attributes to it.
In the citing paper
“Interestingly, astrocytes generated from hiPSC derived from fibroblasts obtained from patients with CNS diseases (usually with a genetic mutation causative of disease or a risk polymorphism) show pathological phenotypes, including dysregulation of lipid metabolism11, alteration in the contents of the extracellular vesicles released by astrocytes80, reduced autophagy81, or altered STAT3 signaling82”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [11]
The cited source says what the claim attributes to it.
In the citing paper
“are rapidly becoming commonplace in basic research11,82 and therapy development109”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [11]
The cited source says what the claim attributes to it.
In the citing paper
“APOE4 microglia-like hiPSCs show decreased phagocytosis and increased inflammatory genes relative to APOE3 microglia143.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [143]
The cited source says what the claim attributes to it.
In the citing paper
“These results demonstrate an isoform-dependent regulation of APOE protein levels, as was previously shown for E3 and E4 in vitro, or in patient cerebrospinal fluid (CSF) (Lin et al., 2018; Mahley, 2016).”
From APOE2, E3, and E4 differentially modulate cellular homeostasis, cholesterol metabolism, and inflammatory response in isogenic iPSC-derived astrocytes (2022) · cites this paper as Lin et al., 2018
The cited source says what the claim attributes to it.
In the citing paper
“ApoE4 astrocytes displayed reduced levels of ApoE and impaired Aβ clearance compared with ApoE3 astrocytes”
From ApoE4-dependent lysosomal cholesterol accumulation impairs mitochondrial homeostasis and oxidative phosphorylation in human astrocytes (2023) · cites this paper as [5]
The cited source says what the claim attributes to it.
In the citing paper
“ApoE4 astrocytes displayed reduced levels of ApoE and impaired Aβ clearance compared with ApoE3 astrocytes”
From ApoE4-dependent lysosomal cholesterol accumulation impairs mitochondrial homeostasis and oxidative phosphorylation in human astrocytes (2023) · cites this paper as [5]
The cited source says what the claim attributes to it.
In the citing paper
“we found a significant accumulation of cholesterol in ApoE4 astrocytes compared with ApoE3 astrocytes”
From ApoE4-dependent lysosomal cholesterol accumulation impairs mitochondrial homeostasis and oxidative phosphorylation in human astrocytes (2023) · cites this paper as [5]
The cited source says what the claim attributes to it.
In the citing paper
“because ApoE is also expressed in neurons under stress conditions (Xu et al., 2006), neurons cultured in vitro (Lin et al., 2018; Xu et al., 1999b), and neurons of selected brain regions in vivo (Han et al., 1994; Xu et al., 1999a)”
From ApoE4 Impairs Neuron-Astrocyte Coupling of Fatty Acid Metabolism (2021) · cites this paper as Lin et al., 2018
The cited source says what the claim attributes to it.
In the citing paper
“In agreement with our data, significantly reduced ApoE levels were also observed in hiPSC-derived ApoE4 astrocytes [15,16,24], as well as in brain homogenates from mouse models expressing the human ApoE4 isoform [43,44].”
From ApoE3 vs. ApoE4 Astrocytes: A Detailed Analysis Provides New Insights into Differences in Cholesterol Homeostasis (2022) · cites this paper as [16]
The cited source says what the claim attributes to it.
In the citing paper
“These results, together with those obtained by transcriptomic and proteomic analyses of hiPSC-derived astrocytes [15,16], further confirm that lipid metabolism is one of the main altered processes in ApoE4 astrocytes.”
From ApoE3 vs. ApoE4 Astrocytes: A Detailed Analysis Provides New Insights into Differences in Cholesterol Homeostasis (2022) · cites this paper as [16]
In the citing paper
“and that the APOE ε4 variant associated with increased risk of Alzheimer’s Disease causes functional changes in neurons, astrocytes and microglia9.”
From CRISPR-based functional genomics for neurological disease (2020) · cites this paper as [9]
In the citing paper
“Furthermore, iPSC-derived cell types from different lineages can be combined into defined three-dimensional cultures, termed assembloids9,94–98.”
From CRISPR-based functional genomics for neurological disease (2020) · cites this paper as [9]
In the citing paper
“APOE ε4 also affects properties of iPSC-derived astrocytes and microglia, notably reducing their ability to clear Aβ9,102.”
