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Introduction
I am a Junior Research Group Leader at the Institute for Stroke and Dementia Research (ISD), Ludwig-Maximilians-University of Munich. My work focuses on aging and Alzheimer's disease, where I study 1) neural mechanisms that support reserve and resilience and 2) mechanisms of tau pathology spread
Publications
Publications (241)
In Alzheimer’s disease, tau pathology spreads hierarchically from the inferior temporal lobe throughout the cortex, ensuing cognitive decline and dementia. Similarly, circumscribed patterns of pathological tau have been observed in normal ageing and small vessel disease, suggesting a spatially ordered distribution of tau pathology across normal age...
The single nucleotide polymorphism (SNP) rs744373 in the bridging integrator-1 gene (BIN1) is a risk factor for Alzheimer’s disease (AD). In the brain, BIN1 is involved in endocytosis and sustaining cytoskeleton integrity. Post-mortem and in vitro studies suggest that BIN1-associated AD risk is mediated by increased tau pathology but whether rs7443...
In Alzheimer’s diseases (AD), tau pathology is strongly associated with cognitive decline. Preclinical evidence suggests that tau spreads across connected neurons in an activity-dependent manner. Supporting this, cross-sectional AD studies show that tau deposition patterns resemble functional brain networks. However, whether higher functional conne...
Microglia activation is the brain's major immune response to amyloid plaques in Alzheimer's disease (AD). Both cerebrospinal fluid (CSF) levels of soluble TREM2 (sTREM2), a biomarker of microglia activation, and microglia PET are increased in AD; however, whether an increase in these biomarkers is associated with reduced amyloid-beta (Aβ) accumulat...
In Alzheimer's disease (AD), the Braak staging scheme suggests a stereotypical tau spreading pattern that does, however, not capture interindividual variability in tau deposition. This complicates the prediction of tau spreading, which may become critical for defining individualized tau-PET readouts in clinical trials. Since tau is assumed to sprea...
In Alzheimer’s disease (AD), amyloid-β (Aβ) triggers the aggregation and spreading of tau pathology, which drives neurodegeneration and cognitive decline. However, the pathophysiological link between Aβ and tau remains unclear, which hinders therapeutic efforts to attenuate Aβ-related tau accumulation. Aβ has been found to trigger neuronal hyperact...
Patients with Alzheimer’s disease (AD) and clinically overlapping neurodegenerative diseases are classified molecularly using the A/T/N classification system. Apart from fluid biomarkers and structural MRI, the three-dimensional A/T/N system incorporates characteristic features from β-amyloid-PET (A), tau-PET (T), and FDG-PET (N). We evaluated if d...
In Alzheimer’s disease (AD), Aβ triggers p-tau secretion, which drives tau aggregation. Therefore, it is critical to characterize modulators of Aβ-related p-tau increases which may alter AD trajectories. Here, we assessed whether factors known to alter tau levels in AD modulate the association between fibrillar Aβ and secreted p-tau 181 determined...
Background
The recent Movement Disorders Society (MDS)‐progressive supranuclear palsy (PSP) diagnostic criteria conceptualized three clinical diagnostic certainty levels: “suggestive of PSP” for sensitive early diagnosis based on subtle clinical signs, “possible PSP” balancing sensitivity and specificity, and “probable PSP” highly specific for PSP...
Traumatic brain injury is widely viewed as a risk factor for dementia, but the biological mechanisms underlying this association are still unclear. In previous studies, traumatic brain injury has been associated with the hallmark pathologies of Alzheimer’s disease, i.e. amyloid-β plaques and neurofibrillary tangles comprised of hyperphosphorylated...
Background
Tau‐PET imaging allows in‐vivo detection of neurofibrillary tangles. One tau‐PET tracer (i.e., [18F]flortaucipir) has received FDA‐approval for clinical use, and multiple other tau‐PET tracers have been implemented into clinical trials for participant selection and/or as a primary or secondary outcome measure. To optimize future use of t...
Background
Positron emission tomography (PET) imaging with [¹⁸F]flortaucipir allows for in‐vivo visualization of aggregated tau in Alzheimer’s disease (AD). The FDA‐approved label for [¹⁸F]flortaucipir PET provides a standardized, clinically applicable definition of tau‐PET positivity by visual interpretation. Here, we studied the concordance betwe...
