Carvedilol is a medication that has been tested for the treatment of memory decline in patients with mild Alzheimer’s disease (AD). It is currently prescribed for the treatment of high blood pressure and heart failure but showed promise as a therapy for AD. It is marketed under the brand name Coreg.

How carvedilol works

Carvedilol is classed as a nonselective “beta blocker”. It works by blocking the receptors on the outside of cells that are essential for cell communication, stopping chemical messengers (neurotransmitters) such as norepinephrine from reaching them.

In patients with high blood pressure and heart failure, it acts to widen blood vessels and improve blood flow. Hypertension can cause nerve cell death and leads to a decline in cognitive ability. Carvedilol could act to ensure a continuous flow of blood through the brain, protecting the brain cells.

Experiments in mouse models suggest that it interferes with the build-up of amyloid-beta fragments in the brain. This is one of the hallmarks of AD and is associated with continuing brain cell death and worsening of symptoms.

Carvedilol in clinical trials

Carvedilol has been previously studied in clinical trials as a therapy for high blood pressure and heart failure. The common side effects of carvedilol therapy are dizziness, fatigue, headache, nausea, and slowness of movement. Carvedilol has been tested as a therapy for AD in one clinical trial so far.

A Phase 4 study (NCT01354444), assessing whether carvedilol has a beneficial effect on an AD patient’s episodic memory (memory regarding personal facts and experiences) compared to a placebo group was completed in 2017. The study aimed to assess whether there was an improvement in memory and whether the 25 mg oral dose was safe and well tolerated in the patients, over the course of six months. The memory of the patients was tested using Hopkins Verbal Learning Test (HVLT), prior to the start of treatment (baseline), and after three and six months of treatment. The trial also measured if carvedilol affected the level of amyloid-beta by taking a cerebrospinal fluid (CSF) sample at the beginning and at the end of the study period (after six months).

Results of the study have been reported. The study recruited 14 patients to the treatment group and 15 to the placebo group. Statistical analysis of the data failed to show a significant difference between the changes in the HVLT scores or changes in CSF levels of amyloid-beta between the treatment group and placebo group, however.


Last updated: Aug. 21, 2019


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