From CRISPR-based functional genomics for neurological disease (2020) · cites this paper as [9]
In the citing paper
“Alterations of ApoE synthesis and release have been shown to characterize hiPSCs-derived ApoE4 astrocytes [15,16,24].”
From ApoE3 vs. ApoE4 Astrocytes: A Detailed Analysis Provides New Insights into Differences in Cholesterol Homeostasis (2022) · cites this paper as [16]
In the citing paper
“studies suggest that lower levels of ApoE receptors in the astrocytic membrane may lead to the reduced ability of ApoE4 astrocytes to clear Aβ [16,73].”
From ApoE3 vs. ApoE4 Astrocytes: A Detailed Analysis Provides New Insights into Differences in Cholesterol Homeostasis (2022) · cites this paper as [16]
In the citing paper
“ApoE4 has been shown to impact on many physiological functions played by astrocytes, affecting their ability to clear Aβ, to uptake glutamate, to promote neuronal synaptogenesis, and to maintain lipid homeostasis [15,16,42].”
From ApoE3 vs. ApoE4 Astrocytes: A Detailed Analysis Provides New Insights into Differences in Cholesterol Homeostasis (2022) · cites this paper as [16]
In the citing paper
“Our results further highlight the link between cholesterol metabolism, astrocyte dysfunction and neurodegeneration, emphasizing the role of cholesterol exposure in driving astrocyte-mediated neurotoxicity70–72.”
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Citations
Cites
Fast and accurate short read alignment with Burrows-Wheeler transform
Li, H., & Durbin, R. (2009) · Bioinformatics · doi:10.1093/bioinformatics/btp324 · Cited by 58,607
Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
STAR: ultrafast universal RNA-seq aligner
Dobin, A., Davis, C. A., Schlesinger, F., Drenkow, J., Zaleski, C., Jha, S., Batut, P., Chaisson, M., & Gingeras, T. R. (2013) · Bioinformatics · doi:10.1093/bioinformatics/bts635 · Cited by 51,709
Robinson, M. D., McCarthy, D. J., & Smyth, G. K. (2010) · Bioinformatics · doi:10.1093/bioinformatics/btp616 · Cited by 41,364
The Genome Analysis Toolkit: A MapReduce framework for analyzing next-generation DNA sequencing data
McKenna, A., Hanna, M., Banks, E., Sivachenko, A., Cibulskis, K., Kernytsky, A., Garimella, K., Altshuler, D., Gabriel, S., Daly, M., et al. (2010) · Genome Research · doi:10.1101/gr.107524.110 · Cited by 27,895
WGCNA: an R package for weighted correlation network analysis
Langfelder, P., & Horvath, S. (2008) · BMC Bioinformatics · doi:10.1186/1471-2105-9-559 · Cited by 27,252
featureCounts: an efficient general purpose program for assigning sequence reads to genomic features
Liao, Y., Smyth, G. K., & Shi, W. (2014) · Bioinformatics · doi:10.1093/bioinformatics/btt656 · Cited by 27,219
Model-based Analysis of ChIP-Seq (MACS)
Zhang, Y., Liu, T., Meyer, C. A., Eeckhoute, J., Johnson, D. S., Bernstein, B. E., Nusbaum, C., Myers, R. M., Brown, M., Li, W., et al. (2008) · Genome Biology · doi:10.1186/gb-2008-9-9-r137 · Cited by 18,386
Robinson, J. T., Thorvaldsdóttir, H., Winckler, W., Guttman, M., Lander, E. S., Getz, G., & Mesirov, J. P. (2011) · Nature Biotechnology · doi:10.1038/nbt.1754 · Cited by 15,390
ANNOVAR: functional annotation of genetic variants from high-throughput sequencing data
Wang, K., Li, M., & Hakonarson, H. H. (2010) · Nucleic Acids Research · doi:10.1093/nar/gkq603 · Cited by 14,724
Flagged first, then by citations
