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Updated: Mar 26, 2026

A Mouse Model for Vascular Cognitive Impairment and Dementia Based on Needle-guided Asymmetric Bilateral Common Carotid Artery Stenosis
Published on: November 22, 2024
Neuronal changes after chronic high blood pressure in animal models and its implication for vascular dementia
Gonzalo Flores1, Gabriel D Flores-Gómez2, Ma de Jesús Gomez-Villalobos1
1Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla. 14 Sur 6301, Puebla, 72570, México.
Insights
Long-lasting high blood pressure, or arterial hypertension, significantly impacts brain structure, leading to vascular dementia. This condition reduces dendritic complexity and spine density in key brain areas, affecting cognitive function.
Area of Science:
- Neuroscience
- Pathophysiology
- Gerontology
Background:
- Vascular dementia (VD) is a prevalent neurocognitive disorder affecting 4% of the elderly, significantly impacting patient independence and family care.
- Arterial hypertension is a primary risk factor for cerebrovascular disease, often preceding VD development.
- Hypertension-induced hypoperfusion and ischemia are linked to neural damage and cognitive decline.
Purpose of the Study:
- To review human and animal model data on the link between chronic hypertension and neural morphological changes in VD.
- To examine the effects of chronic arterial hypertension and aging on vascular dementia.
- To discuss neural dendritic morphology in specific brain regions affected by hypertension.
Main Methods:
- Evaluation of existing human and animal model research.
- Analysis of studies investigating chronic hypertension's impact on neural morphology.
- Focus on prefrontal cortex, dorsal hippocampus, and nucleus accumbens in animal models.
Main Results:
- Chronic hypertension is associated with reduced cerebral blood flow and ischemia.
- Dendritic complexity and spine density are crucial for synaptic contacts and are linked to dementia.
- In aged rats, chronic hypertension led to decreased dendritic length and spine density in key brain areas.
Conclusions:
- Long-lasting arterial hypertension induces significant neural morphological changes.
- These changes, including reduced dendritic complexity, are implicated in the pathophysiology of vascular dementia.
- Animal models provide valuable insights into hypertension-related neural alterations contributing to cognitive decline.
Abstract:
Vascular dementia is a devastating disorder not only for the patient, but also for the family because this neurocognitive disorder breaks the patient's independence, and leads to family care of the patient with a high cost for the family. This complex disorder alters memory, learning, judgment, emotional control and social behavior and affects 4% of the elderly world population. The high blood pressure or arterial hypertension is a major risk factor for cerebrovascular disease, which in most cases leads to vascular dementia. Interestingly, this neurocognitive disorder starts after long lasting hypertension, which is associated with reduced cerebral blood flow or hypoperfusion, and complete or incomplete ischemia with cortical thickness. Animal models have been generated to elucidate the pathophysiology of this disorder. It is known that dendritic complexity determines the receptive synaptic contacts, and the loss of dendritic spine and arbor stability are strongly associated with dementia in humans. This review evaluates relevant data of human and animal models that have investigated the link between long-lasting arterial hypertension and neural morphological changes in the context of vascular dementia. We examined the effect of chronic arterial hypertension and aged in vascular dementia. Neural dendritic morphology in the prefrontal cortex and the dorsal hippocampus and nucleus accumbens after chronic hypertension was diskussed in the animal models of hypertension. Chronic hypertension reduced the dendritic length and spine density in aged rats.
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