RETRACTED ARTICLE: Pericyte loss influences Alzheimer-like neurodegeneration in mice
Open accessAbstract
Pericytes are cells in the blood–brain barrier that degenerate in Alzheimer’s disease (AD), a neurological disorder associated with neurovascular dysfunction, abnormal elevation of amyloid β-peptide (Aβ), tau pathology and neuronal loss. Whether pericyte degeneration can influence AD-like neurodegeneration and contribute to disease pathogenesis remains, however, unknown. Here we show that in mice overexpressing Aβ-precursor protein, pericyte loss elevates brain Aβ40 and Aβ42 levels and accelerates amyloid angiopathy and cerebral β-amyloidosis by diminishing clearance of soluble Aβ40 and Aβ42 from brain interstitial fluid prior to Aβ deposition. We further show that pericyte deficiency leads to the development of tau pathology and an early neuronal loss that is normally absent in Aβ-precursor protein transgenic mice, resulting in cognitive decline. Our data suggest that pericytes control multiple steps of AD-like neurodegeneration pathogenic cascade in Aβ-precursor protein-overexpressing mice. Therefore, pericytes may represent a novel therapeutic target to modify disease progression in AD. Pericytes are cells in the blood–brain barrier that degenerate with the onset of Alzheimer's disease. Here, Sagare et al. show that pericyte loss contributes to disease onset by promoting amyloid-beta accumulation, tau pathology and early loss of neuronal cells.
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LRP1 mediates cellular uptake of Aβ followed by its intracellular degradation and clearance.
“which mediates cellular uptake of A 𝛃 followed by its intracellular degradation and clearance (513, 647).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [513]
The Results section reports that cultured murine brain pericytes clear extracellular Aβ40 through LRP1. The Methods section describes measuring Aβ40 internalization and lysosomal colocalization, but the cited passages do not establish its subsequent intracellular degradation; the claim also generalizes beyond the pericytes studied. Page numbers are not available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredBBB disruption develops early in APP transgenic models carrying human ADAD mutations before Aβ accumulation, CAA, and behavioral deficits.
“Additionally, laboratory studies tell us that BBB disruption develops early in APP transgenic models carrying human ADADmutations (467, 513, 606) before A 𝛃 accumulation, CAA, and behavioral deficits (151, 336, 606, 638)”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [513]
The Results section on vascular damage reports BBB leakage at one month in APPsw/0 mice with additional Pdgfrβ-linked pericyte deficiency. Other Results sections report no change in Aβ levels or behavior at that age, with amyloid deposition and CAA developing later. The claim omits the pericyte-deficiency condition and broadens this finding to APP transgenic models generally; the paper supports BBB disruption before increased Aβ pathology, not before Aβ is present at all. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredProgressive BBB breakdown develops early in APP Sw/0 mice beginning at 1-3 months of age before Aβ deposition, CAA, and behavioral memory recognition deficits that are observed beginning at 10-12 months of age.
“Some studies in transgenic murine models have examined the temporal sequence of appearance of different pathologies, revealing that progressive BBB breakdown develops early in APP Sw/0 mice beginning at 1-3 mo of age (467, 513, 606) before A 𝛃 deposition, CAA, and behavioral memory recognition deficits that are observed beginning at 10-12 mo of age (151, 336, 606, 638).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [513]
The Results section, “Vascular damage in pericyte-deficient APPsw/0 mice” (page unavailable), reports BBB leakage at 1 month that becomes more pronounced later, supporting the early-breakdown sequence. But those measurements concern pericyte-deficient APPsw/0; Pdgfrβ+/− mice, not APPsw/0 mice generally. The Results sections on Aβ pathology and neuronal loss report deposition beginning at 6 months and behavioral deficits at 9 months in the pericyte-deficient mice; they do not establish the claimed 10–12-month onset for Aβ deposition, CAA, and recognition deficits. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn vitro cultured pericytes rapidly clear extracellular Aβ40 via LRP1, while excessive accumulation of Aβ in pericytes over longer periods results in cell death.
“In vitro cultured pericytes were suggested to rapidly clear extracellular Aβ40 via LRP1, while excessive accumulation of Aβ in pericytes over longer periods of time resulted in cell death.506”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [506]
Pericytes express lipoprotein receptor LRP1.
“Pericytes express lipoprotein receptor LRP1 (129, 513), which mediates cellular uptake of A 𝛃 followed by its intracellular degradation and clearance (513, 647).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [513]
In the case of excessive Aβ load, accumulation of Aβ can lead to pericyte cell death.
“In the case of excessive A 𝛃 load, accumulation of A 𝛃 can lead to pericyte cell death (513, 647).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [513]
Loss of pericytes influences AD-associated neurodegeneration.
“Pericytes play a role in cerebral blood flow regulation and support BBB function, are important for maintaining brain homeostasis, 116 and their loss is known to influence AD‐associated neurodegeneration. 117”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [117]
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“In vitro cultured pericytes were suggested to rapidly clear extracellular Aβ40 via LRP1, while excessive accumulation of Aβ in pericytes over longer periods of time resulted in cell death.(506) Pericytes dysfunction may also involve in the pathology of ALS.”
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- Authors
- Sagare, A. P., Bell, R. D., Zhao, Z., Ma, Q., Winkler, E. A., Ramanathan, A., & Zlokovic, B. V.
- Affiliations
- University of Southern California (US)
- University of Rochester Medicine (US)
- Venue
- Nature Communications
- Published
- 2013-12-13
- Volume
- 4
- Issue
- 1
- Pages
- 2932-2932
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC3945879
- OpenAlex
- W2114789645
- Cited by
- 589
- References
- 45
- Citations by year
- 2026: 6 · 2025: 19 · 2024: 49 · 2023: 60 · 2022: 62 · 2021: 81 · 2020: 71 · 2019: 62 · 2018: 38 · 2017: 40 · 2016: 37 · 2015: 44 · 2014: 19
- FWCI
- 23.16
- Type
- journal article
- Language
- en
- Status
- Retracted
- Update notices
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- The Scholars Repository - LLU (Loma Linda University) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG023084, R01AG039452, AG23084, R37AG023084, AG039452, RF1AG039452)
- National Institute of Neurological Disorders and Stroke (R37NS034467, NS34467, R01NS034467)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- pericytes, Alzheimer's disease, amyloid-beta, amyloid precursor protein, amyloid angiopathy, tau pathology, neurovascular dysfunction, blood-brain barrier, cerebral amyloidosis, brain interstitial fluid, cognitive decline, neuronal loss, retracted article
- MeSH terms
- Alzheimer Disease, Animals, Brain, Mice, Transgenic, Neurons, Peptide Fragments, Phosphorylation, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, tau Proteins, Cell Death, Neurodegenerative Diseases, Pericytes, Mice
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