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Items 401–500 of 1,002
Salwa, & Kumar, L. (2021) · Journal of Controlled Release · doi:10.1016/j.jconrel.2021.09.007 · Cited by 32
Microglial transcription profiles in mouse and human are driven by APOE4 and sex
Moser, V. A., Workman, M. J., Hurwitz, S. J., Lipman, R. M., Pike, C. J., & Svendsen, C. N. (2021) · iScience · doi:10.1016/j.isci.2021.103238 · Cited by 29
Liu, Z., Chao, J., Wang, C., Sun, G., Roeth, D., Liu, W., Chen, X., Li, L., Tian, E., Feng, L., et al. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.112841 · Cited by 30
Yang, J., Shi, X., Wang, Y., Ma, M., Liu, H., Wang, J., & Xu, Z. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230593 · Cited by 33
Astrocytes: From the Physiology to the Disease
Trujillo‐Estrada, L., Gómez-Arboledas, Á., Forner, S., Martini, A. C., Gutiérrez, A., Baglietto‐Vargas, D., & LaFerla, F. M. (2019) · Current Alzheimer Research · doi:10.2174/1567205016666190830110152 · Cited by 30
Culprit or Bystander: Defective Mitophagy in Alzheimer’s Disease
Xie, C., Aman, Y., Adriaanse, B. A., Cader, M. Z., Plun‐Favreau, H., Xiao, J., & Fang, E. F. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2019.00391 · Cited by 29
de Sá, R. V., Luna, M. C., & Pasterkamp, R. J. (2021) · Tissue Engineering Part C Methods · doi:10.1089/ten.tec.2020.0337 · Cited by 31
Ojo, J. O., Reed, J. M., Crynen, G. C., Vallabhaneni, P., Evans, J., Shackleton, B., Eisenbaum, M., Ringland, C., Edsell, A., MULLAN, M. J., et al. (2021) · Molecular Brain · doi:10.1186/s13041-021-00803-9 · Cited by 30
Brain Organoids: Filling the Need for a Human Model of Neurological Disorder
Jalink, P., & Caiazzo, M. (2021) · Biology · doi:10.3390/biology10080740 · Cited by 30
Microglia and its Genetics in Alzheimer's Disease
Liang, X., Wu, H., Colt, M., Guo, X., Pluimer, B. R., Zeng, J., Dong, S., & Zhao, Z. (2021) · Current Alzheimer Research · doi:10.2174/1567205018666211105140732 · Cited by 32
Alzheimer's disease and synapse Loss: What can we learn from induced pluripotent stem Cells?
Rodríguez-Jiménez, F. J., Ureña‐Peralta, J. R., Jendelová, P., & Erceg, S. (2023) · Journal of Advanced Research · doi:10.1016/j.jare.2023.01.006 · Cited by 33
Hebisch, M., Klostermeier, S., Wolf, K., Boccaccini, A. R., Wolf, S. E., Tanzi, R. E., & Kim, D. Y. (2023) · Advanced Science · doi:10.1002/advs.202205037 · Cited by 31
Genetic insights into immune mechanisms of Alzheimer’s and Parkinson’s disease
Nott, A., & Holtman, I. R. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1168539 · Cited by 33
Bio–Nano Toolbox for Precision Alzheimer's Disease Gene Therapy
Liu, Y., Xia, X., Zheng, M., & Shi, B. (2024) · Advanced Materials · doi:10.1002/adma.202314354 · Cited by 31
Inflammatory responses revealed through HIV infection of microglia-containing cerebral organoids
Narasipura, S. D., Zayas, J. P., Ash, M. K., Reyes, A. F., Shull, T. L., Gambut, S., Szczerkowski, J. L. A., McKee, C., Schneider, J. R., Lorenzo-Redondo, R., et al. (2025) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03353-2 · Cited by 33
Khan, M. S., Qureshi, N., Khan, R., Son, Y., & Maqbool, T. (2025) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2025.1578138 · Cited by 37
Failure of lysosomal acidification and endomembrane network in neurodegeneration