Background
There is a strong link between tau and progression of Alzheimer’s disease (AD), necessitating an understanding of tau spreading mechanisms. Prior research, predominantly in typical AD, suggested that tau propagates from epicenters (regions with earliest tau) to functionally connected regions. However, given the constrained spatial hetero...
Background
Memory clinic patients typically present with Alzheimer’s disease (AD) and cerebral small vessel disease (SVD) to varying degrees. Therefore, it is crucial to determine the etiology of cognitive deficits for facilitating patient‐centered treatment in memory clinics. Plasma biomarkers (ptau217, Glial Fibrillary Acidic Protein [GFAP], Neur...
Background
Lewy body pathology consisting of aggregated alpha‐Synuclein (a‐Syn) is the hallmark pathology in Parkinson’s disease, yet a‐Syn aggregates are also commonly observed post‐mortem as a co‐pathology in Alzheimer’s disease (AD) patients. Preclinical research has shown that a‐Syn can amplify Ab‐associated tau seeding and aggregation, hence a...
Background
Alzheimer’s disease (AD) is associated with substantial synaptic loss potentially due to synaptotoxicity of fibrillar tau, but the association between tau deposition and synaptic loss remains unclear. Based on previous observations that pathology spreads preferentially between closely connected regions, we tested in the current multi‐PET...
Background
Understanding modulators of Alzheimer's disease’s (AD) progression is crucial for determining optimal treatment windows and targets. Apolipoprotein E e4 (ApoE4), i.e. a key AD risk factor, is associated with earlier tau accumulation at lower Aß levels (Steward et al. 2023), yet, the mechanisms driving this connection remain unclear. Thus...
Background
Neuroimaging studies have revealed age and sex‐specific differences in Alzheimer’s disease (AD) trajectories. However, how age and sex modulate tau spreading remains unclear. Thus, we investigated how age and sex modulate the amyloid‐beta (Aß)‐induced accumulation and spreading of tau pathology from local epicenters across connected brai...
Background
The myelin sheath around axons is of fundamental importance for signal transduction. Myelin is reduced in white matter hyperintensities (WMH), which occur in both small vessel disease (SVD) and Alzheimer’s disease (AD), giving rise to the question to what extent myelin is reduced in these diseases. Here, we employed an advanced MRI based...
Background
In Alzheimer’s disease (AD), cortical tau aggregation is a strong predictor of cortical brain atrophy as shown by MRI and PET studies, particularly driving the degeneration of neuronal somata in the grey matter. However, tau’s physiological role is to stabilize microtubules within axons in the brain’s white matter (WM) pathways. Therefor...
Background
In Alzheimer’s disease, Aß triggers tau spreading which drives neurodegeneration and cognitive decline. However, the mechanistic link between Aß and tau remains unclear, which hinders therapeutic efforts to attenuate Aß‐related tau accumulation. Preclinical research could show that tau spreads across connected neurons in an activity‐depe...
Background
Memory clinic patients typically present with Alzheimer’s disease (AD) and cerebral small vessel disease (SVD) to varying degrees. Therefore, it is crucial to determine the etiology of cognitive deficits for facilitating patient‐centered treatment in memory clinics. Plasma biomarkers (ptau217, Glial Fibrillary Acidic Protein [GFAP], Neur...
Background
Understanding modulators of Alzheimer's disease’s (AD) progression is crucial for determining optimal treatment windows and targets. Apolipoprotein E ε4 (ApoE4), i.e. a key AD risk factor, is associated with earlier tau accumulation at lower Aβ levels (Steward et al. 2023), yet, the mechanisms driving this connection remain unclear. Thus...
Background
White matter hyperintensities (WMH) are prevalent Alzheimer’s disease (AD). However, the role of WMH in the etiology of AD is debated. Specifically, a key question is whether higher WMH is predictive of higher beta‐amyloid (Aβ) and fibrillar tau accumulation. Here, we assessed whether a genetic predisposition to higher WMH (assessed via...
Background
Lewy body pathology consisting of aggregated alpha‐Synuclein (a‐Syn) is the hallmark pathology in Parkinson’s disease, yet a‐Syn aggregates are also commonly observed post‐mortem as a co‐pathology in Alzheimer’s disease (AD) patients. Preclinical research has shown that a‐Syn can amplify Ab‐associated tau seeding and aggregation, hence a...
