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Brain & Heart Dementia and the heart

with a greater risk of developing dementia; however, A potential link between the brain and heart in dementia
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the extent to which this risk is influenced by comorbid may be hypothesized and is potentially related to cerebral
conditions, such as stroke, CAD, and microvascular hypoperfusion. The brain receives about 15% of cardiac
cerebrovascular disease, remains unclear. In a case study output and consumes approximately 20% of the body’s
involving 103,859 patients aged ≥65 years who underwent total oxygen supply, making it particularly vulnerable
coronary angiography, participants were stratified based to reduced perfusion, an issue frequently observed in
on the presence or absence of DM and CAD. The study patients with heart failure. This hypoperfusion in the
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investigated the incidence of all-cause dementia, vascular brain may contribute to the formation of tau-containing
dementia, and Alzheimer’s disease. Of the total population, neurofibrillary tangles and amyloid-beta plaques, both
23,189 (22%) had neither type 2 DM nor CAD, 3,876 (4%) hallmark features of dementia. However, direct evidence
suffered from DM only, 61,020 (59%) suffered from CAD supporting this hypothesis in human studies remains
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only, and 15,774 (15%) had both DM and CAD. After a limited. Cerebral hypoperfusion may disrupt neuronal
median follow-up period of 6.3 years, 5,592 (5.5%) patients energy metabolism, leading to oxidative stress and acidosis.
were diagnosed with all-cause dementia. Patients with DM These metabolic disturbances activate lysosomal enzymes,
and CAD had the highest hazard ratios (HRs) of all-cause which can promote the hyperphosphorylation of amyloid-
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dementia (HR: 1.37, 95% CI: 1.24 – 1.51). This group also beta and tau proteins. Hyperphosphorylated tau proteins
exhibited elevated risks for Alzheimer’s disease (HR: 1.41, aggregate to form neurofibrillary tangles. In addition,
95% CI: 1.23 – 1.62) and vascular dementia (HR: 2.03, altered neuronal metabolism may upregulate beta-
95% CI: 1.69 – 2.45). Interestingly, patients suffering from secretase 1, a protease that facilitates the cleavage of the
DM alone (aHR: 1.14, 95% CI: 0.97 – 1.33) or CAD alone amyloid precursor protein, resulting in the accumulation
(aHR: 1.11, 95% CI: 1.03 – 1.20) also showed a modest of amyloid-beta and the development of amyloid plaques.
but statistically significant increase in all-cause dementia Furthermore, hypoperfusion-induced breakdown of
risk. These findings highlight that the combination of the blood-brain barrier may impair the clearance of
DM and CAD is particularly detrimental and suggest the amyloid-beta, further promoting its deposition and the
importance of CVD prevention in patients with DM to progression of amyloid plaque formation.
reduce the risk of cognitive decline. In patients with Alzheimer’s disease, both the heart
Cardiac enlargement may place patients with and brain may be loaded with amyloid deposits and/or
Alzheimer’s disease at greater risk of developing stroke, angiopathy due to atherosclerosis. This coexisting pathology
and CAD. 20-22 Dementia appears to affect not only the brain predisposes individuals to vascular, cardiac, and cerebral
but also other body systems, including the cardiovascular injury. Amyloid-beta deposition can extend beyond the
system, particularly in patients with comorbidities. 23-26 central nervous system, accumulating in distal organs and
Recent research has emphasized the role of amyloid-beta vessels, such as the kidneys, skin, skeletal muscle, lungs,
proteins in the pathogenesis of Alzheimer’s disease. These and gastrointestinal tract, through the bloodstream. Such
proteins accumulate in the extracellular spaces between systemic deposition may contribute to other amyloid-
brain cells, such as neurons, astrocytes, and microglia, related conditions, including CAD. Amyloid-beta deposits
forming plaques that are thought to contribute to memory in the heart and brain may manifest as idiopathic dilated
dysfunction. Notably, the same protein plaques may also cardiomyopathy. In addition, genetic factors may play
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accumulate in the heart, suggesting a systemic impact. a crucial role in this process, with certain gene variants
The extracellular space is a narrow, fluid-filled space being associated with early-onset dementia, whether
surrounding every cell in the brain, composed of a fluid in familial or sporadic cases. Furthermore, a decline in
similar to cerebrospinal fluid along with extracellular myocardial function during diastole is recognized as a
matrix molecules. In a case study involving 22 patients common physiological event in cardiac aging. However,
with Alzheimer’s disease and 35 patients without dementia in patients with dementia, there may be an accelerated or
aged 78 – 79 years, researchers analyzed stiffness in the more severe decline in diastolic function at a younger age.
left ventricle, which is responsible for pumping blood This dysfunction may be partly attributed to amyloid-beta
throughout the body. Findings indicated that some accumulation in the heart.
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patients with Alzheimer’s disease exhibited an enlarged The findings from the aforementioned studies may be
left ventricle compared to those without the disease. It is crucial in improving care for patients with Alzheimer’s
possible that this thickening of the heart muscle was related disease, as amyloid-beta deposits have been found to
to the same mechanism of amyloid plaque accumulation develop in the myocardium. This knowledge is important
observed in the brains of these patients. for families and healthcare providers, who should be vigilant

Volume 3 Issue 3 (2025) 6 doi: 10.36922/bh.8426