Kim, S.-H., Cho, Y.-S., & Jung, Y. (2025) · Experimental & Molecular Medicine · doi:10.1038/s12276-025-01579-x · Cited by 32
HIV-1 Persistence and Chronic Induction of Innate Immune Responses in Macrophages
Akiyama, H., & Gummuluru, S. (2020) · Viruses · doi:10.3390/v12070711 · Cited by 30
Review of Artificial Intelligence Applications and Algorithms for Brain Organoid Research
Badai, J., Bu, Q., & Zhang, L. (2020) · Interdisciplinary Sciences Computational Life Sciences · doi:10.1007/s12539-020-00386-4 · Cited by 30
MacDougall, G., Brown, L. Y., Kantor, B., & Chiba‐Falek, O. (2021) · Molecular Therapy · doi:10.1016/j.ymthe.2021.01.001 · Cited by 31
Elahi, F. M., Ashimatey, B. S., Bennett, D. J., Walters, S. M., Joie, R. L., Jiang, X., Wolf, A. A., Cobigo, Y., Staffaroni, A. M., Rosen, H. J., et al. (2021) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12181 · Cited by 29
Emerging hiPSC Models for Drug Discovery in Neurodegenerative Diseases
Trudler, D., Ghatak, S., & Lipton, S. A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22158196 · Cited by 30
Chrysanthou, M., Estruch, I. M., Rietjens, I. M. C. M., Wichers, H. J., & Hoppenbrouwers, T. (2022) · Nutrients · doi:10.3390/nu14020363 · Cited by 31
The involvement of microglia in Alzheimer's disease: a new dog in the fight
Moore, Z., Taylor, J. M., & Crack, P. J. (2019) · British Journal of Pharmacology · doi:10.1111/bph.14546 · Cited by 29
Zhang, Y., Bi, K., Zhou, L., Wang, J., Huang, L., Sun, Y., Peng, G., & Wu, W. (2024) · Degenerative Neurological and Neuromuscular Disease · doi:10.2147/dnnd.s471174 · Cited by 30
A framework for translating tauopathy therapeutics: Drug discovery to clinical trials
Feldman, H., Cummings, J. L., Boxer, A. L., Staffaroni, A. M., Knopman, D. S., Rizzo, S. J. S., Territo, P. R., Arnold, S. E., Ballard, C. G., Beher, D., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14250 · Cited by 27
Self-citationLipid metabolism and neuroinflammation: What is the link?
Tiwari, V., & Simons, M. (2025) · The Journal of Experimental Medicine · doi:10.1084/jem.20241232 · Cited by 39
Hollinger, K. R., Zhu, X., Khoury, E. S., Thomas, A. G., Liaw, K., Tallon, C., Wu, Y., Prchalová, E., Kamiya, A., Rojas, C. J., et al. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-190588 · Cited by 28
Seneviratne, U. I., Huang, Z., Ende, C. W. A., Butler, T. W., Cleary, L., Dresselhaus, E. C., Evrard, E., Fisher, E. L., Green, M. E., Helal, C. J., et al. (2020) · Cell chemical biology · doi:10.1016/j.chembiol.2020.09.002 · Cited by 28
Dulewicz, M., Kulczyńska‐Przybik, A., Słowik, A., Borawska, R., & Mroczko, B. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10143009 · Cited by 30
Nuclear dynamics and stress responses in Alzheimer’s disease
Iatrou, A., Clark, E. M., & Wang, Y. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00489-6 · Cited by 31
Kondo, T., Hara, N., Koyama, S., Yada, Y., Tsukita, K., Nagahashi, A., Ikeuchi, T., Ishii, K., Asada, T., Arai, T., et al. (2022) · Nature Aging · doi:10.1038/s43587-021-00158-9 · Cited by 26
Modeling the Human Brain With ex vivo Slices and in vitro Organoids for Translational Neuroscience
Nogueira, G. O., Garcez, P. P., Bardy, C., Cunningham, M. O., & Sebollela, A. S. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.838594 · Cited by 30
Are apolipoprotein E fragments a promising new therapeutic target for Alzheimer’s disease?
