Capillary malformations affect roughly three in every 1,000 newborns and are typically visible as persistent red or purple patches caused by enlarged, tortuous capillaries and post-capillary venules. For many people, the lesions are primarily a cosmetic concern, although they can thicken or darken over time and may cause tissue overgrowth. In some patients, particularly those with facial port-wine stains, the same underlying process is associated with Sturge-Weber syndrome. This neurocutaneous disorder can involve abnormal vessels in the eye and the membranes covering the brain, contributing to glaucoma, seizures, migraines and other neurological complications. Existing interventions—including pulsed-dye laser treatment, surgery and medicines to control eye pressure—can reduce symptoms or improve appearance, but they do not eliminate the abnormal endothelial cells that create the malformation. A treatment directed at the cellular machinery driving the lesions could therefore address a fundamental biological cause rather than only managing its consequences.

The genetic trigger in most cases is a somatic mutation in GNAQ, meaning that it arises after conception and is present only in a subset of cells rather than throughout the body. The most common alteration changes the amino acid arginine to glutamine at position 183 of the Gαq protein, a substitution known as p.R183Q. Gαq normally functions as part of a molecular relay downstream of G protein-coupled receptors. When activated, it stimulates phospholipase C-β, an enzyme that cleaves the membrane lipid PIP2 into two signaling molecules: diacylglycerol and inositol 1,4,5-trisphosphate, or IP3. IP3 releases calcium from intracellular stores, while diacylglycerol activates protein kinase C. Together, these signals influence cell growth, survival, shape and migration. The R183Q mutant appears to keep this relay abnormally active, producing persistent calcium signaling and confusing the instructions that endothelial cells use to organize blood vessels.

To isolate the mutation’s effects, the researchers used CRISPR–Cas9 gene editing to remove endogenous Gαq from immortalized human dermal microvascular endothelial cells. They then reintroduced either normal Gαq or the R183Q mutant using lentiviral vectors. This design allowed the two cell populations to be compared while keeping much of their genetic and environmental background the same. The engineered proteins carried a fluorescent mTurquoise2 tag, enabling the investigators to confirm their expression and localization. Although both rescued cell lines produced similar amounts of Gαq—at levels approximately three times higher than those normally found in the parental cells—the mutant cells developed a distinctly altered shape. They became larger and more elongated, even though their VE-cadherin cell junctions and actin cytoskeleton remained broadly organized. The change in morphology was accompanied by a functional defect: in scratch-wound experiments, mutant endothelial cells moved slowly into the cleared area, leaving the artificial wound open for longer than cells carrying normal Gαq.

The researchers also tested angiogenic sprouting, a process in which endothelial cells extend coordinated projections to form new vessel-like structures. They compacted the cells into three-dimensional spheroids, embedded them in collagen and stimulated them with vascular endothelial growth factor, or VEGF. Compared with normal-Gαq spheroids, those expressing Gαq-R183Q produced substantially fewer and shorter sprouts. This result is notable because vascular malformations are not simply caused by excessive vessel growth; they can also arise when endothelial cells fail to migrate, interpret developmental signals or remodel their surroundings correctly. The mutant cells’ poor performance in both migration and sprouting assays suggested that the mutation was disrupting a network of intracellular signals required for orderly vascular development rather than merely accelerating proliferation. The two cell populations showed no major difference in proliferation rates, further focusing attention on signaling and cell behavior.

To map those signaling changes without presupposing which pathway was involved, the team turned to quantitative phosphoproteomics. Proteins are often regulated by phosphorylation, the reversible addition of phosphate groups to specific amino acids. By measuring thousands of phosphorylation sites, scientists can build a broad picture of which molecular circuits are active or suppressed inside a cell. The researchers grew the normal and mutant endothelial cells in media containing either ordinary amino acids or isotopically heavy versions of lysine and arginine, a strategy called SILAC. After mixing cell lysates, they used mass spectrometry to distinguish the two populations and enriched phosphorylated peptides for analysis. Label-swap experiments helped control for technical bias. Pathway analysis highlighted increased activity associated with the phosphatase PTEN and reduced activity in the integrin-linked kinase pathway. Immunoblotting confirmed lower phosphorylation of Akt, S6K and Paxillin, molecules involved in survival, growth and adhesion, while phosphorylation of ERK was increased, consistent with earlier studies of the mutation.

