The DOI matches its Crossref record; 73 of the 74 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source doesn’t support the claim as written.
In the citing paper
“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]
Checked by a reasoning model — may be wrong.
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]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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.
In the citing paper
“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.”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
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
1 of the 74 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Items 701–800 of 1,002
Epigenetic editing for autosomal dominant neurological disorders
Waldo, J. J., Halmai, J. A. N. M., & Fink, K. D. (2024) · Frontiers in Genome Editing · doi:10.3389/fgeed.2024.1304110 · Cited by 8
Read, J. L., & Suphioglu, C. (2019) · Cellular Physiology and Biochemistry · doi:10.33594/000000147 · Cited by 8
FMR1 loss in a human stem cell model reveals early changes to intrinsic membrane excitability
Susco, S. G., Arias-García, M. A., López-Huerta, V. G., Beccard, A., Bara, A. M., Moffitt, J., Korn, J. A., Fu, Z., & Barrett, L. E. (2020) · Developmental Biology · doi:10.1016/j.ydbio.2020.09.012 · Cited by 9
Modeling SARS-CoV-2 infection in individuals with opioid use disorder with brain organoids
Willner, M. J., Xiao, Y., Kim, H. S., Chen, X., Xu, B., & Leong, K. W. (2021) · Journal of Tissue Engineering · doi:10.1177/2041731420985299 · Cited by 8
Looking at Alzheimer’s Disease Pathogenesis from the Nuclear Side
D’Andrea, L., Stringhi, R., Luca, M. D., & Marcello, E. E. (2021) · Biomolecules · doi:10.3390/biom11091261 · Cited by 8
Potential mechanisms underlying lithium treatment for Alzheimer's disease and COVID-19.
Wei, H.-F., Anchipolovsky, S., Vera, R., Liang, G., & Chuang, D. M. (2022) · PubMed · doi:10.26355/eurrev_202203_28369 · Cited by 8
Screening neuroprotective compounds in herpes-induced Alzheimer's disease cell and 3D tissue models
Silveira, I. A., Mullis, A. S., Cairns, D. M., Shevzov-Zebrun, A., Whalen, J., Galuppo, A., Walsh, K. G., & Kaplan, D. L. (2022) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2022.05.002 · Cited by 9
Modeling neuro-immune interactions using human pluripotent stem cells
Garcia-Epelboim, A., & Christian, K. M. (2023) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2022.102672 · Cited by 7
In vitro characterization on the role of APOE polymorphism in human hippocampal neurogenesis
Lee, H.-A., Price, J., Srivastava, D. P., & Thuret, S. (2023) · Hippocampus · doi:10.1002/hipo.23502 · Cited by 6
de Leeuw, S. M., Kirschner, A. W. T., Lindner, K., Rust, R., Wolski, W., Gavin, A., Nitsch, R. M., & Tackenberg, C. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.07.17.452644 · Cited by 8
Rao, A. T., Chen, N., Kim, M. J., Blumenfeld, J. R., Yip, O., Hao, Y., Liang, Z., Nelson, M. R., Koutsodendris, N., Grone, B. P., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.11.10.566510 · Cited by 8
Kuhn, M. K., Kang, R. Y., Kim, C., Tagay, Y., Morris, N., Tabdanov, E. D., Elcheva, I. A., & Proctor, E. A. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.11.16.567220 · Cited by 9
Lysaker, C. R., Johnson, C. N., Csikós, V., Franczak, E., Benson, M. N., Gilmore, C. A., Birky, C. J., Davis, X. C., McCoin, C. S., Smith, K. P., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.06.15.659811 · Cited by 8