Vecchio, F. L., Bisceglia, P., Imbimbo, B. P., Lozupone, M., Latino, R. R., Resta, E., Leone, M., Solfrizzi, V., Greco, A., Daniele, A., et al. (2022) · Therapeutic Advances in Chronic Disease · doi:10.1177/20406223221081605 · Cited by 28
Nassar, A., Satarker, S., Gurram, P. C., Upadhya, D., Fayaz, S., & Nampoothiri, M. (2023) · Molecular Neurobiology · doi:10.1007/s12035-023-03437-1 · Cited by 27
Xu, D. C., Sas‐Nowosielska, H., Donahue, G., Huang, H., Pourshafie, N., Good, C. R., & Berger, S. L. (2024) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01696-6 · Cited by 35
Astrocyte priming enhances microglial Aβ clearance and is compromised by APOE4
Lee, S. J., Yu, J. J., Lee, H. G., Kim, B., Jang, M. J., Jo, H., Kim, N. Y., Pak, M. E., Kim, J. K., Cho, S., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-62995-1 · Cited by 28
Self-citationYao, A. Y., & Yan, R. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00417-0 · Cited by 26
Honing the Double-Edged Sword: Improving Human iPSC-Microglia Models
Hedegaard, A., Stodolak, S., James, W. S., & Cowley, S. A. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.614972 · Cited by 29
The Breakthroughs and Caveats of Using Human Pluripotent Stem Cells in Modeling Alzheimer’s Disease
Bendtsen, K. M., & Hall, V. J. (2023) · Cells · doi:10.3390/cells12030420 · Cited by 30
Prevention of Alzheimer's disease through diet: An exploratory review
Bhuiyan, N. Z., Hasan, M. K., Mahmud, Z., Hossain, M. S., & Rahman, A. (2023) · Metabolism Open · doi:10.1016/j.metop.2023.100257 · Cited by 35
Lipid mediated brain disorders: A perspective
Singh, A., Kukal, S., Kanojia, N., Singh, M., Saso, L., Kukreti, S., & Kukreti, R. (2023) · Prostaglandins & Other Lipid Mediators · doi:10.1016/j.prostaglandins.2023.106737 · Cited by 27
Jaye, S., Sandau, U. S., & Saugstad, J. A. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1378576 · Cited by 26
Induction of astrocyte reactivity promotes neurodegeneration in human pluripotent stem cell models
Gomes, C., Huang, K.-C., Harkin, J., Baker, A., Hughes, J. M., Pan, Y., Tutrow, K. D., VanderWall, K. B., Lavekar, S. S., Hernandez, M., et al. (2024) · Stem Cell Reports · doi:10.1016/j.stemcr.2024.07.002 · Cited by 29
Modeling Alzheimer’s disease using human cell derived brain organoids and 3D models
Fernandes, S., Revanna, J. S., Pratt, J. M., Hayes, N., Marchetto, M. C., & Gage, F. H. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1434945 · Cited by 33
Alzheimer’s Disease Research Using Human Microglia
Lue, L., Beach, T. G., & Walker, D. G. (2019) · Cells · doi:10.3390/cells8080838 · Cited by 29
Impact of Genetic Risk Factors for Alzheimer’s Disease on Brain Glucose Metabolism
Cho, S., Lee, H., & Seo, J. (2021) · Molecular Neurobiology · doi:10.1007/s12035-021-02297-x · Cited by 25
Self-citationMhatre‐Winters, I., Eid, A., Han, Y., Tieu, K., & Richardson, J. R. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23179829 · Cited by 26
Assaying Microglia Functions In Vitro
Maguire, E., Connor‐Robson, N., Shaw, B., O’Donoghue, R., Stöberl, N., & Hall‐Roberts, H. (2022) · Cells · doi:10.3390/cells11213414 · Cited by 31
Marei, H. E. S., Khan, M. U. A., & Hasan, A. (2023) · Cellular & Molecular Biology Letters · doi:10.1186/s11658-023-00504-2 · Cited by 27
Alzheimer’s Disease: Models and Molecular Mechanisms Informing Disease and Treatments
Nystuen, K., McNamee, S. M., Akula, M., Holton, K. M., DeAngelis, M. M., & Haider, N. B. (2024) · Bioengineering · doi:10.3390/bioengineering11010045 · Cited by 28
Wu, D., Bi, X., & Chow, H. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02987-4 · Cited by 31
Neuro-Immuno-Gene- and Genome-Editing-Therapy for Alzheimer’s Disease: Are We There Yet?
Raikwar, S. P., Thangavel, R., Dubova, I., Ahmed, M. E., Selvakumar, G. P., Kempuraj, D., Zaheer, S. A., Iyer, S. S., & Zaheer, A. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180422 · Cited by 27
Zhao, J., Ikezu, T. C., Lu, W., Macyczko, J. R., Li, Y., Lewis-Tuffin, L. J., Martens, Y. A., Ren, Y., Zhu, Y., Asmann, Y. W., et al. (2023) · Stem Cell Research & Therapy · doi:10.1186/s13287-023-03444-y · Cited by 25
In Vitro Three-Dimensional (3D) Models for Melanoma Immunotherapy
Nomdedeu‐Sancho, G., Gorkun, A. A., Mahajan, N., Willson, K., Schaaf, C. R., Votanopoulos, K. I., Atala, A., & Söker, S. (2023) · Cancers · doi:10.3390/cancers15245779 · Cited by 27
CRISPR/Cas9 and iPSC-Based Therapeutic Approaches in Alzheimer’s Disease
Raffaele, I., Cipriano, G. L., Anchesi, I., Oddo, S., & Silvestro, S. (2025) · Antioxidants · doi:10.3390/antiox14070781 · Cited by 30
Chen, J., Zhao, S., Zhou, Y., Wang, L., Chen, Q., & Zheng, K. (2025) · BioScience Trends · doi:10.5582/bst.2025.01148 · Cited by 29
Microfluidic Platforms to Unravel Mysteries of Alzheimer’s Disease: How Far Have We Come?
