Initial cellular changes include a weakened blood–brain barrier and signs of premature endothelial aging, offering a possible explanation for links between hypertension and cognitive disorders like vascular cognitive impairment and Alzheimer's disease.

Oligodendrocytes fail to properly express genes for myelin maintenance and replacement, risking disrupted neural communication as cognition declines.

By day 42, additional gene expression changes align with observed cognitive decline, highlighting a progression from molecular alterations to functional impairment.

In a mouse model, hypertension induced by angiotensin triggers gene expression changes in endothelial cells, interneurons, and oligodendrocytes as early as three days after induction, indicating rapid brain cell vulnerability.

The study used angiotensin to induce hypertension and single-cell analysis to track molecular changes across brain cell types, highlighting mechanisms beyond mere blood pressure fluctuations.

Damage to interneurons creates an imbalance between inhibitory and excitatory signaling, a pattern associated with cognitive impairment and similar to changes seen in Alzheimer's disease.

Nearly half of Americans have hypertension, with over 119 million US adults affected and about 25% keeping the condition under control, underscoring the broad public health relevance.

Losartan, an angiotensin receptor blocker, reverses some early hypertension-induced effects on endothelial cells and interneurons in mice, suggesting potential cognitive benefits beyond blood pressure reduction.

More specifically, losartan reverses early hypertension effects on endothelial cells and interneurons, implying antihypertensive drugs may offer cognitive protection beyond lowering blood pressure.

Hypertension can trigger early, cell-level brain changes before blood pressure is measurably elevated, suggesting mechanisms beyond vascular pressure that contribute to cognitive decline.

A preclinical Weill Cornell Medicine study in Neuron shows hypertension damages vessels, neurons, and white matter days before a measurable blood pressure rise, indicating early brain vulnerability.

Endothelial cells show premature aging with reduced energy metabolism and increased senescence markers, alongside early signs of a weakened blood–brain barrier.