Adji, A. S., Widjaja, J. S., Wardani, V. A. K., Muhammad, A. H., Handajani, F., Putra, H. B. P., & Rahman, F. S. (2022) · Open Access Macedonian Journal of Medical Sciences · doi:10.3889/oamjms.2022.9053 · Cited by 8
Recent Research Trends in Stem Cells Using CRISPR/Cas-Based Genome Editing Methods
Yoon, D. E., Lee, H., & Kim, K. (2023) · International Journal of Stem Cells · doi:10.15283/ijsc23030 · Cited by 8
Asiamah, E. A., Feng, B., Guo, R., Yaxing, X., Du, X., Liu, X., Zhang, J., Cui, H., & Ma, J. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230658 · Cited by 8
In vivo and ex vivo gene therapy for neurodegenerative diseases: a promise for disease modification
Ebrahimi, P., Davoudi, E., Sadeghian, R., Zadeh, A. Z., Razmi, E., Heidari, R., Morowvat, M. H., & Sadeghian, I. (2024) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-024-03141-4 · Cited by 7
Grenon, M. B., Papavergi, M.-T., Bathini, P., Sadowski, M. J., & Lemere, C. A. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25115754 · Cited by 7
Explainable deep neural networks for predicting sample phenotypes from single-cell transcriptomics
Martorell‐Marugán, J., López-Domínguez, R., Villatoro-García, J. A., Toro‐Domínguez, D., Chierici, M., Jurman, G., & Carmona‐Sáez, P. (2024) · Briefings in Bioinformatics · doi:10.1093/bib/bbae673 · Cited by 9
Significance of gene therapy in neurodegenerative diseases
Wang, L., Ma, L., Gao, Z., Wang, Y., & Qiu, J. (2025) · Frontiers in Neuroscience · doi:10.3389/fnins.2025.1515255 · Cited by 7
Tiwari, P., Dwivedi, R., Kaushik, M., Tripathi, M., & Dada, R. (2025) · Journal of Molecular Neuroscience · doi:10.1007/s12031-025-02363-2 · Cited by 8
Glial Cells in Alzheimer’s Disease: Pathogenic Mechanisms and Therapeutic Frontiers
Sil, M., Mukherjee, N., Chatterjee, I., Ghosh, A., & Goswami, A. (2025) · Journal of Molecular Neuroscience · doi:10.1007/s12031-025-02379-8 · Cited by 9
Niu, T., Wang, S., Zhang, H., Zhu, W., Liu, K., Zhou, X., Sun, R., Niu, D., & Yuan, Y. (2025) · Experimental & Molecular Medicine · doi:10.1038/s12276-025-01534-w · Cited by 7
Advances of therapeutic strategies for Alzheimer’s disease
Guo, X., Yue, R.-Z., Cui, Z., Wang, S., Jia, T., Li, W., Zhang, W., Shan, L., & Li, C. (2025) · Journal of Neurology · doi:10.1007/s00415-025-13456-8 · Cited by 9
Wang, W., Tan, S., Zuo, X., Gao, X., Ma, L., Sun, R., Liang, G., Yin, L., Pu, Y., & Zhang, J. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-05293-7 · Cited by 7
Advances in iPSC Technology in Neural Disease Modeling, Drug Screening, and Therapy
Dai, S., Qiu, L., Veeraraghavan, V. P., Sheu, C., & Mony, U. (2023) · Current Stem Cell Research & Therapy · doi:10.2174/1574888x18666230608105703 · Cited by 8
Zhang, X., Gao, R., Yang, L., Zhu, Y., Zhang, T., Shen, X., Gu, W., Yang, L., & Peng, S. (2024) · Clinical and Translational Discovery · doi:10.1002/ctd2.287 · Cited by 8
Astrocyte–Neuron Interactions in Alzheimer’s Disease
Muñoz‐Castro, C., & Serrano‐Pozo, A. (2024) · Advances in neurobiology · doi:10.1007/978-3-031-64839-7_14 · Cited by 7
Arber, C., Casey, J. M., Crawford, S., Rambarack, N., Yaman, Ü., Wiethoff, S., Augustin, E., Piers, T. M., Price, M., Rostagno, A. A., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02820-z · Cited by 8
Wang, H., Chen, S., Jiang, L., Liu, X., Tang, R., & Tang, M. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1485657 · Cited by 7