Background
The myelin sheath around axons is of fundamental importance for signal transduction. Myelin is reduced in white matter hyperintensities (WMH), which occur in both small vessel disease (SVD) and Alzheimer’s disease (AD), giving rise to the question to what extent myelin is reduced in these diseases. Here, we employed an advanced MRI based...
Background
To understand the progression of Alzheimer's disease (AD), neuroimaging and biomarker research relies increasingly on sophisticated data analysis techniques that are often restricted to expert lab environments. Here, we demonstrate how complex analyses on modeling tau spreading across interconnected brain regions from our previous studie...
Background
Synaptic loss is identified as a strong correlate of cognitive impairment in Alzheimer’s disease (AD). Pathological tau can induce direct toxicity to synapse and spread trans‐synaptically across connected neurons. Recent neuroimaging evidence revealed that tau pathology propagates along interconnected brain regions throughout macroscale...
Background
In Alzheimer’s disease, Aβ triggers tau spreading which drives neurodegeneration and cognitive decline. However, the mechanistic link between Aβ and tau remains unclear, which hinders therapeutic efforts to attenuate Aβ‐related tau accumulation. Preclinical research could show that tau spreads across connected neurons in an activity‐depe...
Background
There is a strong link between tau and progression of Alzheimer’s disease (AD), necessitating an understanding of tau spreading mechanisms. Prior research, predominantly in typical AD, suggested that tau propagates from epicenters (regions with earliest tau) to functionally connected regions. However, given the constrained spatial hetero...
Background
In Alzheimer’s disease (AD), cortical tau aggregation is a strong predictor of cortical brain atrophy as shown by MRI and PET studies, particularly driving the degeneration of neuronal somata in the grey matter. However, tau’s physiological role is to stabilize microtubules within axons in the brain’s white matter (WM) pathways. Therefor...
Background
Tau‐PET imaging allows in‐vivo detection of neurofibrillary tangles. One tau‐PET tracer (i.e., [¹⁸F]flortaucipir) has received FDA‐approval for clinical use, and multiple other tau‐PET tracers have been implemented into clinical trials for participant selection and/or as a primary or secondary outcome measure. To optimize future use of t...
Background
Alzheimer's Disease (AD) is often accompanied by neuroinflammation, which manifests prior to significant cognitive decline. Reactive astrocytosis is a hallmark of such inflammation, potentially serving as an early biomarker for AD pathology. Our study employs [18F]fluorodeprenyl‐D2 ([18F]F‐DED) positron emission tomography (PET) imaging...
Purpose of the report
Adults with Down Syndrome (DS) have a substantially increased risk for Alzheimer’s disease (AD) due to the triplicated amyloid-precursor-protein gene on chromosome 21, resulting in amyloid and tau accumulation. However, tau PET assessments are not sufficiently implemented in DS-AD research or clinical work-up, and second-gener...
Niemann-Pick type C (NPC) disease is an inherited lysosomal storage disorder mainly driven by mutations in the NPC1 gene, causing lipid accumulation within late endosomes/lysosomes and resulting in progressive neurodegeneration. Although microglial activation precedes neuronal loss, it remains elusive whether loss of the membrane protein NPC1 in mi...
In early-stage Alzheimer's disease (AD) amyloid-β (Aβ) deposition can induce neuronal hyperactivity, thereby potentially triggering activity-dependent neuronal secretion of phosphorylated tau (p-tau), ensuing tau aggregation and spread. Therefore, cortical excitability is a candidate biomarker for early AD detection. Moreover, lowering neuronal exc...
Background
Alzheimer’s disease (AD) is associated with substantial synaptic loss potentially due to synaptotoxicity of fibrillar tau, but the association between tau deposition and synaptic loss remains unclear. Based on previous observations that pathology spreads preferentially between closely connected regions, we tested in the current multi‐PET...
Tau PET has attracted increasing interest as an imaging biomarker for 4-repeat (4R)-tauopathy progressive supranuclear palsy (PSP). However, the translation of in vitro 4R-tau binding to in vivo tau PET signals is still unclear. Therefore, we performed a translational study using a broad spectrum of advanced methodologies to investigate the sources...
INTRODUCTION
With the advent of disease‐modifying therapies, accurate assessment of biomarkers indicating the presence of disease‐associated amyloid beta (Aβ) pathology becomes crucial in patients with clinically suspected Alzheimer's disease (AD). We evaluated Aβ levels in cerebrospinal fluid (Aβ CSF) and Aβ levels in positron emission tomography...