The strongest signal, however, involved Calcineurin and the NFAT family of transcription factors. Calcineurin is a calcium- and calmodulin-dependent serine/threonine phosphatase. When intracellular calcium rises, Calcineurin removes phosphate groups from NFAT proteins, allowing them to move from the cytoplasm into the nucleus and regulate gene expression. In the mutant endothelial cells, several phosphorylation sites on NFAT1 and NFAT2 were reduced, indicating enhanced dephosphorylation. Yet imaging revealed an apparent paradox: rather than accumulating in the nucleus, both NFAT proteins remained predominantly in the cytoplasm. The explanation appeared to be a feedback inhibitor called DSCR1.4, also known as RCAN1.4. Its abundance rose sharply in the Gαq-R183Q cells, whereas the related DSCR1.1 isoform did not change. DSCR1.4 can inhibit Calcineurin, creating a feedback loop in which excessive upstream signaling ultimately suppresses the nuclear NFAT activity needed for normal endothelial responses. The mutant cells therefore showed biochemical evidence of persistent pathway stimulation alongside a failure of NFAT-dependent signaling in the nucleus.

Patient tissue provided an important reality check. In skin biopsies from people whose capillary malformations carried the GNAQ p.R183Q mutation, immunofluorescence microscopy showed NFAT1 and NFAT2 concentrated mainly in the cytoplasm of VE-cadherin-positive endothelial cells. Phosphorylated NFAT signals that were detectable in experimental controls were not observed in the endothelial cells of the malformation samples, and DSCR1 protein was present in the affected tissue. These observations were consistent with the engineered-cell experiments, although the researchers noted a significant limitation: matched healthy skin biopsies were not available for direct comparison. The patient samples therefore support the proposed signaling defect but cannot by themselves establish how much NFAT localization or DSCR1.4 expression differs from normal capillaries. Even so, the alignment between patient tissue and the laboratory model strengthens the case that the pathway is relevant to the disease rather than being an artifact of cell culture.

The team next asked whether the pathway could be pharmacologically manipulated. They treated mutant endothelial cells with tacrolimus, also called FK506, an immunosuppressive drug that inhibits Calcineurin after binding to FKBP proteins. A 24-hour treatment restored the nuclear-to-cytoplasmic distribution of NFAT1 and NFAT2 toward the pattern seen in normal cells. It also restored phosphorylation at the NFAT1 and NFAT2 sites that had been depleted by the mutation. Functionally, tacrolimus slightly improved wound closure and partially rescued the number and length of VEGF-induced sprouts. The effect was real but incomplete. The investigators suggest that mutant cells express lower levels of several FKBP proteins needed for tacrolimus to inhibit Calcineurin efficiently, and that additional signaling pathways remain active downstream of Gαq-R183Q. The result is therefore not evidence that tacrolimus is ready to treat capillary malformations, particularly because systemic immunosuppression carries substantial risks, but it does demonstrate that the abnormal pathway is chemically accessible.

A more dramatic rescue came from targeting DSCR1 directly. Using a lentiviral short-hairpin RNA, the researchers reduced expression of both DSCR1.1 and DSCR1.4 in the engineered cells. In Gαq-R183Q endothelial cells, DSCR1 depletion increased phosphorylation of NFAT1 and NFAT2, promoted their movement into the nucleus and almost completely restored migration in scratch assays. It also strongly enhanced angiogenic sprouting in the three-dimensional collagen model. The contrast with tacrolimus is mechanistically informative: blocking Calcineurin from outside the cell produced only a partial functional recovery, whereas removing the mutation-induced feedback brake had a much larger effect. The result identifies DSCR1.4 as a particularly attractive target, although suppressing a gene throughout the body would be technically and biologically challenging. Future therapies might need to deliver a DSCR1.4-directed treatment selectively to affected endothelial cells or develop molecules that interrupt its interaction with Calcineurin without disturbing essential signaling elsewhere.

The findings place capillary malformations within a growing landscape of genetically defined vascular disorders in which different mutations converge on distinct but interconnected signaling networks. The study found reduced Akt/mTOR activity in Gαq-R183Q cells, in contrast to other malformations driven by activating mutations in PIK3CA or loss of PTEN function, where the same pathway is often overactive. That difference underscores why treatments cannot necessarily be transferred from one vascular anomaly to another simply because the lesions look similar. The researchers also caution that their model used cultured human endothelial cells expressing the mutant protein at higher-than-endogenous levels, and that the experiments did not reproduce the full complexity of skin, brain or eye tissue. Animal studies and disease-relevant human models will be needed to determine whether selectively correcting Calcineurin–NFAT–DSCR1.4 signaling can shrink established lesions, prevent progression or improve neurological and ophthalmological complications. Still, the work offers a compelling new route from mutation to mechanism to therapeutic strategy—and suggests that the molecular circuitry beneath a visible birthmark may be far more precisely targetable than previously thought.

