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Article ; Online: Uncovering elevated tau TPP motif phosphorylation in the brain of Alzheimer's disease patients.

Bellier, Jean-Pierre / Cai, Yuqi / Alam, Sarah M / Wiederhold, Thorsten / Aiello, Arica / Vogelgsang, Jonathan S / Berretta, Sabina / Chhatwal, Jasmeer P / Selkoe, Dennis J / Liu, Lei

Alzheimer's & dementia : the journal of the Alzheimer's Association

2023 Volume 20, Issue 3, Page(s) 1573–1585

Abstract: Introduction: A wide array of post-translational modifications of the tau protein occurs in Alzheimer's disease (AD) and they are critical to pathogenesis and biomarker development. Several promising tau markers, pT181, pT217, and pT231, rely on ... ...

Abstract	Introduction: A wide array of post-translational modifications of the tau protein occurs in Alzheimer's disease (AD) and they are critical to pathogenesis and biomarker development. Several promising tau markers, pT181, pT217, and pT231, rely on increased phosphorylation within a common molecular motif threonine-proline-proline (TPP). Methods: We validated new and existing antibodies against pT217, pT231, pT175, and pT181, then combined immunohistochemistry (IHC) and immunoassays (ELISA) to broadly examine the phosphorylation of the tau TPP motif in AD brains. Results: The tau burden, as examined by IHC and ELISA, correlates to Braak stages across all TPP sites. Moreover, we observed regional variability across four TPP motif phosphorylation sites in multiple brains of sporadic AD patients. Discussion: We conclude that there is an elevation of TPP tau phosphorylation in AD brains as disease advances. The regional variability of pTPP tau suggests that examining different phosphorylation sites is essential for a comprehensive assessment of tau pathology.
MeSH term(s)	Humans ; Alzheimer Disease/pathology ; tau Proteins/metabolism ; Phosphorylation ; Threonine/metabolism ; Brain/pathology ; Proline/metabolism
Chemical Substances	tau Proteins ; Threonine (2ZD004190S) ; Proline (9DLQ4CIU6V)
Language	English
Publishing date	2023-12-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.13557
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Article: Fluid biomarkers in cerebral amyloid angiopathy.

Frontiers in neuroscience

2024 Volume 18, Page(s) 1347320

Abstract: Cerebral amyloid angiopathy (CAA) is a type of cerebrovascular disorder characterised by the accumulation of amyloid within the leptomeninges and small/medium-sized cerebral blood vessels. Typically, cerebral haemorrhages are one of the first clinical ... ...

Abstract	Cerebral amyloid angiopathy (CAA) is a type of cerebrovascular disorder characterised by the accumulation of amyloid within the leptomeninges and small/medium-sized cerebral blood vessels. Typically, cerebral haemorrhages are one of the first clinical manifestations of CAA, posing a considerable challenge to the timely diagnosis of CAA as the bleedings only occur during the later disease stages. Fluid biomarkers may change prior to imaging biomarkers, and therefore, they could be the future of CAA diagnosis. Additionally, they can be used as primary outcome markers in prospective clinical trials. Among fluid biomarkers, blood-based biomarkers offer a distinct advantage over cerebrospinal fluid biomarkers as they do not require a procedure as invasive as a lumbar puncture. This article aimed to provide an overview of the present clinical data concerning fluid biomarkers associated with CAA and point out the direction of future studies. Among all the biomarkers discussed, amyloid β, neurofilament light chain, matrix metalloproteinases, complement 3, uric acid, and lactadherin demonstrated the most promising evidence. However, the field of fluid biomarkers for CAA is an under-researched area, and in most cases, there are only one or two studies on each of the biomarkers mentioned in this review. Additionally, a small sample size is a common limitation of the discussed studies. Hence, it is hard to reach a solid conclusion on the clinical significance of each biomarker at different stages of the disease or in various subpopulations of CAA. In order to overcome this issue, larger longitudinal and multicentered studies are needed.
Language	English
Publishing date	2024-01-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2024.1347320
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Article ; Online: Vascular contributions to cognitive decline: Beyond amyloid and tau in the Harvard aging brain study.

