ApoE-Directed Therapeutics Rapidly Clear β-Amyloid and Reverse Deficits in AD Mouse Models
Open accessAbstract
Reversing Decline?: Apolipoprotein E (apoE) normally helps in the clearance of β-amyloid from the brain, a process that is compromised in Alzheimer's disease. Cramer et al. (p. 1503 , published online 9 February; see the Perspective by Strittmatter ) now show that a drug that increases apoE expression rapidly promoted soluble β-amyloid clearance in a mouse model of Alzheimer's disease. The drug also improved cognitive, social, and olfactory performance and rapidly improved neural circuit function. Similar therapeutics may potentially help to ameliorate the symptoms of Alzheimer's disease and its prodromal states.
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Trans-BBB efflux of Aβ into peripheral blood circulation is one of the main pathways of physiological clearance, with ApoE, ApoJ, and ApoA1 as chaperones.
“Several groups have reported that trans-BBB efflux of Aβ into peripheral blood circulation is one of the main pathways of physiological clearance with ApoE, ApoJ, and ApoA1 as chaperones27,31,32.”
From Brain-targeted drug delivery by manipulating protein corona functions (2019) · cites this paper as [32]
The Abstract (page unavailable) says apoE facilitates physiological Aβ clearance from the brain, and the paper reports apoE-dependent clearance in mice. It does not identify efflux across the blood–brain barrier into peripheral blood as a main clearance pathway or name ApoJ and ApoA1 as chaperones. (LLM, conf=0.86)
Experimental — accuracy not yet measuredBexarotene increases apoE levels in mice within hours.
“bexarotene (an RXR agonist) increases apoE levels”
From APOE4-specific Changes in Aβ Accumulation in a New Transgenic Mouse Model of Alzheimer Disease (2012) · cites this paper as [76]
The apoE-expression passage (indexed under Abstract; page not provided) reports increased apoE expression in bexarotene-treated mice after treatment measured in days. The six-hour passage reports a decrease in Aβ, not an increase in apoE, so the added 'within hours' timing is not supported. (LLM, conf=0.88)
Experimental — accuracy not yet measuredTreatment with LXR/RXR agonists increases levels of ABCA1 and APOE and decreases amyloid deposition in APP overexpressing cells and mice.
“Several studies demonstrated that treatment of LXR/RXR agonists increase the levels of ABCA1 and APOE and decrease amyloid deposition in APP overexpressing cells and mice [73-77].”
From MicroRNAs in brain cholesterol metabolism and their implications for Alzheimer's disease (2016) · cites this paper as [74]
The Abstract (passage 6; page unavailable) reports increased apoE and ABCA1 expression and reduced Aβ plaques after short-term bexarotene treatment in APP/PS1 mice. It also reports increased expression in treated primary microglia and astrocytes (passage 2), but does not identify these as APP-overexpressing cells or show decreased amyloid deposition in them. Plaque burden was unchanged after three months of treatment in APP/PS1 mice (passage 5). (LLM, conf=0.87)
Experimental — accuracy not yet measuredTreatment of several AD Tg mice models with liver X receptor or retinoid X receptor agonists, which upregulate ApoE expression and enhance its lipidation status, resulted in reduction of Aβ plaque load through enhancing clearance of Aβ by glial cells.
“In addition, treatment of several AD Tg mice models with liver X receptor or retinoid X receptor agonists, which upregulate ApoE expression and enhance its lipidation status, resulted in reduction of Ab plaque load through enhancing clearance of Ab by glial cells.43,44”
From Blocking the Interaction between Apolipoprotein E and Aβ Reduces Intraneuronal Accumulation of Aβ and Inhibits Synaptic Degeneration (2013) · cites this paper as [44]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredBexarotene facilitates intracellular degradation of soluble Aβ1-42 in a PPARγ-, liver X receptor-, and apolipoprotein E-dependent manner.
“Recently, the RXR agonist bexarotene has been reported to facilitate the intracellular degradation of soluble A 1-42 in a PPAR␥-, liver X receptor-, and apolipoprotein E-dependent manner (Cramer et al., 2012).”
From PPARγ/RXRα-Induced and CD36-Mediated Microglial Amyloid-β Phagocytosis Results in Cognitive Improvement in Amyloid Precursor Protein/Presenilin 1 Mice (2012) · cites this paper as Cramer et al., 2012
In the passage labeled Abstract (page unavailable), the paper reports that bexarotene facilitated degradation of soluble Aβ42 by primary microglia and astrocytes in a PPARγ-, LXR-, and apoE-dependent manner. It does not specify that the degradation was intracellular; a search for “intracellular” found no passage establishing that detail. (LLM, conf=0.86)
Experimental — accuracy not yet measured
ApoE is a central apolipoprotein in cerebral cholesterol metabolism and is involved in brain amyloid metabolism, blood brain barrier integrity, and transport of various lipid species to neuronal cells.
“apoE is a central apolipoprotein in cerebral cholesterol metabolism and is involved in brain amyloid metabolism, blood brain barrier integrity, and transport of various lipid species to neuronal cells [15][16][17][18][19].”