Affaneh, A., Linden, A. K., Tunc‐Ozcan, E., Tsai, Y., Peng, C., & Kessler, J. A. (2024) · Annals of Neurology · doi:10.1002/ana.27149 · Cited by 7
Huynh, T. N. T., Fikse, E. N., Torre, A. L. D. L., Havrda, M. C., Chang, C. C. Y., & Chang, T. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252413690 · Cited by 9
Association of apolipoprotein E ε4 allele and amyotrophic lateral sclerosis in Chinese population
He, D., Shang, L., Liu, Q. F., Shen, D., Sun, X., Cai, Z., Zhao, X., Liu, L., Yang, X., Liu, M., et al. (2021) · Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration · doi:10.1080/21678421.2021.1953077 · Cited by 7
Emerging concepts towards a translational framework in Alzheimer’s disease
Cozachenco, D., Zimmer, E. R., & Lourenco, M. V. (2023) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2023.105246 · Cited by 7
Michalski, C., & Wen, Z. (2023) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2023.1291115 · Cited by 7
The blood-brain barrier models to study apolipoprotein E genotypes in Alzheimer’s disease
Dias, I. H. K., Taiwo, R., & Ma, D. (2021) · Neural Regeneration Research · doi:10.4103/1673-5374.331538 · Cited by 8
Monroe, K. M., Weerakkody, T. N., Sabelström, H., Tatarakis, D., Suh, J. H., Chin, M. Y., Andrews, S. V., Propson, N. E., Balasundar, S., Davis, S. S., et al. (2024) · Research Square · doi:10.21203/rs.3.rs-3954863/v1 · Cited by 7
Wang, S., Li, B., Cai, Z., Hugo, C., Li, J., Sun, Y. E., Lü, Q., Remaley, A. T., Julia, T. C. W., Chui, H. C., et al. (2024) · Research Square · doi:10.21203/rs.3.rs-4373201/v1 · Cited by 7
Cuní-López, C., Root, J. T., Hao, Y., Kowal, I., Blomberg, N., Ghirlando, R., Yang, L. G., Koppes-den Hertog, S. J., Cookson, M. R., van der Kant, R., et al. (2025) · doi:10.1101/2025.08.19.669163 · Cited by 8
Zuniga, N. R., Earls, N. E., Denos, A. E. A., Elison, J. M., Jones, B. S., Smith, E. G., Moran, N. G., Broce, K. L., Romero, G. M., Hyer, C. D., et al. (2024) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1012407 · Cited by 9
Fang, C., Wang, Q., Xiao, Q., Cai, X.-X., Du, R., Xue, L., Tian, X., & Xiong, L. (2025) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-24-01490 · Cited by 7
Unraveling APOE4: The dual role in CNS and peripheral inflammation in Alzheimer's disease
Li, X., Li, Z., Chen, H., Guo, H., Ge, Y., Dong, F., Zhang, F., & Zhang, F. (2025) · International Immunopharmacology · doi:10.1016/j.intimp.2025.115199 · Cited by 7
3D flexible self-folding microelectrode array for organoid electrophysiology analysis
Torres, F. P., Manning, A., Paredes-Espinosa, M. B., Tokranova, N. A., Bertucci, T. B., Kiehl, T. R., Paluh, J. L., Cady, N. C., Xie, Y., & Sharfstein, S. T. (2025) · Cell Biomaterials · doi:10.1016/j.celbio.2025.100179 · Cited by 9
Blenkle, A., Geladaris, A., & Weber, M. S. (2026) · Experimental & Molecular Medicine · doi:10.1038/s12276-026-01647-w · Cited by 6
APOE3 astrocytes can rescue lipid abnormalities and dystrophic neurites of APOE4 human neurons
Halim, D. O., Biase, E. D., Rajon, A., Jordi, L., Hallett, P. J., & Ole Isacson, A. (2026) · PNAS Nexus · doi:10.1093/pnasnexus/pgag053 · Cited by 7
Bello, E., Long, K. R., Iwama, S., Steer, J., Cooper, S., Alasoo, K., Kumasaka, N., Schwartzentruber, J., Panousis, N. I., & Bassett, A. R. (2026) · iScience · doi:10.1016/j.isci.2026.115688 · Cited by 7
Pereira, M. F., Shyti, R., & Testa, G. (2024) · Stem Cell Reports · doi:10.1016/j.stemcr.2024.05.004 · Cited by 8
