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The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Cholesterol Accumulates in Senile plaques of Alzheimer Disease patients and in Transgenic APPswMice

Mori, Takashi, Paris, Daniel, Town, Terrence, Rojiani, Amyn M., Sparks, D. Larry, Delledonne, Anthony, Crawford, Fiona, Abdullah, Laila I., Humphrey, James A., Dickson, Dennis W., Mullan, Michael J.·2001·Journal of Neuropathology & Experimental Neurology
DOI 10.1093/jnen/60.8.778
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Abstract

Mounting evidence suggests that cholesterol may contribute to the pathogenesis of Alzheimer disease (AD). We examined whether cholesterol might be present in senile plaques, a hallmark neuropathological feature of AD. We employed 2 different fluorometric-staining techniques (filipin staining and an enzymatic technique) for the determination of cholesterol in brains of postmortem confirmed AD patients and in nondemented, age-matched histopathologically normal controls. AD patient brains showed abnormal accumulation of cholesterol in congophilic/birefringent dense cores of senile plaques that was essentially absent in histopathologically normal controls. To determine whether increased senile plaque-associated cholesterol occurred generally in all plaques or was restricted to a specific subset, quantitative analysis was performed. Data indicate abnormal accumulation of cholesterol in cores of mature plaques but not in diffuse or immature plaques. Additionally, transgenic mice that overexpress the "Swedish" amyloid precursor protein (Tg APP(SW), line 2576) exhibited a similar pattern of abnormal cholesterol accumulation in mature, congophilic amyloid plaques at 24 months of age that was absent in their control littermates or in 8-month-old Tg APP(SW) mice (an age prior to amyloid deposition). Taken together, our results imply a link between cholesterol and AD pathogenesis and suggest that cholesterol plays an important role in the formation and/or progression of senile plaques.

Overview

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Crossref · 10.1093/jnen/60.8.778

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4 of 4 references verified0 citation errors · 0 not checkable

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  • Cholesterol dysregulation and lipid dyshomeostasis have been identified in several neurodegenerative diseases.

    “Importantly, cholesterol dysregulation6–9 and lipid dyshomeostasis8,10–15 have been identified in several neurodegenerative diseases.”

    From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [6]

  • The altered gene expression and pathways revealed by MAPT R406W HNOs coincide with altered lipid metabolism and cholesterol regulation previously identified in FTLD and AD patients.

    “The altered gene expression and pathways revealed by MAPT R406W HNOs coincide with altered lipid metabolism and cholesterol regulation, which has been previously identified in FTLD and AD patients6,67,68.”

    From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [6]

  • Lipid dyshomeostasis correlates with tau pathology and cognitive deficits in these diseases.

    “Importantly, lipid dyshomeostasis correlates with tau pathology and cognitive deficits in these diseases6,8,29.”

    From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [6]

Citations

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Research works printed but not linked: 24

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Metadata

Authors
Mori, T., Paris, D., Town, T., Rojiani, A. M., Sparks, D. L., Delledonne, A., Crawford, F., Abdullah, L. I., Humphrey, J. A., Dickson, D. W., & Mullan, M. J.
Venue
Journal of Neuropathology & Experimental Neurology
Publisher
Oxford University Press (OUP)
Published
2001-08
Volume
60
Issue
8
Pages
778-785
ISSN
  • 0022-3069
  • 1554-6578
DOI
10.1093/jnen/60.8.778
Cited by
159
References
4
Language
en

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