Subject of Research: Calcineurin–NFAT–DSCR1.4 signaling in Gαq-R183Q-driven capillary malformations

Article Title: Calcineurin-NFAT-DSCR1.4 signaling as druggable axis in Gαq-R183Q–driven capillary malformations

Article References: Xu, T., Janssen, V., Reinhard, N. R. et al. “Calcineurin-NFAT-DSCR1.4 signaling as druggable axis in Gαq-R183Q–driven capillary malformations.” Angiogenesis 29, 16 (2026). Original research article

Image Credits: AI Generated

DOI: 10.1007/s10456-026-10029-9

Keywords: capillary malformations, Sturge-Weber syndrome, GNAQ p.R183Q, endothelial cells, Calcineurin, NFAT signaling, DSCR1.4, tacrolimus, angiogenesis

Stroke remains one of the leading causes of morbidity and mortality worldwide, with the complexity of its pathogenesis posing substantial challenges to both diagnosis and treatment. Central to its development is the dysfunction of the brain’s vasculature, particularly the endothelial cells lining cerebral blood vessels. These cells act as a critical barrier, regulating the exchange between the bloodstream and neural tissue, and their impairment can precipitate the catastrophic cascade of events leading to ischemic injury.

At the heart of this new research is Foxf2, a gene previously implicated in vascular development but not extensively studied in the context of adult cerebrovascular function. The investigative team, led by Todorov-Völgyi and colleagues, employed a combination of genetic, molecular, and cellular techniques to elucidate Foxf2’s role within the endothelial compartment of the brain. Their findings illuminate a complex regulatory network in which Foxf2 orchestrates endothelial cell behavior via modulation of the Tie2 receptor, a tyrosine kinase known for its critical involvement in vascular stability and angiogenesis.

The researchers discovered that loss of Foxf2 expression compromises endothelial integrity, leading to diminished Tie2 signaling and subsequent vascular dysfunction. This cascade ultimately undermines the blood-brain barrier’s selective permeability, rendering neural tissue vulnerable to ischemic insult and inflammatory damage. Such vulnerability aligns with clinical observations linking Foxf2 genetic variants to increased stroke susceptibility, thereby providing a molecular basis for previously observed epidemiological correlations.

One of the study’s significant innovations lies in its use of advanced in vivo models that mimic human cerebrovascular architecture with high fidelity. Through conditional knockout approaches, the team selectively ablated Foxf2 in brain endothelial cells, enabling a precise dissection of its functional consequences. These models revealed marked alterations in endothelial morphology, junctional protein expression, and vessel responsiveness, collectively highlighting Foxf2 as a linchpin of cerebrovascular homeostasis.

The Tie2 receptor, a well-characterized mediator of endothelial survival and vascular quiescence, emerged as the downstream effector through which Foxf2 exerts its protective influence. Reduced Foxf2 correlated with attenuated Tie2 activation, diminishing phosphorylation events essential for endothelial cell resilience. This attenuation precipitated a cascade of pathophysiological changes that compromised vascular integrity, including increased permeability and susceptibility to oxidative stress, both hallmarks of stroke pathology.

Crucially, the study’s findings suggest that therapeutic strategies aimed at augmenting Foxf2 activity or enhancing Tie2 signaling could reinforce the brain’s microvasculature and mitigate stroke risk. Pharmacological agonists of Tie2 or gene therapy approaches to restore Foxf2 expression may hold transformative potential, especially for individuals genetically predisposed to cerebrovascular disorders.

The implications of this research extend beyond stroke, offering insights into broader neurovascular diseases characterized by endothelial cell dysfunction, such as vascular dementia and certain neurodegenerative disorders. The identification of Foxf2 as a master regulator introduces a novel molecular target to potentially slow or prevent the progression of these debilitating conditions.

Moreover, the study highlights the intricate crosstalk between genetic factors and intracellular signaling pathways in vascular biology. By delineating this axis, the researchers contribute to a more nuanced model of cerebrovascular regulation that integrates genetic susceptibility with cellular signaling dynamics, thereby refining our conceptual framework for stroke pathogenesis.

