Age-Related Vascular Pathology in Transgenic Mice Expressing Presenilin 1-Associated Familial Alzheimer's Disease Mutations

Gama Sosa, Miguel A.; Gasperi, Rita De; Rocher, Anne B.; Wang, Athena Ching-Jung; Janssen, William G.M.; Flores, Tony; Perez, Gissel M.; Schmeidler, James; Dickstein, Dara L.; Hof, Patrick R.; Elder, Gregory A.

doi:10.2353/ajpath.2010.090482

Cited by 92Alzheimer's disease research and treatmentsBarrier Structure and Function StudiesNeurological Disease Mechanisms and Treatments

Age-Related Vascular Pathology in Transgenic Mice Expressing Presenilin 1-Associated Familial Alzheimer's Disease Mutations

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Gama Sosa, Miguel A., Gasperi, Rita De, Rocher, Anne B., Wang, Athena Ching-Jung, Janssen, William G.M., Flores, Tony, Perez, Gissel M., Schmeidler, James +3 more·2010·The American Journal of Pathology

DOI 10.2353/ajpath.2010.090482PMC PMC2797896

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Abstract

Mutations in the presenilin 1 (PS1) gene are the most commonly recognized cause of familial Alzheimer's disease (FAD). Besides senile plaques, neurofibrillary tangles, and neuronal loss, Alzheimer's disease (AD) is also accompanied by vascular pathology. Here we describe an age-related vascular pathology in two lines of PS1 FAD-mutant transgenic mice that mimics many features of the vascular pathology seen in AD. The pathology was especially prominent in the microvasculature whose vessels became thinned and irregular with the appearance of many abnormally looped vessels as well as string vessels. Stereologic assessments revealed a reduction of the microvasculature in the hippocampus that was accompanied by hippocampal atrophy. The vascular changes were not congophilic. Yet, despite the lack of congophilia, penetrating vessels at the cortical surface were often abnormal morphologically and microhemorrhages sometimes occurred. Altered immunostaining of blood vessels with basement membrane-associated antigens was an early feature of the microangiopathy and was associated with thickening of the vascular basal laminae and endothelial cell alterations that were visible ultrastructurally. Interestingly, although the FAD-mutant transgene was expressed in neurons in both lines of mice, there was no detectable expression in vascular endothelial cells or glial cells. These studies thus have implications for the role of neuronal to vascular signaling in the pathogenesis of the vascular pathology associated with AD.

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In the PS1 gene familial AD M146V transgenic mouse model, hippocampal augmentation was accompanied by lateral ventricular enlargement.
“In this study the hippocampal augmentation was accompanied by lateral ventricular enlargement (Gama Sosa et al., 2010).”
From Early stage alterations in white matter and decreased functional interhemispheric hippocampal connectivity in the 3xTg mouse model of Alzheimer’s disease. (2019) · cites this paper as Gama Sosa et al., 2010
The section on decreased microvasculature and brain atrophy reports hippocampal atrophy, not augmentation: hippocampal volume was about 30% lower in the PS1 M146V mice than in pooled controls. The Figure 6 caption in the Discussion identifies the lateral ventricle but does not state that it was enlarged. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measured
Mice expressing human PSEN1 M146V mutations driven by the neuronal Thy1 promoter develop BBB breakdown with microhemorrhages and basement membrane degeneration in the absence of Aβ pathology or CAA.
“Similar to humans, mice expressing human PSEN1 M146V mutations driven by the neuronal Thy1 promoter develop BBB breakdown with microhemorrhages and basement membrane degeneration in the absence of A 𝛃 pathology or CAA (191).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [191]
The sections on non-congophilic vascular pathology and ultrastructure report occasional microhemorrhages, no detectable vascular Aβ deposits, and thickening and disruption of the basal lamina in PS1-mutant mice (pages not supplied). But the Genetically Modified Mice section describes M146V expression from a human PS1 PAC, not a Thy1 promoter. The copy does not establish BBB breakdown, and the Discussion notes altered Aβ production despite the absence of amyloid plaques or CAA. (LLM, conf=0.90)
Experimental — accuracy not yet measured
PSEN1 mutant and knockout transgenic models that are not crossed with APP models exhibit significant vascular pathology such as BBB breakdown, hemorrhages, and loss of pericytes.
“Furthermore, PSEN1 mutant and knockout transgenic models that are not crossed with APP models exhibit significant vascular pathology such as BBB breakdown, hemorrhages, and loss of pericytes (191, 641)”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [191]
The introduction and age-related pathology section describe vascular abnormalities in PS1-mutant mice without APP transgenes; the vascular pathology section reports occasional microhemorrhages (Figure 9). The paper does not establish blood–brain barrier breakdown or pericyte loss, and its PS1-null mice were rescued with a PS1 transgene rather than studied as standalone knockouts. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Vascular dysfunction caused by PSEN1 mutations can develop independent of amyloid pathology.
“suggesting that vascular dysfunction caused by PSEN1 mutations can develop independent of amyloid pathology.”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [191]
The Discussion reports microangiopathy in PS1 FAD-mutant mice without congophilic amyloid angiopathy, supporting the narrower claim that vascular pathology can develop without vascular amyloid deposits. It also says the mice have altered Aβ production and that undetected soluble Aβ could be driving the pathology. The study therefore does not establish independence from amyloid-related processes generally. (LLM, conf=0.85)
Experimental — accuracy not yet measured
In the PS1 gene familial AD M146V transgenic mouse model, authors reported an average reduction in hippocampal volume of 30% compared with controls.
“It is noteworthy, that in the PS1 gene familial AD M146V transgenic mouse model, authors reported an average reduction in hippocampal volume of 30% compared with controls (Gama Sosa et al., 2010).”
From Early stage alterations in white matter and decreased functional interhemispheric hippocampal connectivity in the 3xTg mouse model of Alzheimer’s disease. (2019) · cites this paper as Gama Sosa et al., 2010