APOEε4 alters ApoE and Fabp7 in frontal cortex white matter in prodromal Alzheimer's disease
Moreno‐Rodríguez, M., Perez, S. E., Malek‐Ahmadi, M. H., & Mufson, E. J. (2025) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03349-y · Cited by 8
Targeting apolipoprotein E for treating Alzheimer’s disease
Bales, K. R., & Paul, S. M. (2019) · Neuroscience Letters · doi:10.1016/j.neulet.2019.134366 · Cited by 7
Suwito, B. E., Adji, A. S., Wardani, V. A. K., Widjaja, J. S., Angel, S. C. S., & Rahman, F. S. (2022) · Bali Medical Journal · doi:10.15562/bmj.v11i2.3414 · Cited by 6
Fessel, J. (2023) · Discover Mental Health · doi:10.1007/s44192-022-00029-8 · Cited by 6
Rai, A., Ojiakor, O. A., & Rylett, R. J. (2023) · Journal of Neurochemistry · doi:10.1111/jnc.15904 · Cited by 6
Kovalská, M., Hnilicová, P., Kalenská, D., Adamkov, M., Kovalska, L., & Lehotský, J. (2023) · Cells · doi:10.3390/cells12162087 · Cited by 7
Current methods for the microglia isolation: Overview and comparative analysis of approaches
Akhmetzyanova, E. R., Rizvanov, A. A., & Mukhamedshina, Y. O. (2023) · Cell and Tissue Research · doi:10.1007/s00441-023-03853-8 · Cited by 7
Yi, W., Lv, D., Sun, Y., Mu, J., & Lu, X. (2023) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2023.149414 · Cited by 8
Directed Differentiation of Neurons from Human iPSCs for Modeling Neurological Disorders
Wang, C., Cerneckis, J., & Shi, Y. (2024) · Methods in molecular biology · doi:10.1007/978-1-0716-3810-1_12 · Cited by 6
Byrns, C. N., & Bonini, N. M. (2021) · Neuron · doi:10.1016/j.neuron.2020.12.015 · Cited by 6
The Potential of Induced Pluripotent Stem Cells to Treat and Model Alzheimer’s Disease
Schulz, J. M. (2021) · Stem Cells International · doi:10.1155/2021/5511630 · Cited by 6
Canals, I., & Ahlenius, H. (2021) · Methods in molecular biology · doi:10.1007/978-1-0716-1601-7_16 · Cited by 6
Designer Nanodiscs to Probe and Reprogram Membrane Biology in Synapses
Dallo, S., Shin, J., Zhang, S., Ren, Q., & Bao, H. (2022) · Journal of Molecular Biology · doi:10.1016/j.jmb.2022.167757 · Cited by 6
Ngn2 induces diverse neuronal lineages from human pluripotencyPreprint
Lin, H., He, Z., Ebert, S., Schörnig, M., Santel, M., Weigert, A., Hevers, W., Kasri, N. N., Taverna, E., Camp, J. G., et al. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.11.19.389445 · Cited by 6
Penning, A., Snoeck, S., Ormaechea, O. R., Ayyildiz, D., Polzer, O., Buitrago-Arango, M., Capobianco, R., de Winter, F., Balusu, S., Verhaagen, J., et al. (2026) · Acta Neuropathologica Communications · doi:10.1186/s40478-026-02228-8 · Cited by 6
Microglial Drivers of Alzheimer's Disease Pathology: An Evolution of Diverse Participating States
Kuhn, M. K., & Proctor, E. A. (2024) · Proteins Structure Function and Bioinformatics · doi:10.1002/prot.26723 · Cited by 5
Imaging lipid rafts reveals the principle of ApoE4-induced Aβ upregulation in human neurons
Lee, S.-I., Lim, H., Kim, N. Y., Yu, J. J., Cho, J., Lee, H. G., Moon, D. W., & Seo, J. (2025) · iScience · doi:10.1016/j.isci.2025.111893 · Cited by 5
Self-citationExpanding the neuroimmune research toolkit with in vivo brain organoid technologies
Tian, A., Bhattacharya, A., Muffat, J., & Li, Y. (2025) · Disease Models & Mechanisms · doi:10.1242/dmm.052200 · Cited by 6
Naffaa, M. M. (2025) · Regenerative medicine reports . · doi:10.4103/regenmed.regenmed-d-25-00013 · Cited by 5
iPSC-derived neural organoids in dementia research: Recent advances and future directions