Equally compelling is the potential for Foxf2 and Tie2 pathway components to serve as biomarkers for early detection of vascular compromise. Their expression levels or activity states could inform risk stratification and monitoring, enabling clinicians to tailor preventative or therapeutic interventions with greater precision.

The research also points to the importance of endothelial heterogeneity in brain health. Not all endothelial cells are created equal; those within distinct vascular niches may differentially express Foxf2, influencing localized vulnerability to injury. Future work may focus on mapping this spatial variability and exploiting it to develop region-specific therapeutic regimens.

This study consequently invites a reevaluation of existing therapeutic paradigms, many of which focus on symptomatic relief rather than addressing underlying endothelial dysfunction. Targeting the Foxf2–Tie2 signaling axis situates treatment within the realm of molecular correction, offering hope for more durable and efficacious outcomes.

As the field advances, interdisciplinary collaborations integrating genomics, vascular biology, and clinical neurology will be paramount to translating these discoveries into clinical practice. Such collaborations promise to hasten the journey from bench to bedside, ultimately alleviating the global burden of stroke and related disorders.

In sum, the elucidation of Foxf2’s role in safeguarding brain endothelial cells via Tie2 signaling represents a paradigm shift in cerebrovascular research. It underscores the nuanced interplay between genetics and vascular physiology, charting a course toward innovative therapies that address the root causes of stroke and enhance brain resilience.

This seminal work not only broadens the scientific community’s understanding of cerebrovascular function but also invigorates the quest for novel interventions that can transform stroke management from reactive to proactive. As researchers continue to unravel the complexities of vascular biology, Foxf2 stands out as a beacon of promise in the ongoing battle against neurological disease.

The study’s integrative approach, combining genetic manipulation with functional assays and clinical relevance, affirms the critical importance of multi-faceted research in uncovering the biological secrets of the brain’s vasculature. With further exploration, Foxf2 could redefine standards of care and inspire a new generation of targeted cerebrovascular therapeutics.

Subject of Research: The role of the stroke risk gene Foxf2 in brain endothelial cell function mediated through Tie2 signaling.

Article Title: The stroke risk gene Foxf2 maintains brain endothelial cell function via Tie2 signaling.

Article References:
Todorov-Völgyi, K., González-Gallego, J., Müller, S.A. et al. The stroke risk gene Foxf2 maintains brain endothelial cell function via Tie2 signaling. Nat Neurosci (2025). https://doi.org/10.1038/s41593-025-02136-5

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41593-025-02136-5

The research, published in the Journal of the American Heart Association, involved female spontaneously hypertensive rats subjected to either a refined control diet devoid of plant foods or a nutrient-matched plant-based diet rich in fruits, vegetables, nuts, and legumes. Over six months, the investigation focused not only on the preventative capacity of this diet but remarkably, also its restorative effects on established CMD. This dual approach provides vital insights into dietary interventions as a potentially powerful tool in cardiovascular disease management.

CMD’s pathophysiology implicates the dysfunction of endothelial cells — the critical regulators of vascular tone in coronary microvessels. Normally, these cells facilitate vasodilation, ensuring adequate myocardial perfusion especially under stress. However, hypertension induces oxidative stress and inflammation, leading to endothelial damage. Such damage results in improper vasoconstriction and inadequate blood flow, manifesting clinically as chest pain and contributing to heart failure risk. Notably, CMD presents with a higher severity in women and correlates with increased hospitalization rates, underscoring an urgent need for more effective therapies.

Traditional pharmacological treatments for CMD yield limited success, often failing to adequately restore microvascular function. This shortcoming prompted the Georgia State team to investigate non-pharmacological alternatives targeting the underlying vascular cell dysfunction. Rooted in the hypothesis that antioxidants found abundantly in plant-based foods may counteract oxidative vascular damage, the study tested a diet comprising 28% plant-based components—a composition analogous to a human diet featuring black beans, red bell peppers, Brussels sprouts, lemons, sweet potatoes, walnuts, and blueberries.

One of the study’s most compelling findings was that the plant-based diet improved coronary flow reserve—a clinical measure of microvascular function—even while systemic hypertension remained unabated. This suggests that vascular endothelial health can be selectively enhanced independent of blood pressure control. MRI-based assessments of myocardial blood flow corroborated these improvements, revealing restored perfusion correlating with improved endothelial responsiveness.