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Additional file 1 of The pathogenic role of c-Kit+ mast cells in the spinal motor neuron-vascular niche in ALS
Kovacs, M., Alamón, C., Maciel, C., Varela, V., Ibarburu, S., Tarragó, L., King, P. H., Si, Y., Kwon, Y., Hermine, O., et al. (2021) · Figshare · doi:10.6084/m9.figshare.15178512
Additional file 1 of No observed effect on brain vasculature of Alzheimer’s disease-related mutations in the zebrafish presenilin 1 gene
Barthelson, K., Newman, M., Nowell, C. J., & Lardelli, M. T. (2021) · Figshare · doi:10.6084/m9.figshare.13642328
Additional file 1 of Repetitive transcranial magnetic stimulation increases the brain’s drainage efficiency in a mouse model of Alzheimer’s disease
Lin, Y., Jin, J., Lv, R., Luo, Y., Dai, W., Li, W., Tang, Y., Wang, Y., Ye, X., & Lin, W.-J. (2021) · Figshare · doi:10.6084/m9.figshare.14722040
Additional file 2 of Repetitive transcranial magnetic stimulation increases the brain’s drainage efficiency in a mouse model of Alzheimer’s disease
Lin, Y., Jin, J., Lv, R., Luo, Y., Dai, W., Li, W., Tang, Y., Wang, Y., Ye, X., & Lin, W.-J. (2021) · Figshare · doi:10.6084/m9.figshare.14722043
Non-viral vasculogenic reprogramming restores cognition and mitigates pathology in Alzheimer’s diseasePreprint
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Authors: Gama Sosa, M. A., Gasperi, R. D., Rocher, A. B., Wang, A. C.-J., Janssen, W. G. M., Flores, T., Perez, G. M., Schmeidler, J., Dickstein, D. L., Hof, P. R., & Elder, G. A.
Affiliations: James J. Peters VA Medical Center (US)
Boston University (US)
Icahn School of Medicine at Mount Sinai (US)
Corresponding author: Elder, Gregory A.
ORCID: Gasperi, Rita De
Rocher, Anne B.
Janssen, William G.M.
Schmeidler, James
Dickstein, Dara L.
Hof, Patrick R.
Elder, Gregory A.
Venue: The American Journal of Pathology
Publisher: Elsevier BV
Published: 2010-01
Volume: 176
Issue: 1
Pages: 353-368
ISSN: 0002-9440 (ISSN-L)
DOI: 10.2353/ajpath.2010.090482
PMC: PMC2797896
OpenAlex: W2055083885
Cited by: 92
References: 59
Citations by year: 2026: 7 · 2025: 3 · 2024: 2 · 2023: 3 · 2022: 5 · 2021: 12 · 2020: 4 · 2019: 4 · 2018: 8 · 2017: 8 · 2016: 5 · 2015: 4 · 2014: 7 · 2013: 8 · 2012: 3
FWCI: 2.66
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 3667 d)
Locations: American Journal Of Pathology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute on Aging (AG20139, AG029361, AG010491, AG05138, AG02219)
Alzheimer's Association (IIRG-07-57318)
U.S. Department of Veterans Affairs (5I01BX000342-02)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords: Alzheimer's disease, vascular pathology, presenilin 1, familial Alzheimer's disease mutations, transgenic mice, microangiopathy, hippocampal atrophy, microhemorrhages, basement membrane thickening, endothelial ultrastructure, vascular aging
MeSH terms: Aging, Alzheimer Disease, Animals, Atrophy, Basement Membrane, Blood Vessels, Brain, Dendrites, Humans, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Extracellular Matrix Proteins, Transgenes, Chromosomes, Artificial, P1 Bacteriophage, Mutant Proteins, Mice, Presenilin-1, Microvessels

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Age-Related Vascular Pathology in Transgenic Mice Expressing Presenilin 1-Associated Familial Alzheimer's Disease Mutations

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