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Cited by 370Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Overexpression of ABCA1 reduces amyloid deposition in the PDAPP mouse model of Alzheimer disease

Open access
Wahrle, Suzanne E., Jiang, Hong, Parsadanian, Maia, Kim, Jungsu, Li, Aimin, Knoten, Amanda, Jain, Sanjay, Hirsch-Reinshagen, Veronica +4 more·2008·Journal of Clinical Investigation
DOI 10.1172/jci33622PMC PMC2200302
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Abstract

APOE genotype is a major genetic risk factor for late-onset Alzheimer disease (AD). ABCA1, a member of the ATP-binding cassette family of active transporters, lipidates apoE in the CNS. Abca1(-/-) mice have decreased lipid associated with apoE and increased amyloid deposition in several AD mouse models. We hypothesized that mice overexpressing ABCA1 in the brain would have increased lipidation of apoE-containing lipoproteins and decreased amyloid deposition. To address these hypotheses, we created PrP-mAbca1 Tg mice that overexpress mouse Abca1 throughout the brain under the control of the mouse prion promoter. We bred the PrP-mAbca1 mice to the PDAPP AD mouse model, a transgenic line overexpressing a mutant human amyloid precursor protein. PDAPP/Abca1 Tg mice developed a phenotype remarkably similar to that seen in PDAPP/Apoe(-/-) mice: there was significantly less amyloid beta-peptide (Abeta) deposition, a redistribution of Abeta to the hilus of the dentate gyrus in the hippocampus, and an almost complete absence of thioflavine S-positive amyloid plaques. Analyses of CSF from PrP-mAbca1 Tg mice and media conditioned by PrP-mAbca1 Tg primary astrocytes demonstrated increased lipidation of apoE-containing particles. These data support the conclusions that increased ABCA1-mediated lipidation of apoE in the CNS can reduce amyloid burden and that increasing ABCA1 function may have a therapeutic effect on AD.

AI snapshot

Written from the paper’s full text.

TL;DR

Overexpression of ABCA1 in the brain increased lipidation of apoE-containing lipoproteins and markedly reduced fibrillar amyloid deposition in PDAPP mice. The phenotype resembled PDAPP/Apoe−/− mice, supporting ABCA1/apoE lipidation as a potential AD therapeutic target.

Key findings

  • PrP-mAbca1 transgenic mice overexpressed ABCA1 throughout the brain at approximately 2- to 14-fold across five lines; when crossed to PDAPP mice, PDAPP/Abca1 Tg mice had significantly less Aβ deposition, redistribution of Aβ to the hilus of the dentate gyrus, and almost no thioflavine S–positive amyloid plaques, similar to PDAPP/Apoe−/− mice.
  • At 12 months, Aβ levels were approximately 2.5-fold lower in PDAPP/Abca1 line D and approximately 3-fold lower in line E versus non-Tg littermates; thioflavine S–positive amyloid was decreased by approximately 50% with 2-fold ABCA1 overexpression and to almost 0 with 6-fold or greater overexpression.
  • At 3 months, before histological Aβ deposition, PDAPP/Abca1 line D and E Tg mice had 15%–50% higher Aβ levels than non-Tg controls, with no differences in APP or APP C-terminal fragments, suggesting altered clearance/transport rather than increased production.
  • ABCA1 overexpression increased apoE lipidation: CSF apoE particles tended to be larger, astrocyte-conditioned media had a greater proportion of apoE particles larger than 11 nm, and lipoprotein fractions showed a significantly greater cholesterol-to-apoE ratio. High-expressing lines also had lower apoE in hippocampus (approximately 40%) and CSF (approximately 40%–70%), but line D reduced Aβ without lowering apoE.

Methods

  • Mouse Abca1 cDNA was cloned into the MoPrP.HD-N171 vector to create PrP-mAbca1 Tg mice; five lines (D, E, L, J, G) with 2- to 14-fold brain ABCA1 overexpression were characterized, and lines D, E, and J were bred to the PDAPP AD mouse model.
  • Mice were analyzed at 3 or 12 months with non-Tg littermate controls; outcomes included Aβ and thioflavine S histology/stereology, Aβ and apoE ELISAs, Western blotting, real-time RT-PCR, CSF and astrocyte-conditioned media lipoprotein analyses by nondenaturing gradient gel electrophoresis and size-exclusion chromatography, and testis histology/TUNEL/immunohistochemistry.
  • Statistical comparisons used two-tailed Student’s t test or Mann-Whitney U test, with P < 0.05 considered significant.