Further cellular investigations isolated blood vessel endothelial cells from heart tissues to delineate the mechanistic underpinnings of this dietary intervention. Results indicated that the antioxidant-rich diet mitigated markers of oxidative damage and inflammation within these cells, enhancing their ability to mediate vasodilation. Moreover, histological analyses highlighted reduced tissue injury and fibrosis, implicating improved vascular integrity as a central mediator of the observed functional recovery.

By switching a subset of rats from the control to the plant-based diet after CMD was established, researchers demonstrated that dietary modification not only prevents but also partially reverses microvascular disease progression. This finding has profound clinical implications, as it provides a potential low-cost, low-risk therapeutic strategy to halt and regress CMD pathology, a feature rarely achieved with current therapies.

The study’s translation to human health is particularly promising. Given the diet’s similarity to feasible human dietary patterns rich in whole, plant-based foods, these findings support initiating clinical trials to evaluate whether corresponding dietary regimens might similarly benefit patients with CMD. Such trials could pioneer a paradigm shift in cardiovascular disease prevention and management, especially for those with hypertension who remain at risk despite pharmacologic control.

Importantly, this research also sheds light on the sex-specific vulnerability of CMD, as women disproportionately suffer from this microvascular disorder. Future investigations could explore whether plant-based diets confer differential benefits across sexes and dissect the molecular pathways implicated in CMD pathogenesis unique to female physiology.

The robust methodology employed—including prolonged dietary exposure, advanced imaging modalities, and cellular-level analysis—provides rigorous validation of the diet’s effects. This integrative approach reinforces the validity and applicability of findings, ensuring that they resonate beyond animal models to inform clinical strategies.

While the study underscores the antioxidant potential of plant-based foods as a key factor, it also opens avenues for investigating other components such as fiber, micronutrients, and phytochemicals that may synergistically influence vascular health. Understanding the composite effect of these nutrients could refine dietary guidelines further, tailoring interventions to optimize cardiovascular outcomes.

Overall, the demonstrated ability of a thoughtfully composed plant-based diet to counteract and even reverse hypertension-induced coronary microvascular dysfunction marks a pivotal advancement in cardiovascular research. It reaffirms the vital connection between nutrition and heart health and offers a tangible, actionable pathway to mitigate a disease that disproportionately burdens millions worldwide.

This pioneering work lays essential groundwork for future clinical trials and mechanistic studies aimed at dissecting the complexities of diet-induced vascular repair. By illuminating the substantial reparative capacity of plant-derived nutrients, the study empowers patients and healthcare providers alike to reconsider dietary prescriptions as fundamental components of cardiovascular disease management.

Subject of Research: Animals

Article Title: Prevention and Reversal of Hypertension‐Induced Coronary Microvascular Dysfunction by a Plant‐Based Diet

News Publication Date: 11-Nov-2025

Web References: https://www.ahajournals.org/doi/full/10.1161/JAHA.125.045515

References: Najjar, R.S., et al. (2025). Prevention and Reversal of Hypertension-Induced Coronary Microvascular Dysfunction by a Plant-Based Diet. Journal of the American Heart Association. DOI: 10.1161/JAHA.125.045515

Image Credits: Georgia State University

Keywords: Heart disease, Dietetics

Tau protein has long been implicated in the characteristic neurofibrillary tangles found in Alzheimer’s disease, predominantly associated with neuronal damage and cognitive decline. However, recent histopathological observations have detected accumulations of tau aggregates not only within neural tissue but distinctly localized along the cerebrovascular endothelium. This vascular tau deposition has eluded mechanistic understanding until now, with early vascular changes increasingly recognized as precursors to symptomatic dementia. The current study elucidates how fibrillar, protofibrillar tau species alter cerebral endothelial cell function at a molecular level, driving a cascade of vascular dysfunction instrumental in disease progression.

To dissect this phenomenon, researchers developed an in vitro model mimicking the neurovascular unit’s endothelial barrier, exposing these cells to protofibrillar tau extracted to replicate early-stage Alzheimer’s pathology. The experiments revealed that tau exposure induces a metabolic shift within endothelial cells, specifically modulating glycolytic activity and mitochondrial function. This energy reprogramming is accompanied by an upregulation of pro-inflammatory gene pathways and endothelial activation markers, culminating in increased barrier permeability. The consequence is a breach in the BBB, allowing potentially neurotoxic substances and peripheral immune cells to infiltrate the brain parenchyma, thereby exacerbating neuroinflammation and neuronal injury.