Prasanna, P., Rathee, S., Rahul, V., Mandal, D., Goud, M. S. C., Yadav, P., Hawthorne, S. J., Sharma, A., Gupta, P. K., Ojha, S. K., et al. (2021) · Life · doi:10.3390/life11101022 · Cited by 25
Interfacing brain organoids with precision medicine and machine learning
Zheng, H., Feng, Y., Tang, J., & Ma, S. (2022) · Cell Reports Physical Science · doi:10.1016/j.xcrp.2022.100974 · Cited by 26
Lozupone, M., Imbimbo, B. P., Balducci, C., Vecchio, F. L., Bisceglia, P., Latino, R. R., Leone, M. A., Dibello, V., Solfrizzi, V., Greco, A., et al. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12728 · Cited by 28
APOE4 is a Risk Factor and Potential Therapeutic Target for Alzheimer's Disease
Ayyubova, G. (2023) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1871527322666230303114425 · Cited by 23
Complexity of Sex Differences and Their Impact on Alzheimer’s Disease
Kadlecová, M., Freude, K., & Haukedal, H. (2023) · Biomedicines · doi:10.3390/biomedicines11051261 · Cited by 27
Implication of tau propagation on neurodegeneration in Alzheimer’s disease
Lamontagne-Kam, D., Ulfat, A. K., Hervé, V., Vu, T.-M., & Brouillette, J. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1219299 · Cited by 28
Thapar, N., Eid, M. A. F., Raj, N., Kantas, T., Billing, H. S., & Sadhu, D. (2023) · Annals of Medicine and Surgery · doi:10.1097/ms9.0000000000001500 · Cited by 28
Back to the origins: Human brain organoids to investigate neurodegeneration
Faravelli, I., Costamagna, G., Tamanini, S., & Corti, S. (2020) · Brain Research · doi:10.1016/j.brainres.2019.146561 · Cited by 25
Wenzel, T. J., Desjarlais, J. D., & Mousseau, D. D. (2024) · Stem Cell Research & Therapy · doi:10.1186/s13287-024-03876-0 · Cited by 27
A manifesto for Alzheimer’s disease drug discovery in the era of disease-modifying therapies
Hering, H., Bussière, T., Liu, C., Glajch, K. E., Weihofen, A., Grogan, J. L., & Walsh, D. M. (2025) · Molecular Neurodegeneration · doi:10.1186/s13024-025-00872-7 · Cited by 28
Espinoza, A. P. V., Na, N., Campanati, L., Ngo, P., Baldwin, K. K., & Cline, H. T. (2025) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2516103122 · Cited by 23
The Use of Patient-Derived Induced Pluripotent Stem Cells for Alzheimer’s Disease Modeling
Lee, C., Willerth, S. M., & Nygaard, H. B. (2020) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2020.101804 · Cited by 24
Brain Organoids: Studying Human Brain Development and Diseases in a Dish
Xu, J., & Wen, Z. (2021) · Stem Cells International · doi:10.1155/2021/5902824 · Cited by 25
CRISPRroots: on- and off-target assessment of RNA-seq data in CRISPR–Cas9 edited cells
Corsi, G. I., Gadekar, V. P., Gorodkin, J., & Seemann, S. E. (2021) · Nucleic Acids Research · doi:10.1093/nar/gkab1131 · Cited by 25
Bhattacharya, A., Choi, W. W. Y., Muffat, J., & Li, Y. (2021) · Journal of Molecular Biology · doi:10.1016/j.jmb.2021.167386 · Cited by 24
Geerts, H., Walker, M., Rose, R., Bergeler, S., van der Graaf, P. H., Schuck, E. L., Koyama, A., Yasuda, S., Hussein, Z., Reyderman, L., et al. (2023) · CPT Pharmacometrics & Systems Pharmacology · doi:10.1002/psp4.12912 · Cited by 24
Lavekar, S. S., Harkin, J., Hernandez, M., Gomes, C., Patil, S., Huang, K.-C., Puntambekar, S. S., Lamb, B. T., & Meyer, J. S. (2023) · Scientific Reports · doi:10.1038/s41598-023-40382-4 · Cited by 24
