Researchers find ACE inhibitors can stop memory loss in lupus patients

Researchers at the in claim that – a class of drugs that are widely used in hypertension treatment can be beneficial for patients by preventing in them.

According to the data published by the researchers in the Journal of Experimental Medicine, the ACE Inhibitors could prevent cognitive decline in mice.

A complex autoimmune disease, Lupus develops when the body generates antibodies that target its own healthy cells by specifically identifying DNA. Lupus is characterized by cognitive impairments like memory loss or confusion.

The scientists in their research found that brain cells like Microglia when activated, contribute to memory loss and other cognitive abnormalities in many lupus patients. ACE inhibitors have been known to prevent microglia activation.

Feinstein Institute researchers discovered that an ACE inhibitor called captopril shielded neurons from activated microglia and thereby prevented cognitive impairments in mice.

Betty Diamond and her team at The Feinstein Institute for Medical Research claim that ACE inhibitors used in hypertension drugs can stop memory loss in lupus patients
and her team at The Feinstein Institute for Medical Research claim that ACE inhibitors used in hypertension drugs can stop memory loss in lupus patients. Photo courtesy of PRNewsfoto/The Feinstein Institute for Medical Research.

Betty Diamond – professor and head of the Center for Autoimmune, Musculoskeletal and Hematopoietic Diseases at the Feinstein Institute, commenting on the potential role of ACE inhibitors, said: “Our study suggests that ACE inhibitors are a promising class of therapeutics that can easily move into clinical trials aimed at mitigating the cognitive dysfunction associated with neuropsychiatric lupus”.

Lupus patients with memory loss produce DNRAbs which recognize DNA and NMDAR, a NMDA receptor which is a critical brain protein.

Antibodies mostly do not enter the brain but following an infection or injury, DNRAbs are believed to get temporary access to the brain and they target neurons expressing NMDAR. Then the neurons die or lose synapses to connect with other neighboring nerve cells, resulting in memory loss or cognitive impairment, said Feinstein Institute for Medical Research.

The researchers suspected that microglia may be responsible for cutting connections between neurons after they are exposed to DNRAbs. Due to this, Betty Diamond and her team experimented on mice that produce DNRAbs which can enter into the brain and induce memory loss.

The researchers found that microglia gets activated when DNRAbs penetrate the brain and that a protein called C1q attracts the particular brain cells to the synapses of neurons targeted by the antibodies. The action of removing the C1q protein or depletion of the microglial cells themselves prevents neurons from losing their synapses upon being exposed to DNRA.

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