Limitations

  • The paper states that it is unclear whether increasing ABCA1 in adulthood may compromise male fertility, or whether ABCA1 can be selectively targeted to brain versus testes or other organs; male mice overexpressing ABCA1 at 6-fold or greater were infertile, with approximately 50% reduced testes mass and approximately 3-fold more apoptotic testicular cells.
  • The paper notes that mechanisms linking increased apoE lipidation to altered Aβ transport, clearance, or aggregation were not directly tested, and that behavioral studies in APP Tg mice can be difficult to interpret.
  • Evident from the text: findings are from transgenic mouse models with supraphysiological ABCA1 overexpression, some high-expressing lines had peripheral cholesterol changes of unknown mechanism, and several supporting observations are reported as data not shown.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1172/jci33622

Cites

66 of 66 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 16 cited sources checked · 0 supported · 0 flagged

  • Findingown data

    The five PrP-mAbca1 Tg lines examined had different levels of ABCA1 overexpression in the cortex, ranging from approximately 2-fold in line D to approximately 14-fold in line G.

    “ranging from approximately 2-fold in line D to approximately 14-fold in line G (Figure 1A).”
    Quote in the paperNot a substantial claim
  • Findingown data

    PrP-mAbca1 Tg mice overexpress ABCA1 throughout the brain.

    “Analysis of tissue from the occipital cortex, frontal cortex, hippocampus, cerebellum, striatum, septum, and thalamus showed that PrP-mAbca1 Tg mice overexpressed ABCA1 throughout the brain (Figure 1B).”
    Quote in the paperSubstantial claim
  • Findingown data

    In the CSF, apoE levels were decreased by approximately 40%-70% in all lines overexpressing ABCA1.

    “In the CSF, apoE levels were decreased by approximately 40%-70% in all lines overexpressing ABCA1 (Figure 6C).”
    Quote in the paperSubstantial claim
  • Findingown data

    There was no difference between Tg and non-Tg apoE mRNA levels in either the hippocampus or cortex of PrP-mAbca1 line E and line J mice.

    “We found no difference between Tg and non-Tg apoE mRNA levels in either the hippocampus or cortex of either line (Figure 6D and data not shown).”
    Quote in the paperSubstantial claim
  • Findingown data

    Overexpression of ABCA1 by 6-fold or greater resulted in reductions in hippocampal apoE of approximately 40% compared with non-Tg littermate control mice.

    “overexpression of ABCA1 by 6-fold or greater resulted in reductions in hippocampal apoE of approximately 40% compared with non-Tg littermate control mice (Figure 6A).”
    Quote in the paperSubstantial claim
  • May combine two claims. 16
  • Classified as probably not a substantial claim. 4

  • May combine two claims.

    Findingown data

    PDAPP/Abca1 non-Tg mice had frequent punctate Aβ deposits in the cortex and hippocampus, including the molecular layer, but almost no Aβ deposits in the hilus of the dentate gyrus.

    “The PDAPP mice with wild-type ABCA1 levels (PDAPP/Abca1 non-Tg mice) had frequent punctate Aβ deposits in the cortex and hippocampus (Figure 3A, top left panel), including the molecular layer of the hippocampus, but almost no Aβ deposits in the hilus of the dentate gyrus of the hippocampus (Figure 3A, middle left panel).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    PDAPP/Abca1 Tg mice had rare Aβ deposition in the cortex, occasional Aβ deposition in the molecular layer, and frequent Aβ deposition in the hilus of the dentate gyrus.

    “In contrast, the PDAPP mice with ABCA1 overexpression (PDAPP/Abca1 Tg mice) had rare Aβ deposition in the cortex (Figure 3A, top middle panel), occasional Aβ deposition in the molecular layer, and frequent Aβ deposition in the hilus of the dentate gyrus (Figure 3A, middle panel).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingnone given

    Decreases or increases in ABCA1 expression alter the absolute level of apoE without affecting Apoe transcription.

    “Since decreases or increases in ABCA1 expression alter the absolute level of apoE without affecting Apoe transcription, understanding how ABCA1 alters apoE metabolism in the brain will be important.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    PDAPP/Abca1 Tg mice had almost no thioflavine S-positive amyloid plaques in the cortex and hippocampus, unlike PDAPP/Abca1 non-Tg mice.

