Managing cardiovascular risk factors—including adopting healthy habits such as a nutritious diet and regular physical activity—is a highly effective preventative strategy against dementia, asserts
MADRID (EUROPA PRESS) – Marta Cortés, a researcher at the Cajal Neuroscience Center of the Spanish National Research Council (CNC-CSIC), emphasized that cardiovascular health is a “critical pillar” in the development of Alzheimer’s disease. She explained that high vascular risk directly leads to reduced brain metabolism, neuronal damage, and immunothrombosis, “redefining the condition as a systemic issue, not just a neurological one.”
Cortés shared these insights during her participation in a discussion hosted by the Ramón Areces Foundation and the Royal Academy of Pharmacy, which also featured other Spanish researchers focused on improving dementia and Alzheimer’s treatments.
She highlighted the promising state of Alzheimer’s research, noting that “over 100 compounds for the disease are currently undergoing clinical trials.”
She also directly linked heart health with brain health: “High cardiovascular risk (especially hypertension) leads to reduced metabolism in brain areas affected by Alzheimer’s, even in healthy individuals, establishing a direct causal relationship,” Cortés pointed out.
Cortés stated, “The prevalence of Alzheimer’s triples in individuals with atherosclerosis, and an increase in atheroma plaque is directly associated with decreased brain metabolism and higher markers of neuronal death in the blood.”
She further noted that “immune cells (TH17) and immunothrombosis processes, exacerbated by cardiovascular risk factors, harm the blood-brain barrier, clog microvessels, and actively contribute to the formation of amyloid plaques.”
In her address, this researcher from the Cajal Neuroscience Center of the Spanish National Research Council explained that “managing cardiovascular risk factors—including habits like a healthy diet and physical exercise—is a high-impact prevention strategy for dementia, potentially avoiding up to 45 percent of cases by mitigating the vascular damage that accelerates cognitive decline.”
She also discussed her research into the role of microRNA 721 in cognitive decline using a ‘knockout’ mouse model, aiming to develop new biomarkers and therapies. “Maintaining high cardiovascular risk for five years causes a process of partial neuronal death, evidenced by elevated levels of the axonal damage biomarker (NfL) in plasma,” added Cortés.
THE CONNECTION BETWEEN ATHEROSCLEROSIS, HYPERTENSION, AND ALZHEIMER’S
Meanwhile, María Pilar Martín from the National Center for Cardiovascular Research (CNIC), agreed with her colleague Cortés that cardiovascular risk, neuroinflammation (IL-17), and immunothrombosis (NETs) are interconnected mechanisms that drive cognitive decline, offering new therapeutic targets. “Immunothrombosis, caused by Neutrophil Extracellular Traps (NETs), is considered a central mechanism in both acute stroke damage and chronic deterioration in dementia,” she stated.
This expert noted, “Subclinical atherosclerosis and hypertension in middle-aged individuals, even if asymptomatic, are already linked to reduced brain metabolism in Alzheimer’s vulnerable regions.” She referred to chronic inflammation due to aging (‘inflammaging’), strongly connected to cardiovascular risk factors, “which drives cognitive decline by allowing specific immune cells to damage the brain.”
Among the projects underway, this researcher highlighted microRNA 721 as a potential therapeutic target, “since its inhibition in animal models delays immune system aging and enhances cognitive function.”
“Dysfunction of the cerebral lymphatic drainage leads to an accumulation of inflammatory T cells, causing cognitive impairment and opening new therapeutic avenues for neurodegenerative diseases,” she added. “We also know that cervical lymph nodes are crucial regulators of T cells in the brain; their dysfunction leads to an accumulation that causes neuroinflammation and cognitive decline.”
Thus, she explained that an excess of T cells can damage the blood-brain barrier, cause neurovascular dysfunction, and directly affect neurons, accelerating neurological damage. “Manipulating the lymphatic system or regulating specific T cell populations represents a potential therapeutic target for Alzheimer’s, multiple sclerosis, and strokes,” she affirmed.
NEURODEGENERATIVE AND VASCULAR FACTORS
María Ángeles Moro, also from the National Center for Cardiovascular Research (CNIC), pointed out that “most dementias, even those diagnosed as Alzheimer’s, present a mixed pathology that combines neurodegenerative and vascular factors.”
She agreed with her predecessors that controlling cardiovascular risk is crucial as it is directly associated with reduced brain metabolism. “As we often say, what’s bad for the heart is also bad for the brain,” she summarized. “Immunothrombosis and vascular inflammation are emerging as key pathogenic mechanisms in dementia, opening up new therapeutic pathways beyond the traditional focus on amyloid. It is postulated that NETs-mediated immunothrombosis is a central pathogenic factor in dementia, causing damage through both microvascular occlusions and direct inflammation,” explained Moro.
She also referred to specific therapeutic targets such as NETs inhibition (with drugs like DNase), the IL-17 pathway, and the regulation of microRNA 721 to combat neuroinflammation.
Lastly, Honorio Bando, honorary professor at the Faculty of Medicine at the Autonomous University of Madrid and academician at the Royal Academy of Pharmacy, applauded “the rapid scientific progress, particularly in innovative drugs, which is outpacing legal regulations, creating a critical regulatory gap.” “Science, driven by new technologies and drugs, is advancing significantly faster than legal frameworks,” he concluded.