White matter hyperintensities of presumed vascular origin (WMH) are associated with cognitive impairment and are a key imaging marker in evaluating brain health. However, WMH volume alone does not fully account for the extent of cognitive deficits and the mechanisms linking WMH to these deficits remain unclear. Lesion network mapping (LNM) enables...
Background and Objective: Frontotemporal dementia (FTD) is a highly heritable disorder. The majority of genetic cases are caused by autosomal dominant pathogenic variants in the c9orf72, GRN and MAPT gene. Behavioural and neuropsychiatric symptoms are frequent in genetic FTD. We aimed to describe behavioural and neuropsychiatric phenotypes in genet...
INTRODUCTION
Recent advances in biomarker research have improved the diagnosis and monitoring of Alzheimer's disease (AD), but in vivo biomarker‐based workflows to assess 4R‐tauopathy (4RT) patients are currently missing. We suggest a novel biomarker‐based algorithm to characterize AD and 4RTs.
METHODS
We cross‐sectionally assessed combinations of...
Background
Microglial activation is one hallmark of Alzheimer disease (AD) neuropathology but the impact of the regional interplay of microglia cells in the brain is poorly understood. We hypothesized that microglial activation is regionally synchronized in the healthy brain but experiences regional desynchronization with ongoing neurodegenerative...
Purpose
Current therapy strategies still provide only limited success in the treatment of glioblastoma, the most frequent primary brain tumor in adults. In addition to the characterization of the tumor microenvironment, global changes in the brain of patients with glioblastoma have been described. However, the impact and molecular signature of neur...
Rates of cognitive decline in Alzheimers disease (AD) are extremely heterogeneous, with ages of symptom onset ranging from age 40 to 100 years and conversion from mild cognitive impairment to AD dementia taking 2 to 20 years. Development of biomarkers for amyloid-beta (AB) and tau protein aggregates, the hallmark pathologies of AD, have improved pa...
Background
Preclinical, postmortem, and positron emission tomography (PET) imaging studies have pointed to neuroinflammation as a key pathophysiological hallmark in primary 4‐repeat (4R) tauopathies and its role in accelerating disease progression.
Objective
We tested whether microglial activation (1) progresses in similar spatial patterns as the...
Four-repeat (4R) tauopathies are neurodegenerative diseases characterized by cerebral accumulation of 4R tau pathology. The most prominent 4R tauopathies are progressive supranuclear palsy (PSP) and corticobasal degeneration characterized by subcortical tau accumulation and cortical neuronal dysfunction, as shown by PET-assessed hypoperfusion and g...
Background
Several magnetic resonance imaging (MRI) measures have been suggested as progression biomarkers in progressive supranuclear palsy (PSP), and some PSP staging systems have been recently proposed.
Objective
Comparing structural MRI measures and staging systems in tracking atrophy progression in PSP and estimating the sample size to use th...
Purpose
[¹⁸F]PI-2620 positron emission tomography (PET) detects misfolded tau in progressive supranuclear palsy (PSP) and Alzheimer’s disease (AD). We questioned the feasibility and value of absolute [¹⁸F]PI-2620 PET quantification for assessing tau by regional distribution volumes (VT). Here, arterial input functions (AIF) represent the gold stand...
Tau-PET receives growing interest as an imaging biomarker for the 4-repeat tauopathy progressive supranuclear palsy (PSP). However, the translation of in vitro 4R-tau binding to in vivo tau-PET signals is still unclear. Therefore, we conducted a longitudinal [18F]PI-2620 PET/MRI study in a 4-repeat-tau mouse model (PS19) and found elevated [18F]PI-...
Local therapy strategies still provide only limited success in the treatment of glioblastoma, the most frequent primary brain tumor in adults, indicating global involvement of the brain in this fatal disease. To study the impact of neuroinflammation distant of the primary tumor site on the clinical course of patients with glioblastoma, we performed...
Introduction: White matter hyperintensities of presumed vascular origin (WMH) are associated with cognitive impairment and are a key imaging marker in evaluating cognitive health. However, WMH volume alone does not fully account for the extent of cognitive deficits and the mechanisms linking WMH to these deficits remain unclear. We propose that les...