From APOE and vascular disease: Sequencing and genotyping in general population cohorts (2023) · cites this paper as [18]
The paper’s introductory passage (indexed under Abstract; page unavailable) describes apoE’s role in forming HDL particles and promoting soluble β-amyloid degradation, supporting its involvement in lipid and brain amyloid metabolism. It does not say that apoE maintains blood–brain barrier integrity or transports lipid species to neuronal cells; its blood–brain barrier statement concerns bexarotene, not apoE. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe similar findings for rare APOE variants with low apoE may reflect that the intracerebral vasculature, brain tissue and blood-brain barrier are dependent on normal levels of apoE for sufficient local lipid transport and β-amyloid clearance.
“The similar findings presently observed for rare APOE variants with low apoE may reflect that the intracerebral vasculature, brain tissue and blood-brain barrier are dependent on normal levels of apoE for sufficient local lipid transport and βamyloid clearance [17,18,31,43].”
From APOE and vascular disease: Sequencing and genotyping in general population cohorts (2023) · cites this paper as [18]
The paper's main text (indexed under Abstract; page unavailable) links apoE and lipid transport to soluble β-amyloid clearance, and reports that enhanced clearance in mice required apoE. It does not establish that intracerebral vasculature or the blood-brain barrier depend on normal apoE levels, or test the rare APOE variants in the citing sentence. (LLM, conf=0.84)
Experimental — accuracy not yet measuredBexarotene is an FDA-approved liver X receptor/retinoid X receptor agonist for use in refractory cutaneous T cell lymphoma and has been shown to enhance Aβ clearance and improve cognitive performance in plaque-depositing mouse models.
“Bexarotene is an FDA-approved liver X receptor/retinoid X receptor agonist for use in refractory cutaneous T cell lymphoma and has been shown to enhance Aβ clearance and improve cognitive performance in plaque-depositing mouse models209.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [209]
The paper’s text indexed under Abstract (page not specified) identifies bexarotene as an FDA-approved RXR agonist and reports enhanced Aβ clearance and improved cognition in plaque-depositing mouse models. It describes activation of LXR:RXR but does not call bexarotene an LXR agonist or specify FDA approval for refractory cutaneous T-cell lymphoma. (LLM, conf=0.88)
Experimental — accuracy not yet measuredBexarotene significantly reduces insoluble Aβ after 3 days.
“significantly reduces insoluble A after 3 days”
From APOE4-specific Changes in Aβ Accumulation in a New Transgenic Mouse Model of Alzheimer Disease (2012) · cites this paper as [76]
Plaque levels at 3 months remained unchanged after bexarotene.
“although plaque levels at 3 months remained unchanged (76).”
From APOE4-specific Changes in Aβ Accumulation in a New Transgenic Mouse Model of Alzheimer Disease (2012) · cites this paper as [76]
Bexarotene decreases soluble Aβ in mice within hours.
“decreases soluble A in mice within hours”
From APOE4-specific Changes in Aβ Accumulation in a New Transgenic Mouse Model of Alzheimer Disease (2012) · cites this paper as [76]
RXR activation facilitates Aβ clearance in an ApoE-dependent manner.
“Cramer et al. demonstrated that RXR activation facilitate Aβ clearance in an ApoE dependent manner [74].”
From MicroRNAs in brain cholesterol metabolism and their implications for Alzheimer's disease (2016) · cites this paper as [74]
Published data indicate that the ApoE/Aβ interaction may result in multidirectional effects that may promote Aβ degradation by nonneuronal cells while enhancing Aβ accumulation in neurons.
“These published data indicate that the ApoE/Ab interaction may result in multidirectional effects that may promote Ab degradation by nonneuronal cells 43,44 while enhancing Ab accumulation in neurons.”
From Blocking the Interaction between Apolipoprotein E and Aβ Reduces Intraneuronal Accumulation of Aβ and Inhibits Synaptic Degeneration (2013) · cites this paper as [44]
Activation of the Retinoid X Receptor rapidly reverses AD pathology in mouse models of AD.
“Recently, we have shown that activation of the Retinoid X Receptor, the obligate heterodimeric partner of PPARγ and LXRs, rapidly reverses AD pathology in mouse models of AD, and many of the beneficial effects seen in that study may occur through activation of PPAR signaling pathways (Cramer et al., 2012).”
From Mechanisms Underlying the Rapid Peroxisome Proliferator-Activated Receptor-γ-Mediated Amyloid Clearance and Reversal of Cognitive Deficits in a Murine Model of Alzheimer's Disease (2012) · cites this paper as Cramer et al., 2012
Increasing apoE lipidation, either through genetic or pharmacological approaches, promotes Aβ clearance and improves cognitive performance in mice.
“In addition, several studies have demonstrated that increasing apoE lipidation, either through genetic or pharmacological approaches, promotes Aβ clearance and improves cognitive performance in mice (27, 44, 45).”