Shirzadi, Zahra / Boyle, Rory / Yau, Wai-Ying W / Coughlan, Gillian / Fu, Jessie Fanglu / Properzi, Michael J / Buckley, Rachel F / Yang, Hyun-Sik / Scanlon, Catherine E / Hsieh, Stephanie / Amariglio, Rebecca E / Papp, Kathryn / Rentz, Dorene / Price, Julie C / Johnson, Keith A / Sperling, Reisa A / Chhatwal, Jasmeer P / Schultz, Aaron P

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

2024 , Page(s) 271678X241237624

Abstract: In addition to amyloid and tau pathology, elevated systemic vascular risk, white matter injury, and reduced cerebral blood flow contribute to late-life cognitive decline. Given the strong collinearity among these parameters, we proposed a framework to ... ...

Abstract	In addition to amyloid and tau pathology, elevated systemic vascular risk, white matter injury, and reduced cerebral blood flow contribute to late-life cognitive decline. Given the strong collinearity among these parameters, we proposed a framework to extract the independent latent features underlying cognitive decline using the Harvard Aging Brain Study (N = 166 cognitively unimpaired older adults at baseline). We used the following measures from the baseline visit: cortical amyloid, inferior temporal cortex tau, relative cerebral blood flow, white matter hyperintensities, peak width of skeletonized mean diffusivity, and Framingham Heart Study cardiovascular disease risk. We used exploratory factor analysis to extract orthogonal factors from these variables and their interactions. These factors were used in a regression model to explain longitudinal Preclinical Alzheimer Cognitive Composite-5 (PACC) decline (follow-up = 8.5 ±2.7 years). We next examined whether gray matter volume atrophy acts as a mediator of factors and PACC decline. Latent factors of systemic vascular risk, white matter injury, and relative cerebral blood flow independently explain cognitive decline beyond amyloid and tau. Gray matter volume atrophy mediates these associations with the strongest effect on white matter injury. These results suggest that systemic vascular risk contributes to cognitive decline beyond current markers of cerebrovascular injury, amyloid, and tau.
Language	English
Publishing date	2024-03-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	604628-9
ISSN	1559-7016 ; 0271-678X
ISSN (online)	1559-7016
ISSN	0271-678X
DOI	10.1177/0271678X241237624
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Article ; Online: Plasma VEGFA and PGF impact longitudinal tau and cognition in preclinical Alzheimer's disease.

Yang, Hyun-Sik / Yau, Wai-Ying W / Carlyle, Becky C / Trombetta, Bianca A / Zhang, Can / Shirzadi, Zahra / Schultz, Aaron P / Pruzin, Jeremy J / Fitzpatrick, Colleen D / Kirn, Dylan R / Rabin, Jennifer S / Buckley, Rachel F / Hohman, Timothy J / Rentz, Dorene M / Tanzi, Rudolph E / Johnson, Keith A / Sperling, Reisa A / Arnold, Steven E / Chhatwal, Jasmeer P

Brain : a journal of neurology

2024

Abstract: Vascular dysfunction is increasingly recognized as an important contributor to the pathogenesis of Alzheimer's disease. Alterations in vascular endothelial growth factor (VEGF) pathways have been implicated as potential mechanisms. However, the specific ... ...