Significantly, the metabolic switch induced by tau involves heightened glycolysis—a phenomenon reminiscent of metabolic adaptations seen in other inflammatory and pathological contexts. This glycolytic induction appears to be an early event, occurring rapidly after tau exposure and preceding overt barrier compromise. Such metabolic reprogramming not only serves as a mechanistic driver of endothelial dysfunction but also presents a potential therapeutic target to restore BBB integrity before irreversible neurodegeneration unfolds. The identification of this early metabolic alteration is poised to shift the paradigm of Alzheimer’s research toward neurovascular intervention strategies.

The in vitro findings were corroborated by in vivo studies using tau transgenic mice engineered to accumulate human tau aggregates akin to Alzheimer’s pathology. Examination of these animals’ cerebrovascular architecture showcased hallmark changes consistent with tau-mediated endothelial injury, including amplified inflammatory responses and diminished tight junction protein expression integral to BBB maintenance. These vascular pathologies parallel the metabolic disturbances observed in cultured cells, reinforcing the concept that tau-induced endothelial dysfunction is a foundational event in the Alzheimer’s disease cascade.

Importantly, this study delineates the heterogeneity of tau species, focusing on protofibrillar forms that are thought to develop prior to the formation of insoluble neurofibrillary tangles. The research suggests that these intermediate aggregates exert potent and deleterious effects on cerebrovascular cells, in contrast to fibrillar forms traditionally associated with neuronal damage. By pinpointing this specific tau conformation, interventions can be tailored to intercept early-stage tau toxicity, targeting the neurovascular interface to prevent subsequent neurodegenerative outcomes.

The weakening of the BBB due to tau-driven endothelial pathology signifies not only physical barrier disruption but also the loss of critical neuroprotective functions. The BBB’s role extends beyond a mere physical blockade; it actively regulates nutrient transport, waste clearance, and immune surveillance. Tau-mediated impairment compromises these processes, fostering a pro-inflammatory brain milieu conducive to progressive neuronal loss. Thus, vascular contributions to cognitive impairment and dementia (VCID) gain substantial credence, with tau pathology serving as a molecular nexus linking neurodegeneration and vascular dysfunction.

Looking forward, the research team is delving deeper into the mechanisms of tau internalization by endothelial cells and the signaling pathways precipitating glycolytic upregulation. Moreover, investigations aim to elucidate tau’s effects on other constituents of the neurovascular unit, particularly glial cells such as astrocytes and pericytes, which synergistically maintain BBB homeostasis. Disentangling this complex cellular interplay is essential to comprehensively understand and therapeutically target neurovascular degeneration in Alzheimer’s disease.

This study marks a significant leap in Alzheimer’s research by highlighting a non-neuronal, vascular dimension of tau pathology. It propels the field toward early detection and treatment paradigms centered on preserving BBB function to forestall cognitive decline. Targeting metabolic and inflammatory pathways within cerebral endothelial cells presents a promising avenue for novel therapeutics, potentially altering the trajectory of Alzheimer’s and similar dementias before irreversible damage ensues.

The implications for clinical translation are profound, fostering a new generation of diagnostic biomarkers sensitive to neurovascular dysfunction and endothelial metabolic changes induced by tau. Such biomarkers could enable earlier intervention windows and tailored treatment modalities. Furthermore, understanding tau’s vascular effects may unlock insights into overlapping pathologies such as cerebral amyloid angiopathy and other forms of vascular dementia, broadening the impact of these findings.

In summary, the intricate relationship between pathogenic tau species and cerebral endothelial metabolism illuminates a critical axis of Alzheimer’s disease progression. By disrupting energy homeostasis and promoting inflammatory activation, tau compromises the blood-brain barrier’s protective functions, opening new vistas for exploring therapeutic strategies to maintain cerebrovascular health and cognitive integrity.

Subject of Research: The pathological effects of protofibrillar tau on cerebral endothelial cell metabolism, vascular inflammation, and blood-brain barrier integrity in Alzheimer’s disease.

Article Title: Fibrillar tau alters cerebral endothelial cell metabolism, vascular inflammatory activation, and barrier function in vitro and in vivo.

News Publication Date: 20-Mar-2025.

Web References:
Alzheimer’s & Dementia – DOI: 10.1002/alz.70077

Keywords

Alzheimer disease, Human brain, Blood vessels, Blood brain barrier, Tau proteins, Memory formation, Inflammation, Discovery research, Molecular mechanisms, Neural mechanisms, Academic researchers, Academic journals, Cell pathology, Human health