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The researcher of Cajal Neuroscience Center of the Higher Council for Scientific Research (CNC-CSIC) Martha Cortes has highlighted that cardiovascular health is a “fundamental pillar” in Alzheimer’s pathogenesissince elevated vascular risk directly causes cerebral hypometabolism, neuronal damage and immunothrombosis, “redefining the disease as a systemic and not just a neurological problem.”
This was shown during his participation in a debate organized by the Ramón Areces Foundation and the Royal Academy of Pharmacy in which other Spanish researchers who are working for a better approach to dementia and, in particular, Alzheimer’s, have participated.
Cortés has highlighted the good times that research into Alzheimer’s is going through, since “more than 100 compounds for this disease are in clinical trials“. And she has directly linked the evolution of the heart with that of the brain: “A high cardiovascular risk (especially hypertension) causes a reduction in metabolism in the same brain areas affected by Alzheimer’s, even in healthy people, establishing a direct causal link,” the researcher highlighted.
According to Cortés, “the prevalence of Alzheimer’s triples in individuals with atherosclerosis, and the increase in atheromatous plaque is directly associated with a decrease in brain metabolism and an increase in markers of neuronal death in the blood.” In this sense, he stated that “immune cells (TH17) and immunothrombosis processes, exacerbated by cardiovascular risk factors, damage the blood-brain barrier, occlude microvessels and actively contribute to the formation of amyloid plaques.”
During her intervention, this researcher from the Cajal Neuroscience Center of the Higher Council for Scientific Research explained that “the control of cardiovascular risk factors – among them, healthy habits such as good nutrition, physical exercise – is a high-impact prevention strategy for dementia, which can avoid up to 45 percent of cases by mitigating vascular damage that accelerates cognitive decline.
He has also mentioned how he is investigating the role of microRNA 721 in cognitive impairment using a mouse model knockoutwith the aim of developing new biomarkers and therapies. “Maintaining a high cardiovascular risk for five years causes a process of partial neuronal death, evidenced by high levels of the biomarker of axonal damage (NfL) in plasma,” added Cortés.
Relationship between atherosclerosis and hypertension and Alzheimer’s
For its part, María Pilar Martín, from the National Center for Cardiovascular Research (CNIC), has agreed with his colleague Cortés that cardiovascular risk, neuroinflammation (IL-17) and immunothrombosis (NETs) are identified as interconnected mechanisms that drive the cognitive impairmentoffering new therapeutic objectives. “Immunothrombosis, caused by Neutrophil Extracellular Traps (NETs), is postulated as a central mechanism in both acute damage due to stroke and chronic deterioration in dementia,” he stated.
For this expert, “subclinical atherosclerosis and hypertension in middle-aged people, even asymptomatic, are already associated with a reduction in brain metabolism in regions vulnerable to Alzheimer’s.” And he has referred to chronic inflammation due to aging (‘inflammaging’), strongly linked to cardiovascular risk factors, which “drives cognitive decline by allowing specific immune cells to damage the brain.”
Of all the work that is being carried out, this researcher has highlighted the microRNA 721 as a possible therapeutic target, “since its inhibition in animal models delays the aging of the immune system and improves cognitive function.”
“Dysfunction of cerebral lymphatic drainage causes an accumulation of inflammatory T cells, causing cognitive impairment and opening new therapeutic avenues for neurodegenerative diseases“He added. “We also know that cervical lymph nodes are crucial regulators of T cells in the brain; “its dysfunction causes a buildup that causes neuroinflammation and cognitive impairment.”
Thus, he explained that the excess of T cells It can damage the blood-brain barrier, cause neurovascular dysfunction, and directly affect neurons, accelerating neurological damage. “Manipulation of the lymphatic system or regulation of specific populations of T cells represents a potential therapeutic target for Alzheimer’s, multiple sclerosis and stroke,” he said.
Neurodegenerative and vascular factors
For its part, María Ángeles Moro, from the National Center for Cardiovascular Research (CNIC), has highlighted how “the majority of dementias, even those diagnosed as Alzheimer’s, present a mixed pathology that combines neurodegenerative and vascular factors.”
She agrees with her predecessors in the speaking session on the importance of controlling that cardiovascular risk being directly associated with lower brain metabolism. “As we often say, what is bad for the heart is also bad for the brain,” he summarized. “Immunothrombosis and vascular inflammation are emerging as key pathogenic mechanisms in dementiaopening new therapeutic avenues beyond the traditional focus on amyloid. It is postulated that immunothrombosis mediated by NETs is a central pathogenic factor in dementia, causing damage both by vascular micro-occlusions and by direct inflammation,” explained Moro.
He has also referred to specific therapeutic targets such as inhibition of NETs (with drugs such as DNASA), the IL-17 pathway and the regulation of micro RNA 721 to combat neuroinflammation. Finally, Honorio Bando, honorary professor of the Faculty of Medicine of the Autonomous University of Madrid and academic of the Royal Academy of Pharmacyhas applauded “the rapid scientific advance, especially in innovative drugs, which is surpassing the legal system, creating a critical regulatory gap.” “Science, driven by new technologies and drugs, advances significantly faster than the legal system,” he concluded.
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