Abstract	Vascular dysfunction is increasingly recognized as an important contributor to the pathogenesis of Alzheimer's disease. Alterations in vascular endothelial growth factor (VEGF) pathways have been implicated as potential mechanisms. However, the specific impact of VEGF proteins in preclinical Alzheimer's disease and their relationships with other Alzheimer's disease and vascular pathologies during this critical early period remain to be elucidated. We included 317 older adults from the Harvard Aging Brain Study, a cohort of individuals who were cognitively unimpaired at baseline and followed longitudinally for up to 12 years. Baseline VEGF family protein levels (VEGFA, VEGFC, VEGFD, PGF, and FLT1) were measured in fasting plasma using high-sensitivity immunoassays. Using linear mixed effects models, we examined the interactive effects of baseline plasma VEGF proteins and amyloid PET burden (Pittsburgh Compound-B) on longitudinal cognition (Preclinical Alzheimer Cognitive Composite-5). We further investigated if effects on cognition were mediated by early neocortical tau accumulation (Flortaucipir PET burden in the inferior temporal cortex) or hippocampal atrophy. Lastly, we examined the impact of adjusting for baseline cardiovascular risk score or white matter hyperintensity volume. Baseline plasma VEGFA and PGF each showed a significant interaction with amyloid burden on prospective cognitive decline. Specifically, low VEGFA and high PGF were associated with greater cognitive decline in individuals with elevated amyloid, i.e. those on the Alzheimer's disease continuum. Concordantly, low VEGFA and high PGF were associated with accelerated longitudinal tau accumulation in those with elevated amyloid. Moderated mediation analyses confirmed that accelerated tau accumulation fully mediated the effects of low VEGFA and partially mediated (31%) the effects of high PGF on faster amyloid-related cognitive decline. The effects of VEGFA and PGF on tau and cognition remained significant after adjusting for cardiovascular risk score or white matter hyperintensity volume. There were concordant but non-significant associations with longitudinal hippocampal atrophy. Together, our findings implicate low VEGFA and high PGF in accelerating early neocortical tau pathology and cognitive decline in preclinical Alzheimer's disease. Additionally, our results underscore the potential of these minimally-invasive plasma biomarkers to inform the risk of Alzheimer's disease progression in the preclinical population. Importantly, VEGFA and PGF appear to capture distinct effects from vascular risks and cerebrovascular injury. This highlights their potential as new therapeutic targets, in combination with anti-amyloid and traditional vascular risk reduction therapies, to slow the trajectory of preclinical Alzheimer's disease and delay or prevent the onset of cognitive decline.
Language	English
Publishing date	2024-02-05
Publishing country	England
Document type	Journal Article
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awae034
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Article ; Online: A peptide-centric quantitative proteomics dataset for the phenotypic assessment of Alzheimer's disease.

Merrihew, Gennifer E / Park, Jea / Plubell, Deanna / Searle, Brian C / Keene, C Dirk / Larson, Eric B / Bateman, Randall / Perrin, Richard J / Chhatwal, Jasmeer P / Farlow, Martin R / McLean, Catriona A / Ghetti, Bernardino / Newell, Kathy L / Frosch, Matthew P / Montine, Thomas J / MacCoss, Michael J

Scientific data

2023 Volume 10, Issue 1, Page(s) 206

Abstract: Alzheimer's disease (AD) is a looming public health disaster with limited interventions. Alzheimer's is a complex disease that can present with or without causative mutations and can be accompanied by a range of age-related comorbidities. This diverse ... ...

Abstract	Alzheimer's disease (AD) is a looming public health disaster with limited interventions. Alzheimer's is a complex disease that can present with or without causative mutations and can be accompanied by a range of age-related comorbidities. This diverse presentation makes it difficult to study molecular changes specific to AD. To better understand the molecular signatures of disease we constructed a unique human brain sample cohort inclusive of autosomal dominant AD dementia (ADD), sporadic ADD, and those without dementia but with high AD histopathologic burden, and cognitively normal individuals with no/minimal AD histopathologic burden. All samples are clinically well characterized, and brain tissue was preserved postmortem by rapid autopsy. Samples from four brain regions were processed and analyzed by data-independent acquisition LC-MS/MS. Here we present a high-quality quantitative dataset at the peptide and protein level for each brain region. Multiple internal and external control strategies were included in this experiment to ensure data quality. All data are deposited in the ProteomeXchange repositories and available from each step of our processing.
MeSH term(s)	Humans ; Alzheimer Disease/genetics ; Brain/pathology ; Chromatography, Liquid ; Peptides ; Proteomics ; Tandem Mass Spectrometry
Chemical Substances	Peptides
Language	English
Publishing date	2023-04-14
Publishing country	England
Document type	Dataset ; Journal Article
ZDB-ID	2775191-0
ISSN	2052-4463 ; 2052-4463
ISSN (online)	2052-4463
ISSN	2052-4463
DOI	10.1038/s41597-023-02057-7
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Article: Physical activity is associated with increased resting-state functional connectivity in networks predictive of cognitive decline in clinically unimpaired older adults.