    “However, almost no thioflavine S-positive amyloid plaques were seen in the PDAPP/Abca1 Tg mice (Figure 3A, bottom middle panel) or in PDAPP/Apoe -/-mice (Figure 3A, bottom right panel), even in sections with extensive Aβ deposits.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In the cortex, apoE was decreased by only approximately 20% in Tg mice from PrP-mAbca1 lines L, J, and G and was not decreased significantly in lines D or E.

    “In the cortex, apoE was decreased by only approximately 20% in Tg mice from PrP-mAbca1 lines L, J, and G and was not decreased significantly in lines D or E (Figure 6B).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    The Aβ load in the entire hippocampus did not vary significantly according to the presence of the mABCA1 transgene, but the distribution of Aβ within the hippocampus was altered by the transgene.

    “The Aβ load in the entire hippocampus did not vary significantly according to the presence of the mABCA1 transgene, but the distribution of Aβ within the hippocampus was altered by the transgene.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    PDAPP/Abca1 Tg mice had more Aβ deposition in the hilus of the dentate gyrus and less in the molecular layer than non-Tg mice.

    “PDAPP/Abca1 Tg mice had more Aβ deposition in the hilus of the dentate gyrus and less in the molecular layer (Figure 4A).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    PDAPP/Abca1 Tg mice had decreased deposition of Aβ, a near absence of thioflavine S-positive amyloid plaques, and a redistribution of Aβ deposits in the hippocampus from the molecular layer to the hilus of the dentate gyrus.

    “We found that PDAPP/Abca1 Tg mice had (a) decreased deposition of Aβ; (b) a near absence of thioflavine S-positive amyloid plaques; and (c) a redistribution of Aβ deposits in the hippocampus from the molecular layer to the hilus of the dentate gyrus.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    APP Tg mice crossed to mice lacking Apoe develop significantly less Aβ deposition, and the plaques that do form are almost all nonfibrillar and are not associated with neuritic dystrophy.

    “APP Tg mice that are crossed to mice lacking Apoe develop significantly less Aβ deposition, and strikingly, the Aβ plaques that do form are almost all nonfibrillar and are not associated with neuritic dystrophy (20,23,24).”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [20]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [23]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [24]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Premisecitation

    Deletion of Abca1 either has no effect on or even increases Aβ deposition in four different mouse models of AD.

    “3 laboratories independently found that deletion of Abca1 either has no effect on or even increases Aβ deposition in 4 different mouse models of AD (20,23,24).”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [20]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [23]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [24]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Interpretationcitation

    Lipid-poor apoE binds to fibrillar Aβ in vivo and likely promotes amyloidogenesis.

    “demonstrating that lipid-poor apoE binds to fibrillar Aβ in vivo and likely promotes amyloidogenesis.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [23]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [24]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Classified as probably not a substantial claim.

    Study design and conductreasoning

    Non-Tg littermate mice were always used as controls in experiments with the PrP-mAbca1 Tg mice from the appropriate line to control for genetic background effects.

    “To control for genetic background effects, non-Tg littermate mice were always used as controls in experiments with the PrP-mAbca1 Tg mice from the appropriate line.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data

    The size of the decrease in hippocampal apoE did not vary between lines that overexpressed ABCA1 6-fold to 14-fold, indicating that the effect is saturable.

    “The size of the decrease did not vary between lines that overexpressed ABCA1 6-fold to 14-fold, indicating that the effect is saturable.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Activation of the transcription factor LXR increases transcription of ABCA1 and many other genes involved in lipid metabolism and other pathways.

    “Activation of the transcription factor LXR has been shown to increase transcription of ABCA1 and many other genes involved in lipid metabolism and other pathways (50)(51)(52).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites (50)(51)(52)

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Interpretationreasoning

    Overexpression of ABCA1 in the brain decreases the amyloidogenic properties of apoE, and increased apoE lipidation results in a phenotype very similar to apoE deficiency with respect to Aβ metabolism.

    “This phenotype strongly argues that overexpression of ABCA1 in the brain decreases the amyloidogenic properties of apoE and, further, that increased apoE lipidation results in a phenotype very similar to apoE deficiency with respect to Aβ metabolism.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The PDAPP mouse model of AD recapitulates key features of human AD such that findings in this model are relevant to AD.
    • Rests on an assumption: Aβ deposition and fibrillogenesis in mouse models are appropriate measures of AD pathology.