Vicente, M. C., Addo-Osafo, K., & Vossel, K. A. (2024) · Frontiers in Neurology · doi:10.3389/fneur.2024.1277613 · Cited by 25
Kim, Y. W., Al‐Ramahi, I., Koire, A. M., Wilson, S. J., Konecki, D. M., Mota, S., Soleimani, S., Botas, J., & Lichtarge, O. (2020) · Alzheimer s & Dementia · doi:10.1002/alz.12240 · Cited by 22
Staurenghi, E., Leoni, V., Lo Iacono, M., Sottero, B., Testa, G., Giannelli, S., Leonarduzzi, G., & Gamba, P. (2022) · Antioxidants · doi:10.3390/antiox11112168 · Cited by 24
Wang, J., Fourrière, L., & Gleeson, P. A. (2024) · Biochemical Journal · doi:10.1042/bcj20240056 · Cited by 26
Chen, X., Sun, G., Feng, L., Tian, E., & Shi, Y. (2025) · Communications Biology · doi:10.1038/s42003-024-07401-0 · Cited by 23
WWOX-Related Neurodevelopmental Disorders: Models and Future Perspectives
Steinberg, D. J., & Aqeilan, R. I. (2021) · Cells · doi:10.3390/cells10113082 · Cited by 22
Panda, S. P., & Soni, U. (2022) · Ageing Research Reviews · doi:10.1016/j.arr.2022.101560 · Cited by 22
Qu, W., Canoll, P., & Hargus, G. (2023) · Neuroscience · doi:10.1016/j.neuroscience.2022.05.006 · Cited by 24
Lipid Dys-Homeostasis Contributes to APOE4-Associated AD Pathology
Lazar, A. N., Hanbouch, L., Boussicaut, L., Fourmaux, B., Daira, P., Millan, M. J., Bernoud‐Hubac, N., & Potier, M. (2022) · Cells · doi:10.3390/cells11223616 · Cited by 23
BACE2: A Promising Neuroprotective Candidate for Alzheimer’s Disease
Yeap, Y. J., Kandiah, N., Nižetić, D., & Lim, K. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220867 · Cited by 25
Scott‐Hewitt, N., Huang, Y., & Stevens, B. (2023) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.15010 · Cited by 22
Koutsodendris, N., Blumenfeld, J. R., Agrawal, A., Traglia, M., Yip, O., Rao, A. T., Kim, M. J., Nelson, M. R., Wang, Y.-H., Grone, B. P., et al. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.113252 · Cited by 25
When glia meet induced pluripotent stem cells (iPSCs)
Li, L., & Shi, Y. (2020) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2020.103565 · Cited by 24
Watanabe, H., Murakami, R., Tsumagari, K., Morimoto, S., Hashimoto, T., Imaizumi, K., Sonn, I., Yamada, K., Saito, Y., Murayama, S., et al. (2023) · Stem Cell Reports · doi:10.1016/j.stemcr.2023.08.002 · Cited by 24
Cell type-specific functions of Alzheimer's disease endocytic risk genes
Maninger, J.-K., Nowak, K., Goberdhan, S., O'Donoghue, R., & Connor-Robson, N. (2024) · Philosophical Transactions of the Royal Society B: Biological Sciences · doi:10.1098/rstb.2022.0378 · Cited by 22
Ding, Y., Palecek, S. P., & Shusta, E. V. (2024) · Fluids and Barriers of the CNS · doi:10.1186/s12987-024-00580-2 · Cited by 22
Joseph, G. U., Oyovwi, M. O., Jeroh, E., Esuku, D. T., & Ben‐Azu, B. (2025) · Journal of Molecular Pathology · doi:10.3390/jmp6020012 · Cited by 23
Gao, M., Bai, J., Lou, F., Sun, Y., Wang, Z., Cai, X., Li, Y., Zhang, F., Liang, J., Li, X., et al. (2025) · Nature Aging · doi:10.1038/s43587-025-00976-1 · Cited by 25
Asante, I., Louie, S. G., & Yassine, H. N. (2022) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.14907 · Cited by 23
iPSC-derived PSEN2 (N141I) astrocytes and microglia exhibit a primed inflammatory phenotype