Pruzin, Jeremy J / Klein, Hannah / Rabin, Jennifer S / Schultz, Aaron P / Kirn, Dylan R / Yang, Hyun-Sik / Buckley, Rachel F / Scott, Mathew R / Properzi, Michael / Rentz, Dorene M / Johnson, Keith A / Sperling, Reisa A / Chhatwal, Jasmeer P

Alzheimer's & dementia (Amsterdam, Netherlands)

2022 Volume 14, Issue 1, Page(s) e12319

Abstract: Introduction: Physical activity (PA) promotes resilience with respect to cognitive decline, although the underlying mechanisms are not well understood. We examined the associations between objectively measured PA and resting-state functional ... ...

Abstract	Introduction: Physical activity (PA) promotes resilience with respect to cognitive decline, although the underlying mechanisms are not well understood. We examined the associations between objectively measured PA and resting-state functional connectivity magnetic resonance imaging (rs-fcMRI) across seven anatomically distributed neural networks. Methods: rs-fcMRI, amyloid beta (Aβ) positron emission tomography (PET), PA (steps/day × 1 week), and longitudinal cognitive (Preclinical Alzheimer's Cognitive Composite) data from 167 cognitively unimpaired adults (ages 63 to 90) were used. We used linear and linear mixed-effects regression models to examine the associations between baseline PA and baseline network connectivity and between PA, network connectivity, and longitudinal cognitive performance. Results: Higher PA was associated selectively with greater connectivity in three networks previously associated with cognitive decline (default, salience, left control). This association with network connectivity accounted for a modest portion of PA's effects on Aβ-related cognitive decline. Discussion: Although other mechanisms are likely present, PA may promote resilience with respect to Aß-related cognitive decline, partly by increasing connectivity in a subset of cognitive networks.
Language	English
Publishing date	2022-07-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2832898-X
ISSN	2352-8729
ISSN	2352-8729
DOI	10.1002/dad2.12319
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Article ; Online: Tau Mediates Synergistic Influence of Vascular Risk and Aβ on Cognitive Decline.

Yau, Wai-Ying Wendy / Shirzadi, Zahra / Yang, Hyun-Sik / Ikoba, Akpevweoghene P / Rabin, Jennifer S / Properzi, Michael J / Kirn, Dylan R / Schultz, Aaron P / Rentz, Dorene M / Johnson, Keith A / Sperling, Reisa A / Chhatwal, Jasmeer P

Annals of neurology

2022 Volume 92, Issue 5, Page(s) 745–755

Abstract: ... Aβ on greater ITC tau accumulation (p = 0.004), even in individuals with Aβ burden below ... both p < 0.0001). ITC tau accumulation mediated 33% of the interactive association of FHS-CVD and Aβ ...

Abstract	Objective: Elevated vascular risk and beta-amyloid (Aβ) burden have been synergistically associated with cognitive decline in preclinical Alzheimer's disease (AD), although the underlying mechanisms remain unclear. We examined whether accelerated longitudinal tau accumulation mediates the vascular risk-Aβ interaction on cognitive decline. Methods: We included 175 cognitively unimpaired older adults (age 70.5 ± 8.0 years). Baseline vascular risk was quantified using the office-based Framingham Heart Study general cardiovascular disease risk score (FHS-CVD). Baseline Aβ burden was measured with Pittsburgh Compound-B positron emission tomography (PET). Tau burden was measured longitudinally (3.6 ± 1.5 years) with Flortaucipir PET, focusing on inferior temporal cortex (ITC). Cognition was assessed longitudinally (7.0 ± 2.0 years) using the Preclinical Alzheimer's Cognitive Composite. Linear mixed effects models examined the interactive effects of baseline vascular risk and Aβ on longitudinal ITC tau. Additionally, moderated mediation was used to determine whether tau accumulation mediated the FHS-CVDAβ effect on cognitive decline. Results:* We observed a significant interaction between elevated baseline FHS-CVD and Aβ on greater ITC tau accumulation (p = 0.004), even in individuals with Aβ burden below the conventional threshold for amyloid positivity. Examining individual vascular risk factors, we found elevated systolic blood pressure and body mass index showed independent interactions with Aβ on longitudinal tau (both p < 0.0001). ITC tau accumulation mediated 33% of the interactive association of FHS-CVD and Aβ on cognitive decline. Interpretation: Vascular risks interact with subthreshold levels of Aβ to promote cognitive decline, partially by accelerating early neocortical tau accumulation. Our findings support vascular risk reduction, especially treating hypertension and obesity, to attenuate Aβ-related tau pathology and reduce late-life cognitive decline. ANN NEUROL 2022;92:745-755.
MeSH term(s)	Humans ; Aged ; Middle Aged ; tau Proteins ; Cognitive Dysfunction/diagnostic imaging ; Amyloid beta-Peptides ; Alzheimer Disease/diagnostic imaging ; Alzheimer Disease/psychology ; Positron-Emission Tomography ; Cardiovascular Diseases ; Biomarkers
Chemical Substances	tau Proteins ; Amyloid beta-Peptides ; Biomarkers
Language	English
Publishing date	2022-08-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80362-5
ISSN	1531-8249 ; 0364-5134
ISSN (online)	1531-8249
ISSN	0364-5134
DOI	10.1002/ana.26460
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Article ; Online: Association of β-Amyloid and Vascular Risk on Longitudinal Patterns of Brain Atrophy.