INTRODUCTION
White matter hyperintensities (WMH) are associated with key dementia etiologies, in particular arteriolosclerosis and amyloid pathology. We aimed to identify WMH locations associated with vascular risk or cerebral amyloid‐β1‐42 (Aβ42)‐positive status.
METHODS
Individual patient data (n = 3,132; mean age 71.5 ± 9 years; 49.3% female) f...
This paper provides an overview of the role of neuroinflammation in Alzheimer’s disease and other neurodegenerative diseases, highlighting the potential of anti-inflammatory treatments to slow or prevent decline. This research focuses on the use of positron emission tomography (PET) imaging to visualize and quantify molecular brain changes in patie...
Purpose
We hypothesized that severe tau burden in brain regions involved in direct or indirect pathways of the basal ganglia correlate with more severe striatal dopamine deficiency in four-repeat (4R) tauopathies. Therefore, we correlated [¹⁸F]PI-2620 tau-positron-emission-tomography (PET) imaging with [¹²³I]-Ioflupane single-photon-emission-comput...
Background and objectives
18-kDa translocator protein position-emission-tomography (TSPO-PET) imaging emerged for in vivo assessment of neuroinflammation in Alzheimer’s disease (AD) research. Sex and obesity effects on TSPO-PET binding have been reported for cognitively normal humans (CN), but such effects have not yet been systematically evaluated...
In Alzheimer’s disease, amyloid-beta (Aβ) triggers the trans-synaptic spread of tau pathology, and aberrant synaptic activity has been shown to promote tau spreading. Aβ induces aberrant synaptic activity, manifesting in increases in the presynaptic growth-associated protein 43 (GAP-43), which is closely involved in synaptic activity and plasticity...
Background
In aging, tau pathology develops in the medial temporal lobe (MTL), but spreads extensively to the cortex in the presence of amyloid‐beta, driving neurodegeneration and Alzheimer’s disease (AD) dementia development. This suggests that earliest age‐related MTL tau is a pre‐requisite for cortical tau spreading and the development of AD. Us...
Background
In clinical trials, an important question is which brain regions show high tau accumulation within 1‐2 years. Building upon our previous epicenter‐connectivity‐based distance model for predicting the progression of tau‐PET accumulation from initial seed regions of high tau (epicenters) to other regions (Franzmeier et al. Sci Adv. 2020),...
Background
Recent post‐mortem studies suggest that cerebrovascular disease contributes to Alzheimer’s disease (AD) pathophysiology and clinical progression. In particular, cerebral amyloid angiopathy is highly common in AD and has been linked to faster cognitive decline. Yet, in‐vivo evidence on the contribution of cerebrovascular disease to pathob...
Background
Alzheimer’s disease (AD) is characterized by the accumulation of amyloid beta (Aβ) plaques in the brain. Blood‐brain barrier (BBB) dysfunction has been associated with AD. Aβ‐plaques have been found to disrupt the BBB, leading to increased permeability and invasion of immune cells into the CNS and triggering an inflammatory response, and...
Background
In Alzheimer’s disease (AD), Amyloid‐beta deposition (Ab) is associated with tau spreading from epicenters to connected regions. Yet, Ab and tau accumulate in strikingly different patterns, and it is unclear how Abdrives tau spreading. We envision two mechanisms, i.e. i) that cortical Ab exerts remote effects and “pulls” tau out of conne...
Background
Targeting amyloid (Aß) may show highest clinical efficacy when preventing downstream tau spreading and subsequent neurodegeneration. Thus, it’s critical to establish Aß‐PET thresholds at which tau spreading is triggered, which may depend on ApoE4, i.e. a key genetic risk factor for Aß, tau and cognitive decline. Yet, ApoE4’s impact on Aß...
Background
Animal and in vitro studies of Alzheimer’s disease (AD) found that tau spreads trans‐synaptically in an activity‐dependent manner, suggesting that synapses are key routes for tau spread. Importantly, amyloid‐beta (Ab) induces synaptic remodeling and aberrant synaptic activity, which may accelerate trans‐synaptic tau spread. In AD patient...
Background
Myelin is the cholesterol‐rich layer ensheathing axons in the white matter (WM). The APOE ε4 allele has been associated with both reduced cholesterol transport to myelin layers in mice and with faster tau progression in individuals with AD. Here we asked the questions whether 1) APOE ε4 is associated with lower myelin and 2) any myelin d...