Sullivan, M. A., Lane, S. D., McKenzie, A. D. J., Ball, S. R., Sunde, M., Neely, G. G., Moreno, C. L., Maximova, A., Werry, E. L., & Kassiou, M. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02951-2 · Cited by 23
Brain Organoids: A Promising Living Biobank Resource for Neuroscience Research
Li, S., Wang, M., & Zhou, J. (2020) · Biopreservation and Biobanking · doi:10.1089/bio.2019.0111 · Cited by 23
Liu, A., Wang, T., Yang, L., & Zhou, Y. (2025) · Brain Sciences · doi:10.3390/brainsci15070675 · Cited by 23
ABCA7 variants impact phosphatidylcholine and mitochondria in neurons
von Maydell, D., Wright, S. E., Pao, P.-C., Staab, C., King, O., Spitaleri, A., Bonner, J. M., Liu, L., Yu, C. J., Chiu, C.-C., et al. (2025) · Nature · doi:10.1038/s41586-025-09520-y · Cited by 35
Self-citationModeling cell-cell interactions in the brain using cerebral organoids
Oliveira, B., Yahya, A. Ç., & Novarino, G. (2019) · Brain Research · doi:10.1016/j.brainres.2019.146458 · Cited by 20
Integrating CRISPR Engineering and hiPSC-Derived 2D Disease Modeling Systems
Rehbach, K., Fernando, M. B., & Brennand, K. (2020) · Journal of Neuroscience · doi:10.1523/jneurosci.0518-19.2019 · Cited by 22
Song, S., Ashok, A., Williams, D. J., Kaufman, M. E., Duff, K., & Sproul, A. A. (2021) · Current Protocols · doi:10.1002/cpz1.141 · Cited by 16
Metadata
- Authors
- Lin, Y.-T., Seo, J., Gao, F., Feldman, H. M., Wen, H.-L., Penney, J., Cam, H. P., Gjoneska, E., Raja, W. K., Cheng, J., Rueda, R., Kritskiy, O., Abdurrob, F., Peng, Z., Milo, B., Yu, C. J., Elmsaouri, S., Dey, D., Ko, T., Yankner, B. A., & Tsai, L.-H.
- Affiliations
- Massachusetts Institute of Technology (US)
- Harvard University (US)
- Corresponding author
- Tsai, Li-Huei
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2018-06
- Volume
- 98
- Issue
- 6
- Pages
- 1141-1154.e7
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC6023751
- OpenAlex
- W2805798400
- Cited by
- 1,125
- References
- 74
- Citations by year
- 2026: 94 · 2025: 152 · 2024: 175 · 2023: 167 · 2022: 159 · 2021: 151 · 2020: 142 · 2019: 66 · 2018: 18
- FWCI
- 64.81
- Type
- journal article
- Language
- en
- Update notices
- erratum (2018-06-27)
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc-nd)
- IslandScholar (University of Prince Edward Island) (submittedVersion)
- Funders
- Basic Science Research Program (2014R1A6A3A03055359)
- NIH (RF1 AG048056, RC1 AG036106, RF1 AG048029)
- Glenn Foundation for Medical Research
- Robert A. and Renee E. Belfer Family Foundation
- Cure Alzheimer's Fund
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- APOE ε4, sporadic Alzheimer's disease, induced pluripotent stem cells, APOE3, neurons, astrocytes, microglia-like cells, amyloid-beta, synaptic function, lipid metabolism, cholesterol accumulation, cell type-specific gene expression, CRISPR/Cas9 genome editing
- MeSH terms
- Alzheimer Disease, Astrocytes, Brain, Cell Differentiation, Humans, Synaptic Transmission, Neuroglia, Neurons, Organoids, Peptide Fragments, Phosphoproteins, Amyloid beta-Peptides, tau Proteins, Microglia, Lipid Metabolism, Apolipoprotein E3, Apolipoprotein E4, Induced Pluripotent Stem Cells, Transcriptome, CRISPR-Cas Systems
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