Evidence of beta amyloid independent small vessel disease in familial Alzheimer's disease
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We studied small vessel disease (SVD) pathology in Familial Alzheimer's disease (FAD) subjects carrying the presenilin 1 (PSEN1) p.Glu280Ala mutation in comparison to those with sporadic Alzheimer's disease (SAD) as a positive control for Alzheimer's pathology and Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) bearing different NOTCH3 mutations, as positive controls for SVD pathology. Upon magnetic resonance imaging (MRI) in life, some FAD showed mild white matter hyperintensities and no further radiologic evidence of SVD. In post‐mortem studies, total SVD pathology in cortical areas and basal ganglia was similar in PSEN1 FAD and CADASIL subjects, except for the feature of arteriosclerosis which was higher in CADASIL subjects than in PSEN1 FAD subjects. Further only a few SAD subjects showed a similar degree of SVD pathology as observed in CADASIL. Furthermore, we found significantly enlarged perivascular spaces in vessels devoid of cerebral amyloid angiopathy in FAD compared with SAD and CADASIL subjects. As expected, there was greater fibrinogen‐positive perivascular reactivity in CADASIL but similar reactivity in PSEN1 FAD and SAD groups. Fibrinogen immunoreactivity correlated with onset age in the PSEN1 FAD cases, suggesting increased vascular permeability may contribute to cognitive decline. Additionally, we found reduced perivascular expression of PDGFRβ AQP4 in microvessels with enlarged PVS in PSEN1 FAD cases. We demonstrate that there is Aβ‐independent SVD pathology in PSEN1 FAD, that was marginally lower than that in CADASIL subjects although not evident by MRI. These observations suggest presence of covert SVD even in PSEN1, contributing to disease progression. As is the case in SAD, these consequences may be preventable by early recognition and actively controlling vascular disease risk, even in familial forms of dementia.
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More integrative hypotheses have suggested that inflammation, excitatory-inhibitory imbalance, or vascular impairment is involved in the series of initial reactions that eventually become chronic and result in irreversible brain dyshomeostasis, neurodegeneration, and AD.
“Therefore, more integrative hypotheses have suggested that inflammation, excitatory‐inhibitory imbalance, or vascular impairment is involved in the series of initial reactions that eventually become chronic and result in irreversible brain dyshomeostasis, neurodegeneration, and AD [42, 66, 69].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [66]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredPrevious reports show reduced perivascular AQP4 in E280A carriers.
“previous reports of reduced AQP4 perivascular in E280A carriers [66]”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [66]
The Results (Astrocytosis and astrocyte end feet pathology in PSEN1 FAD) report reduced perivascular AQP4 reactivity in dilated versus non-dilated vessels within PSEN1 p.Glu280Ala FAD cases. They also report no difference in perivascular AQP4 reactivity between the FAD, SAD and CADASIL groups. The claim omits the vessel-specific condition and could imply a general reduction in E280A carriers. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe distribution of CAA in this case contrasted to more generalized distribution of CAA in other PSEN1 E280A cases.
“which contrasted to more generalized distribution of CAA in other PSEN1 E280A cases [7, 22].”
From Distinct tau neuropathology and cellular profiles of an APOE3 Christchurch homozygote protected against autosomal dominant Alzheimer’s dementia (2022) · cites this paper as [22]
We have previously reported small vessel disease in SAD, FAD, and APOEch.
“We have previously reported small vessel disease in SAD, FAD [66, 67], and APOEch [65].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [66]
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- Authors
- Littau, J. L., Velilla, L., Hase, Y., Villalba‐Moreno, N. D., Hagel, C., Drexler, D., Osorio Restrepo, S., Villegas, A., Lopera, F., Vargas, S., Glatzel, M., Krasemann, S., Quiroz, Y. T., Arboleda‐Velasquez, J. F., Kalaria, R., & Sepulveda‐Falla, D.
- Affiliations
- University Medical Center Hamburg-Eppendorf (DE)
- Universidad de Antioquia (CO)
- Newcastle University (GB)
- Department of Radiology, Neuroradiology Section Universidad de Antioquia Medellín Colombia
- Neuroscience Group of Antioquia University of Antioquia Medellín
- Harvard University (US)
- Schepens Eye Research Institute of Mass Eye and Ear and the Department of Ophthalmology at Harvard Medical School Boston Massachusetts
- Neurovascular Research Group Translational and Clinical Research Institute, Newcastle University Newcastle upon Tyne
- Institute of Neuropathology University Medical Center Hamburg‐Eppendorf Hamburg Germany
- ORCID
- Venue
- Brain Pathology
- Publisher
- Wiley
- Published
- 2022-06-13
- Volume
- 32
- Issue
- 6
- Pages
- e13097-e13097
- ISSN
- 1015-6305 (ISSN-L)
- 1750-3639
- PMC
- PMC9616091
- OpenAlex
- W4282555638
- Cited by
- 20
- References
- 60
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 7 · 2023: 2 · 2022: 2
- FWCI
- 1.97
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Brain Pathology (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity) (cc-by-nc-nd)
- Funders
- Bundesministerium für Bildung und Forschung
- National Institute of Neurological Disorders and Stroke (RF1NS110048)
- Topics
- Health Sciences › Medicine › Neurology › Cerebrovascular and genetic disorders
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- cerebral small vessel disease, familial Alzheimer's disease, CADASIL, Notch3, perivascular spaces, fibrinogen, PDGFRβ, aquaporin-4, cerebral amyloid angiopathy, arteriosclerosis, white matter hyperintensities, vascular permeability, age of onset, cognitive decline
- MeSH terms
- Alzheimer Disease, Fibrinogen, Humans, Amyloid beta-Peptides, CADASIL
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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