Background
Corticobasal syndrome (CBS) with underlying 4‐repeat tauopathy is a progressive neurodegenerative disorder characterized by declining cognitive and motor functions. Biomarkers for assessing pathological brain changes in CBS including tau‐ and microglia‐PET or neurofilament light chain (NfL) have recently been evaluated for differential d...
Background
Traumatic brain injury (TBI) is widely viewed as a risk factor for dementia. Since amyloid‐β and tau pathology have been reported in up to a third of individuals with TBI – even after a single TBI event – their accumulation could be a potential mechanism underlying this association. The aim of this study was to examine the relationship b...
Background
State‐of‐the‐art preprocessing of MRI and PET data is crucial for Alzheimer’s disease (AD) neuroimaging research. Therefore, standardization and harmonization of neuroimaging preprocessing across sites is key to generate comparable and sharable datasets and to reduce potential bias introduced by different preprocessing strategies. Furthe...
Background
Reliable biomarkers for detecting different abnormal tau protein isoforms between neurodegenerative diseases are currently missing. Phosphorylated tau (p‐tau) in the cerebrospinal fluid (CSF) is acknowledged as a 3/4R tau biomarker in AD but not in other tauopathies. The positron emission tomography (PET) radiotracer ¹⁸ F‐PI‐2620 has the...
Background
Alzheimer’s disease is characterized by cortical hyperexcitability in the early stages, which may be attributed to the intricate interplay between tau and amyloid β pathologies. To combat the propagation of tau pathology and cognitive decline, it may be beneficial to maintain a high degree of functional brain network segregation. Additio...
Background
State‐of‐the‐art preprocessing of MRI and PET data is crucial for Alzheimer’s disease (AD) neuroimaging research. Therefore, standardization and harmonization of neuroimaging preprocessing across sites is key to generate comparable and sharable datasets and to reduce potential bias introduced by different preprocessing strategies. Furthe...
Background
Recent post‐mortem studies suggest that cerebrovascular disease contributes to Alzheimer’s disease (AD) pathophysiology and clinical progression. In particular, cerebral amyloid angiopathy is highly common in AD and has been linked to faster cognitive decline. Yet, in‐vivo evidence on the contribution of cerebrovascular disease to pathob...
Background
Animal and in vitro studies of Alzheimer’s disease (AD) found that tau spreads trans‐synaptically in an activity‐dependent manner, suggesting that synapses are key routes for tau spread. Importantly, amyloid‐beta (Ab) induces synaptic remodeling and aberrant synaptic activity, which may accelerate trans‐synaptic tau spread. In AD patient...
Background
Targeting amyloid (Aß) may show highest clinical efficacy when preventing downstream tau spreading and subsequent neurodegeneration. Thus, it’s critical to establish Aß‐PET thresholds at which tau spreading is triggered, which may depend on ApoE4, i.e. a key genetic risk factor for Aß, tau and cognitive decline. Yet, ApoE4’s impact on Aß...
Background
Alzheimer’s disease (AD) is characterized by the accumulation of amyloid beta (Aß) plaques in the brain. Blood‐brain barrier (BBB) dysfunction has been associated with AD. Aß‐plaques have been found to disrupt the BBB, leading to increased permeability and invasion of immune cells into the CNS and triggering an inflammatory response, and...
Background
In Alzheimer’s disease (AD), Amyloid‐beta deposition (Ab) is associated with tau spreading from epicenters to connected regions. Yet, Ab and tau accumulate in strikingly different patterns, and it is unclear how Abdrives tau spreading. We envision two mechanisms, i.e. i) that cortical Ab exerts remote effects and “pulls” tau out of conne...
Background
In aging, tau pathology develops in the medial temporal lobe (MTL), but spreads extensively to the cortex in the presence of amyloid‐beta, driving neurodegeneration and Alzheimer’s disease (AD) dementia development. This suggests that earliest age‐related MTL tau is a pre‐requisite for cortical tau spreading and the development of AD. Us...
Background: Previous studies investigating disruptions in central nervous system (CNS) barriers in schizophrenia spectrum disorders (SSD) mainly focused on cerebrospinal fluid (CSF) markers, that cannot adequately assess blood-brain barrier (BBB) integrity. Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) represents a sensitive method...