  • May combine two claims.

    Interpretationreasoning

    A 2-fold overexpression of ABCA1 in the brain is insufficient to significantly alter either apoJ or apoE levels.

    “Because this difference in apoJ levels was not observed in ABCA1 line D mice (data not shown), a 2-fold overexpression of ABCA1 in the brain is insufficient to significantly alter either apoJ or apoE levels (Figure 6A).”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Lipidated apoE binds with a much higher affinity than poorly lipidated apoE to soluble Aβ.

    “In addition, lipidated apoE binds with a much higher affinity than poorly lipidated apoE to soluble Aβ (60).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [60]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Lipidated apoE forms an SDS-stable complex with Aβ to a greater extent than nonlipidated apoE.

    “Previous in vitro work has shown that lipidated apoE forms an SDS-stable complex with Aβ to a greater extent than nonlipidated apoE (58,59).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [58]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [59]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Interpretationown data

    The higher Aβ levels at 3 months in PDAPP/Abca1 Tg mice do not represent deposited Aβ, as the mice did not have histological evidence of Aβ deposition at that age.

    “These higher levels do not represent deposited Aβ, as the mice did not have histological evidence of Aβ deposition at this age.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data

    There were no differences in levels of APP and C-terminal fragments between PDAPP/Abca1 line E Tg and PDAPP/non-Tg mice, suggesting that Aβ production was not likely to account for the differences in Aβ levels at 3 months.

    “There were no differences between PDAPP/Abca1 line E Tg and PDAPP/non-Tg mice (Figure 5E), suggesting that Aβ production was not likely to account for the differences in Aβ levels at 3 months.”
    Quote in the paperSubstantial claim
20 of 20

  • The paper relies on this without support.

    The PDAPP mouse model of AD recapitulates key features of human AD such that findings in this model are relevant to AD.

    “PDAPP AD mouse model, a transgenic line overexpressing a mutant human amyloid precursor protein.”
    “increasing ABCA1 function may have a therapeutic effect on AD.”

  • The paper relies on this without support.

    Aβ deposition and fibrillogenesis in mouse models are appropriate measures of AD pathology.

    “These data support the conclusions that increased ABCA1-mediated lipidation of apoE in the CNS can reduce amyloid burden and that increasing ABCA1 function may have a therapeutic effect on AD.”

  • The paper relies on this without support.

    The effects of ABCA1 overexpression on Aβ deposition are not due to altered expression of other proteins outside those tested.

    “No differences were found in the levels of low-density lipoprotein receptor (LDLR), LDLR-related protein 1 (LRP1), and apoA-I when comparing ABCA1 line E Tg mice to non-Tg littermates (Figure 8, A and B).”
3 of 3

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?

  • Increasing Abca1 expression, and subsequently apoE lipidation, reduces Aβ peptides and plaque deposition.

    “Conversely, increasing Abca1 expression, and subsequently apoE lipidation, reduces Aβ peptides and plaque deposition. 13”

    From Deletion of miR-33, a regulator of the ABCA1–APOE pathway, ameliorates neuropathological phenotypes in APP/PS1 mice (2024) · cites this paper as [13]

    The Discussion reports reduced Aβ deposition and near-absent fibrillar plaques in PDAPP mice overexpressing ABCA1; the apoE results report increased lipidation of apoE-containing particles. But the Results section on amyloid deposition reports higher, not lower, Aβ levels in these mice at three months, so the unqualified claim that Aβ peptides are reduced overstates the findings (page unavailable in our copy). (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • ABCA1 overexpression or LXR/RXR agonist treatment decreases amyloid deposition in APP transgenic mouse models.

    “ABCA1 overexpression or LXR/RXR agonist treatment decreased amyloid deposition [66-69].”

    From MicroRNAs in brain cholesterol metabolism and their implications for Alzheimer's disease (2016) · cites this paper as [69]

    The Introduction reports that ABCA1 overexpression reduced amyloid deposition in PDAPP mice, an APP transgenic model. The Discussion says LXR agonists affect Aβ levels, but does not establish that LXR/RXR agonist treatment decreased amyloid deposition in these mice. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Both overexpression and deletion of ABCA1 in the mouse brain result in a decrease in apoE protein level.

    “Both the overexpression and deletion of ABCA1 in the mouse brain resulted in a decrease in apoE protein level [28-30].”