Shima, S., Kondo, T., & Inoue, H. (2025) · Neuroscience Research · doi:10.1016/j.neures.2025.104980 · Cited by 6
Advances in Alzheimer’s disease: mechanistic insights and therapeutic targets
Jia, Y.-J., Ge, Y., Li, B., Yang, Y., Chen, H., Liu, J., Guo, J., Yu, J., Ye, K., Wang, J., et al. (2026) · Science China Life Sciences · doi:10.1007/s11427-025-2991-7 · Cited by 6
Anastacio, H. T. D., Matosin, N., & Ooi, L. (2024) · Life · doi:10.3390/life14050625 · Cited by 6
Systems genetics identifies methionine as a high risk factor for Alzheimer's disease
Wang, C., Hei, Y., Liu, Y., Bajpai, A. K., Li, Y., Guan, Y., Xu, F., & Yao, C. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1381889 · Cited by 5
Andromidas, F., MacKinnon, B., Myers, A. J., Shaffer, M. M., Brahimi, A., Atashpanjeh, S., Vazquez, T. L., Le, T., Jellison, E. R., Staurovsky, S., et al. (2024) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2024.103975 · Cited by 4
Tiwari, S. K., & Ginhoux, F. (2025) · hLife · doi:10.1016/j.hlife.2025.02.002 · Cited by 5
Modelling sex differences of neurological disorders in vitro
Castro‐Aldrete, L., Einsiedler, M., Cuní‐López, C., Vanhaelen, Q., Silvestri, A., Ferretti, M. T., de Gennaro, M. E., Putignano, G., Guix, M., Marino, N., et al. (2025) · Nature Reviews Bioengineering · doi:10.1038/s44222-025-00355-w · Cited by 4
Verheijen, B. M. (2019) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2019.00277 · Cited by 5
RetractedGoldstein, L. S. B., & Das, U. (2020) · Progress in molecular biology and translational science · doi:10.1016/bs.pmbts.2020.08.001 · Cited by 5
Weller, A. E., Doyle, G. A. R., Reiner, B. C., Crist, R. C., & Berrettini, W. H. (2021) · Neuroscience Research · doi:10.1016/j.neures.2021.10.010 · Cited by 5
Eren, N., Gerike, S., Üsekes, B., Peters, O., Cosma, N. C., & Hellmann‐Regen, J. (2023) · Immunity & Ageing · doi:10.1186/s12979-023-00376-2 · Cited by 6
Dissection of Neurochemical Pathways Across Complexity and Scale
Abbondanza, A., Kim, N., Lima‐Filho, R. A. S., Amin, A., Anversa, R. G., Almeida, F. B., Cardozo, P. L., Carello‐Collar, G., Carsana, E. V., Folarin, R. O., et al. (2025) · Journal of Neurochemistry · doi:10.1111/jnc.70160 · Cited by 4
Apolipoprotein E4 inhibits γ‐secretase activity via binding to the γ‐secretase complex
Sun, Y., Islam, S., Gao, Y., Nakamura, T., Zou, K., & Michikawa, M. (2022) · Journal of Neurochemistry · doi:10.1111/jnc.15750 · Cited by 5
Aggregate Trends of Apolipoprotein E on Cognition in Transgenic Alzheimer’s Disease Mice
Watson, Y., Nelson, B., Kluesner, J. H., Tanzy, C., Ramesh, S., Patel, Z., Kluesner, K. H., Singh, A., Murthy, V., & Mitchell, C. S. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210492 · Cited by 5
Arnaud, L., Benech, P. D., Greetham, L., Stephan, D., Jimenez, A., Jullien, N. D., García‐González, L., Tsvetkov, P. O., Devred, F., Sancho-Martinez, I., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.04.16.440108 · Cited by 5
Xu, J., Duan, J., Cai, Z., Arai, C., Di, C., Venters, C. C., Xu, J., Jones, M., So, B. R., & Dreyfuss, G. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.10.09.617477 · Cited by 7
Protective ApoE variants support neuronal function by extracting peroxidated lipids
Ralhan, I., Do, A. D., Bae, J.-Y., Feringa, F. M., Cai, W., Chang, J., Chik, K., Lee, N. Y., Gerry, C., van der Kant, R., et al. (2025) · bioRxiv · doi:10.1101/2025.03.05.641722 · Cited by 4