Rabin, Jennifer S / Pruzin, Jeremy / Scott, Matthew / Yang, Hyun-Sik / Hampton, Olivia / Hsieh, Stephanie / Schultz, Aaron P / Buckley, Rachel F / Hedden, Trey / Rentz, Dorene / Johnson, Keith A / Sperling, Reisa A / Chhatwal, Jasmeer P

Neurology

2022 Volume 99, Issue 3, Page(s) e270–e280

Abstract: Background and objectives: Vascular risk factors and elevated β-amyloid (Aβ) are commonly observed together among older adults. Here, we examined the interactive vs independent effects of systemic vascular risk and Aβ burden on longitudinal gray matter ... ...

Abstract	Background and objectives: Vascular risk factors and elevated β-amyloid (Aβ) are commonly observed together among older adults. Here, we examined the interactive vs independent effects of systemic vascular risk and Aβ burden on longitudinal gray matter atrophy and how their co-occurrence may be related to cognitive decline in a cohort of clinically normal adults. A secondary goal was to examine whether vascular risk influences gray matter atrophy independently from markers of white matter injury. Methods: Participants were 196 adults (age 73.8 ± 6.1 years) from the Harvard Aging Brain Study. Baseline Aβ burden was quantified with Pittsburgh compound B PET. Baseline vascular risk was measured with the Framingham Heart Study cardiovascular disease risk score. Brain atrophy was quantified longitudinally with structural MRI over a median of 4.50 (±1.26) years. Cognition was assessed yearly with the Preclinical Alzheimer Cognitive Composite over a median of 6.25 (±1.40) years. Linear mixed-effects models examined vascular risk and Aβ burden as interactive vs independent predictors of gray matter atrophy, with adjustment for age, sex, years of education, Results: Higher vascular risk and elevated Aβ burden interacted to predict more severe atrophy in frontal and temporal lobes, thalamus, and striatum. Higher Aβ burden, but not vascular risk, was associated with more severe atrophy in parietal and occipital lobes, as well as the hippocampus. Adjusting for diffusion- and FLAIR-based markers of white matter injury had little impact on the above associations. Gray matter atrophy mediated the association between vascular risk and cognitive decline at higher levels of Aβ burden. Discussion: We observed an interaction between elevated vascular risk and higher Aβ burden with longitudinal brain atrophy, which in turn influenced cognitive decline. These results support vascular risk factor management as a potential intervention to slow neurodegeneration and cognitive decline in preclinical Alzheimer disease.
MeSH term(s)	Humans ; Aged ; Amyloid beta-Peptides/metabolism ; Brain/pathology ; Alzheimer Disease/pathology ; Gray Matter/pathology ; Cognitive Dysfunction/diagnostic imaging ; Cognitive Dysfunction/pathology ; Longitudinal Studies ; Magnetic Resonance Imaging ; Atrophy/pathology ; Positron-Emission Tomography
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2022-07-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000200551
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Article ; Online: Functional MRI of mnemonic networks across the spectrum of normal aging, mild cognitive impairment, and Alzheimer's disease.

