Pathophysiological Association of Alzheimer’s Disease and Hypertension: A Clinical Concern for Elderly Population

Figures & data

Figure 1 Figurative description of a modified risk factor for AD developments.

Figure 2 Molecular levels factors involved in neural death—from β-secretase processing to synaptic dysfunction and neuronal cell death in AD development.

Figure 3 Depicts the consequences of biological aging and high blood pressure on a person’s life over time. Both are linked to cognitive, functional, and structural brain damage (cognitive loss, reduced cerebral blood flow, altered distribution of blood flow in response to the cognitive and physiological challenge, reduced grey matter volume, presence of white matter high intensities, greater diffusion within white matter tracts, more porous blood brain barrier, and presence of reactive oxygen species).

Figure 4 A detailed description of the pathophysiological association between Alzheimer’s Disease and hypertension.

Table 1 The Studies on the Relationship Between AHM Drug Use and AD Therapy

Antihypertensive Class	Antihypertensive Drug	Alzheimer Disease Related Observation	References
Calcium Channel Blockers	Isradipine Nilvadipine Nimodipine Lisinopril	Neuronal malfunction, cell death, and apoptosis are all caused by increased intracellular calcium. Production of amyloid-beta (Aβ) protein. Clearance by glial and neuronal cells by autophagy.	[165–168]
Angiotensin-Converting Enzyme Inhibitors	Captopril Perindopril	Reduce symptoms of cognitive decline in patients with “Alzheimer”s disease. Decrease levels of the neurotoxic 3-hydroxykynurenine (3-HK). Decrease levels of the reactive oxygen species (ROS) hydrogen peroxide. Attenuation of Human Lysozyme. Amyloid Fibrillation.	[169–171]
Angiotensin Receptor Blockers	Valsartan Candesartan Telmisartan Losartan	AT4Rs (angiotensin IV receptors) are associated with cognitive, cerebrovascular, and neuro-inflammatory rescue. Reduces dense core Aβ plaques but not diffuse plaques or Aβ species. Decrease level of hyperphosphorylated tau protein.	[172–175]
Beta Blockers	Propranolol Carvedilol	Potentiate peripheral inflammation following systemic LPS. Potentiate microglial phagocytosis of synaptosomes.	[176,177]

Figure 5 A coordination of different domains as HTN-team to knowledge the general public about HTN.

Evans AK, Ardestani PM, Yi B, et al. Beta-adrenergic receptor antagonism is proinflammatory and exacerbates neuroinflammation in a mouse model of Alzheimer’s disease. Neurobiol Dis. 2020;146:105089. doi:10.1016/j.nbd.2020.105089

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