A recent scientific statement from the American Heart Association (AHA) underscores a significant connection between cardiovascular diseases—such as heart failure, atrial fibrillation (AFib), and coronary heart disease—and a heightened risk of cognitive decline and dementia. This research highlights how heart health plays a crucial role in brain function, indicating that conditions like hypertension and type 2 diabetes can contribute to cognitive deterioration.
In another study, researchers have proposed that the anticoagulant heparin might delay the onset of Alzheimer’s disease by disrupting harmful protein interactions within the brain, although further investigation is necessary. An expert report published in the journal Stroke reviews the latest findings and asserts that three prevalent cardiovascular conditions in adults—heart failure, AFib, and coronary heart disease—are associated with cognitive impairment and an elevated risk of dementia.
The authors emphasize that stroke and cognitive decline, both significant aspects of brain health, are chronic and debilitating conditions that profoundly affect individuals and society at large. It is imperative to maintain heart health from an early age to mitigate the risk of cardiovascular diseases, safeguard brain function, and reduce the likelihood of cognitive decline in later years.
While dementia is often regarded as an incurable and progressive condition, research suggests that adopting a healthy lifestyle and proactively managing vascular risk factors may help preserve cognitive abilities.
Heart Issues and Cognitive Decline
Research cited in the AHA report indicates that approximately 50% of individuals with cognitive challenges, such as difficulties in memory and language, also suffer from heart failure. AFib, the most prevalent heart rhythm disorder, is linked to a 39% increased likelihood of cognitive impairment, while coronary heart disease raises the dementia risk by 27%. Notably, up to 50% of individuals who survive heart attacks experience some form of cognitive decline.
Previous studies have revealed that patients with AFib treated with direct oral anticoagulants (DOACs) faced a 12% lower risk of developing dementia compared to those receiving traditional blood thinners like warfarin.
Investigating Heparin’s Role in Alzheimer’s Risk
A new study published in Molecular Psychiatry has examined the effects of heparin treatment on the onset of Alzheimer’s symptoms, discovering that patients receiving this anticoagulant experienced symptom onset up to two years later than average. This suggests a potential protective advantage of heparin, a common blood thinner.
Earlier research has indicated that the risk of developing Alzheimer’s may be associated with the Apolipoprotein E (ApoE) protein, which interacts with heparan sulfate proteoglycans (HSPGs). The ApoE4 variant poses the greatest risk, whereas a rare variant known as ApoE Christchurch appears to lower the Alzheimer’s risk in genetically susceptible individuals. Furthermore, HSPGs contribute to the accumulation of tau protein, another critical element in the brain damage seen in Alzheimer’s disease.
Proteins that attach to HSPGs may build up in the brain well before symptoms emerge, and a gene involved in heparan sulfate production has been identified as a risk factor for Alzheimer’s.
Heparin, a type of heparan sulfate that has been utilized since the 1930s to prevent blood clots, does not penetrate the brain. However, researchers theorize that it might delay Alzheimer’s onset by interrupting the interactions between ApoE and HSPG.
The Connection Between Heparin and Alzheimer’s Delay
In this study, researchers analyzed medical records from two major health systems: the Mount Sinai Health System (MSHS) and Columbia University Medical Center (CUMC). They employed a retrospective, longitudinal approach to compare patients who had received heparin with those who had not.
Within the MSHS cohort, 24.7% of the 15,183 patients had undergone heparin treatment, while 51.5% of the 6,207 patients at CUMC received heparin. All participants eventually received an Alzheimer’s diagnosis, but those treated with heparin were diagnosed approximately one year later than those who did not receive the treatment.
Dr. Benjamin Readhead, a research associate professor at the ASU-Banner Neurodegenerative Disease Research Center and the study’s first author, shared key findings with Medical News Today. “Some of our co-authors previously identified a rare genetic mutation in the APOE gene that offers considerable protection against Alzheimer’s disease, linked to how this variant interacts with heparin-like molecules in the body,” Readhead explained. “Our investigation into heparin indicated that its use was associated with a significant delay of around one year in the clinical diagnosis of Alzheimer’s disease dementia across both health systems.”
Implications for Future Alzheimer’s Research
Dr. Eric M. Reiman, the study’s senior author, noted that while the findings do not suggest current heparin formulations should be used for treating or preventing Alzheimer’s, they could inform the development of new therapies for the disease, especially for individuals carrying the APOE4 gene, a major genetic risk factor. Reiman highlighted that the study focused on a specific demographic with an elevated genetic risk for Alzheimer’s.
The observation that a rare form of APOE might confer some protection against Alzheimer’s symptoms led researchers to hypothesize that blocking ApoE’s interaction with HSPG could facilitate the development of preventive treatments for Alzheimer’s.
Dr. Clifford Segil, a neurologist at Providence Saint John’s Health Center in Santa Monica, CA, who was not involved in the study, cautioned that while it is difficult to assert that a blood-thinning medication like heparin could influence Alzheimer’s disease progression, it may help prevent certain types of dementia stemming from recurrent strokes, such as multi-infarct dementia or vascular dementia. He expressed a desire for follow-up studies to investigate whether heparin use in hospital settings could reduce the risk of stroke-related dementias.
Reiman emphasized that the study illustrates the potential of using large electronic health record datasets to evaluate the effects of various drugs on Alzheimer’s disease treatment and prevention. “This information could support further exploration of repurposed medications for Alzheimer’s disease or, as demonstrated in this case, provide insights into the biological processes that could be targeted in developing new therapeutic options.”
The researchers also explored the possibility of heparin providing broader protection for brain health. However, given that most heparin formulations do not easily penetrate the brain and are typically administered over short periods, the effectiveness of heparin as a neuroprotective agent remains uncertain.
As more research is conducted, the insights gained from large-scale patient data analyses may pave the way for new drugs targeting these mechanisms, potentially leading to experimental treatments in the future.