Julia, T. C. W., & Arranz, A. M. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00612-9 · Cited by 4
Pasteris, M., Çakır, S., Bellizzi, A., & Sariyer, I. K. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251359633 · Cited by 4
The Janus face of CaMKII: from memory consolidation to neurotoxic switch in Alzheimer’s disease
Tang, L., Liu, F., Sun, X., Yang, J., Liu, Y., Pan, X., Hao, L., Lou, F., & Su, J. (2025) · Archives of Toxicology · doi:10.1007/s00204-025-04160-7 · Cited by 5
Lessons from ex vivo and in vitro models in microglia research
Cserép, C., Berki, P., Mars, M., Pósfai, B., Pasterkamp, R. J., Benkő, S., & Dénes, Á. (2025) · Trends in Neurosciences · doi:10.1016/j.tins.2025.10.004 · Cited by 5
Banerjee, S., Chandu, P. M., Sarkar, M., Soni, T. K., Saha, M., Fathah Muhammad, L., Chatterjee, B., & Das, U. (2025) · Neurological Research · doi:10.1080/01616412.2025.2600434 · Cited by 5
Gao, C., Lin, Z., Chen, Y., Gan, R., Wang, K., He, X., & Han, H. (2025) · Neuropharmacology and Therapy · doi:10.15212/npt-2025-0015 · Cited by 5
Wang, Y., Anchipolovsky, S., Bhuiyan, P., Sato, L., Liang, G., Chuang, D., & Wei, H. (2026) · Neurotherapeutics · doi:10.1016/j.neurot.2026.e00860 · Cited by 4
Liu, Y., Initiative, A. D. N., Wang, X.-J., Tan, L., Tan, C., & Xu, W. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230516 · Cited by 5
CRISPR/Cas9 gene editing: A new hope for Alzheimer's disease
Shareena, G., Viswalingam, V., Rajput, M. S., & Kumar, D. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-23841-3.00014-5 · Cited by 4
Lipid trajectories improve risk models for Alzheimer’s disease and mild cognitive impairment
Chase, B. A., Frigerio, R., Yucus, C. J., Patel, S. V., Maraganore, D. M., Sanders, A. R., Duan, J., & Markopoulou, K. (2024) · Journal of Lipid Research · doi:10.1016/j.jlr.2024.100714 · Cited by 5
Schulten, W., Czaniera, N. J., Buschheuer, A. L., Liermann, A., Wiegand, A., Kaltschmidt, B., & Kaltschmidt, C. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26199283 · Cited by 4
den Hoedt, S., Dorst‐Lagerwerf, K. Y., de Vries, H. E., Rozemüller, A. J. M., Scheltens, P., Walter, J., Sijbrands, E. J. G., Martínez‐Martínez, P., Verhoeven, A. J. M., Teunissen, C. E., et al. (2023) · Journal of Alzheimer s Disease Reports · doi:10.3233/adr220072 · Cited by 4
Recapitulation and investigation of human brain development with neural organoids
Tamada, A., & Muguruma, K. (2023) · IBRO Neuroscience Reports · doi:10.1016/j.ibneur.2023.12.006 · Cited by 7
ApoE maintains neuronal integrity via microRNA and H3K27me3-mediated repression
Tan, J., Tan, Y.-Y., Ngian, Z., Chong, S. Y., Rao, V. K., Wang, J., Zeng, X., & Ong, C. (2024) · iScience · doi:10.1016/j.isci.2024.109231 · Cited by 5
Modeling Alzheimer's disease using cerebral organoids: Current challenges and prospects
Abijo, A. Z., Olatunji, S., Adelodun, S. T., Asamu, M. O., & Omeiza, N. A. (2024) · Brain Organoid and Systems Neuroscience Journal · doi:10.1016/j.bosn.2024.09.001 · Cited by 6
Is the Relationship Between Cardiovascular Disease and Alzheimer’s Disease Genetic? A Scoping Review
Moore, A. K., & Ritchie, M. D. (2024) · Genes · doi:10.3390/genes15121509 · Cited by 5
The Impact of Apolipoprotein E Allelic Variants on Alzheimer’s Disease
Serrano, E., Sanz, P. G., & Barrantes, F. J. (2021) · Springer eBooks · doi:10.1007/978-3-030-61721-9_29 · Cited by 4
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