    From Measurement of apolipoprotein E and amyloid β clearance rates in the mouse brain using bolus stable isotope labeling (2012) · cites this paper as [30]

    The Introduction reports markedly lower brain apoE in mice lacking ABCA1. In “ApoE levels and solubility in PrP-mAbca1 Tg mice,” overexpression of sixfold or more reduced hippocampal apoE, but twofold overexpression did not alter it; the reduction also varied by brain region. The claim omits those limits on the overexpression finding. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • The apoE-containing lipoprotein particles isolated from the CSF of ABCA1−/− mice are poorly lipidated, while those from the CSF of mice overexpressing ABCA1 have higher levels of lipidation compared to wild-type animals.

    “However, the apoE containing lipoprotein particles isolated from the cerebral spinal fluid (CSF) of ABCA1−/− mice were poorly lipidated, while those from the CSF of mice overexpressing ABCA1 had higher levels of lipidation compared to Wt animals [28,30].”

    From Measurement of apolipoprotein E and amyloid β clearance rates in the mouse brain using bolus stable isotope labeling (2012) · cites this paper as [30]

    The Introduction reports abnormally small apoE-containing particles in the CSF of ABCA1-deficient mice and describes their apoE as poorly lipidated. In “ApoE levels and solubility in PrP-mAbca1 Tg mice” (page unavailable), CSF particles from overexpressing mice only tended to be larger than controls, which the authors say suggests greater lipidation. The claim states that greater CSF lipidation as a definite finding; the paper’s direct lipidation measurement was instead of particles secreted by cultured astrocytes. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • 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 [44]

    The Discussion reports that genetic overexpression of ABCA1 increased apoE lipidation and reduced Aβ deposition in PDAPP mice. It describes increased Aβ clearance as a possibility for future testing, not an established result; it also proposes cognitive-performance studies rather than reporting improvement. The cited study does not establish the pharmacological part of the claim. (LLM, conf=0.89)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

  • Three-month cortical Aβ40 total does not equal its components

    Minor

    For the line D transgenic group, carbonate Aβ40 of 0.23 plus guanidine Aβ40 of 0.05 gives 0.28, not the reported total of 0.73.

    Reported 0.73 · recomputed 0.28

1 of 1

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Related

Authors
Wahrle, S. E., Jiang, H., Parsadanian, M., Kim, J., Li, A., Knoten, A., Jain, S., Hirsch-Reinshagen, V., Wellington, C. L., Bales, K. R., Paul, S. M., & Holtzman, D. M.
Affiliations
  • Washington University in St. Louis (US)
  • University of British Columbia (CA)
  • Eli Lilly (United States) (US)
Corresponding author
Holtzman, David M.
ORCID
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
2008-01-17
Volume
118
Issue
2
Pages
671-82
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci33622
PMC
PMC2200302
OpenAlex
W2165895874
Semantic Scholar
d3897f2ef12c640d78228188112f4cc8ebffe747
Cited by
370
References
65
Citations by year
2026: 4 · 2025: 15 · 2024: 16 · 2023: 15 · 2022: 20 · 2021: 24 · 2020: 22 · 2019: 17 · 2018: 13 · 2017: 20 · 2016: 14 · 2015: 24 · 2014: 33 · 2013: 25 · 2012: 30
FWCI
15.67
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed (publishedVersion)
  • Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
  • Europe PMC (PubMed Central) (submittedVersion)
  • PubMed Central (submittedVersion)
Funders
  • American Health Assistance Foundation
  • Eli Lilly and Company
  • National Institutes of Health (AG13956)
  • Canadian Institutes of Health Research
  • National Institute on Aging (R01 AG013956, R37AG013956, AG13956)
  • National Institute of Diabetes and Digestive and Kidney Diseases (P30DK079333)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD047396, K08 HD047396)
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
ABCA1, Alzheimer's disease, amyloid-beta deposition, amyloid plaques, apolipoprotein E, amyloid precursor protein overexpression, transgenic mice, dentate gyrus, cerebrospinal fluid, astrocytes, APOE genotype, therapeutic target
MeSH terms
Alzheimer Disease, Animals, Apolipoproteins E, Astrocytes, Brain, Brain Chemistry, Disease Models, Animal, Lipoproteins, Male, Mice, Transgenic, Amyloid beta-Peptides, ATP-Binding Cassette Transporters, Mice, ATP Binding Cassette Transporter 1

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