Chhatwal, Jasmeer P / Sperling, Reisa A

Journal of Alzheimer's disease : JAD

2012 Volume 31 Suppl 3, Page(s) S155–67

Abstract: Functional magnetic resonance imaging (fMRI) is a non-invasive technique that has come into common use to examine neural network function in normal and impaired cognitive states. Using this promising type of analysis, researchers have identified the ... ...

Abstract	Functional magnetic resonance imaging (fMRI) is a non-invasive technique that has come into common use to examine neural network function in normal and impaired cognitive states. Using this promising type of analysis, researchers have identified the presence of anatomically distributed regions operating as large-scale neural networks, which are observed both during the performance of associative memory tasks and in the resting state. The assembly of these anatomically distinct regions into functional ensembles and their choreographed activation and deactivation sets the stage for complex behaviors such as the formation and retrieval of associative memories. We review progress in the use of task-related and task-free MRI to elucidate the changes in neural activity in normal older individuals, patients with mild cognitive impairment, and those with Alzheimer's disease, focusing on the altered activity of the default mode network and medial temporal lobe. We place task-free fMRI studies into the larger context of more traditional, task-based fMRI studies of human memory, which have firmly established the critical role of the medial temporal lobe in associative encoding. Lastly, we discuss the data from our group and others that suggests task-free MRI and task-based fMRI may prove useful as non-invasive biomarkers in studying the progression of memory failure over the course of Alzheimer's disease.
MeSH term(s)	Aging/pathology ; Alzheimer Disease/pathology ; Alzheimer Disease/psychology ; Cognitive Dysfunction/pathology ; Cognitive Dysfunction/psychology ; Humans ; Magnetic Resonance Imaging/methods ; Memory/physiology ; Nerve Net/anatomy & histology ; Nerve Net/pathology ; Rest ; Temporal Lobe/pathology
Language	English
Publishing date	2012-08-10
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-2012-120730
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Article ; Online: Progression of cerebral amyloid angiopathy: a pathophysiological framework.

Koemans, Emma A / Chhatwal, Jasmeer P / van Veluw, Susanne J / van Etten, Ellis S / van Osch, Matthias J P / van Walderveen, Marianne A A / Sohrabi, Hamid R / Kozberg, Mariel G / Shirzadi, Zahra / Terwindt, Gisela M / van Buchem, Mark A / Smith, Eric E / Werring, David J / Martins, Ralph N / Wermer, Marieke J H / Greenberg, Steven M

The Lancet. Neurology

2023 Volume 22, Issue 7, Page(s) 632–642

Abstract: Cerebral amyloid angiopathy, which is defined by cerebrovascular deposition of amyloid β, is a common age-related small vessel pathology associated with intracerebral haemorrhage and cognitive impairment. Based on complementary lines of evidence from in ... ...

Abstract	Cerebral amyloid angiopathy, which is defined by cerebrovascular deposition of amyloid β, is a common age-related small vessel pathology associated with intracerebral haemorrhage and cognitive impairment. Based on complementary lines of evidence from in vivo studies of individuals with hereditary, sporadic, and iatrogenic forms of cerebral amyloid angiopathy, histopathological analyses of affected brains, and experimental studies in transgenic mouse models, we present a framework and timeline for the progression of cerebral amyloid angiopathy from subclinical pathology to the clinical manifestation of the disease. Key stages that appear to evolve sequentially over two to three decades are (stage one) initial vascular amyloid deposition, (stage two) alteration of cerebrovascular physiology, (stage three) non-haemorrhagic brain injury, and (stage four) appearance of haemorrhagic brain lesions. This timeline of stages and the mechanistic processes that link them have substantial implications for identifying disease-modifying interventions for cerebral amyloid angiopathy and potentially for other cerebral small vessel diseases.
MeSH term(s)	Mice ; Animals ; Amyloid beta-Peptides ; Cerebral Amyloid Angiopathy/complications ; Brain/pathology ; Cerebral Hemorrhage/complications ; Cognitive Dysfunction/pathology
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2023-05-23
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2081241-3
ISSN	1474-4465 ; 1474-4422
ISSN (online)	1474-4465
ISSN	1474-4422
DOI	10.1016/S1474-4422(23)00114-X
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