From <i>APOE3</i> -Jacksonville (V236E) variant reduces self-aggregation and risk of dementia (2021) · cites this paper as [45]
Expression of apoE in the brain mediates clearance of amyloid-b peptides.
“This should be seen in the context that b-amyloid markers do become abnormal up to 20 years before clinical symptoms become overt [114], and because expression of apoE in the brain mediates clearance of amyloid-b peptides [89], a clearance that is impaired in Alzheimer disease [90].”
From Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review (2016) · cites this paper as [89]
Induction of murine Apoe expression improves amyloid-b clearance and cognition.
“Additionally, induction of murine Apoe expression improves amyloid-b clearance and cognition; this finding also underlines the importance of the level of apoE [89].”
From Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review (2016) · cites this paper as [89]
Administration of RXR or LXR agonists reduces Aβ aggregation and restores cognitive function in AD mouse model.
“the administration of RXR or LXR agonists reduces Aβ aggregation and restores cognitive function in AD mouse model (11, 12)”
From Nuclear SphK2/S1P signaling is a key regulator of ApoE production and Aβ uptake in astrocytes (2024) · cites this paper as [11]
Bexarotene has shown therapeutic effects in AD model mice.
“Bexarotene has shown therapeutic effects in AD model mice (11)”
From Nuclear SphK2/S1P signaling is a key regulator of ApoE production and Aβ uptake in astrocytes (2024) · cites this paper as [11]
Oral administration of the RXR agonist bexarotene in an Alzheimer disease mouse model facilitates rapid clearance of soluble amyloid-beta, linked to increased ApoE levels and TREM2 expression.
“Oral administration of the RXR agonist bexarotene in a mouse model of AD facilitated rapid clearance of soluble Aβ (103). The therapeutic effect was linked to the induction of increased levels of ApoE. Moreover, a recent study showed that bexarotene induces TREM2 expression in microglia (197).”
From Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017) · cites this paper as [103]
Bexarotene has been reported to improve memory, cognition, and pathology in mouse models of Alzheimer's disease and aging.
“Bexarotene has been reported to improve memory, cognition, and pathology in mouse models of AD819 and aging11 and is now in early phase clinical trials2021.”
From Neuronally-directed effects of RXR activation in a mouse model of Alzheimer’s disease (2017) · cites this paper as [8]
Bexarotene has previously been shown to reduce amyloid plaque pathology in APP/PS1, APPPS1-21, and Tg2576 mouse models of Alzheimer's disease.
“Bexarotene has previously been shown to reduce amyloid plaque pathology in APP/PS1, APPPS1–21, and Tg2576 mouse models of AD8.”
From Neuronally-directed effects of RXR activation in a mouse model of Alzheimer’s disease (2017) · cites this paper as [8]
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- Authors
- Cramer, P. E., Cirrito, J. R., Wesson, D. W., Lee, C. Y. D., Karlo, J. C., Zinn, A. E., Casali, B. T., Restivo, J. L., Goebel, W. D., James, M. J., Brunden, K. R., Wilson, D. A., & Landreth, G. E.
- Affiliations
- Case Western Reserve University (US)
- Washington University in St. Louis (US)
- Nathan Kline Institute for Psychiatric Research (US)
- University of Pennsylvania (US)
- Corresponding author
- Landreth, Gary E.
- ORCID
- Venue
- Science
- Published
- 2012-03-23
- Volume
- 335
- Issue
- 6075
- Pages
- 1503-1506
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3651582
- OpenAlex
- W2081388499
- Cited by
- 1,050
- References
- 31
- Citations by year
- 2026: 27 · 2025: 31 · 2024: 41 · 2023: 37 · 2022: 53 · 2021: 67 · 2020: 59 · 2019: 71 · 2018: 57 · 2017: 68 · 2016: 90 · 2015: 106 · 2014: 131 · 2013: 123 · 2012: 88
- FWCI
- 96.72
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG037693, AG030482-03S1, R01AG030482, K01AG029524, P50AG005681)
- National Institute on Deafness and Other Communication Disorders (DC-003906, R01DC003906)
- Topics
- Health Sciences › Medicine › Physiology › 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
- Alzheimer's disease, amyloid-beta clearance, apolipoprotein E, bexarotene, retinoid X receptor, PPARγ, liver X receptor, nuclear receptor agonists, amyloid plaques, cognitive impairment, social dysfunction, olfactory dysfunction, neural circuit function
- MeSH terms
- Liver X Receptors, Bexarotene, Alzheimer Disease, Amyloidosis, Animals, Apolipoproteins E, Astrocytes, Behavior, Animal, Brain, Disease Models, Animal, Male, Mice, Inbred C57BL, Mice, Transgenic, Odorants, Olfactory Pathways, Phagocytosis, Tetrahydronaphthalenes, Amyloid beta-Peptides, Microglia, Extracellular Fluid, Retinoid X Receptors, PPAR gamma, Mice, Orphan Nuclear Receptors, Plaque, Amyloid, Molecular Targeted Therapy
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