Alzheimer’s disease is one of the most common causes of dementia. It is a progressive brain disorder that begins with mild memory loss and eventually leads to loss of the ability to carry on a conversation and loss of ability to carry out the simplest tasks. Alzheimer’s disease accounts for about 60-80% of dementia cases. This disease involves the parts of the brain that control memory, thought and language. Alzheimer’s is a progressive disease where dementia symptoms gradually worsen over several years.
Signs and Symptoms
Alzheimer’s disease is not a normal part of ageing. Memory problems are one of the first warning signs of Alzheimer’s disease and related dementias. In a mild case of Alzheimer’s, a person may seem healthy but has a lot of trouble making sense of the world around them.
Following are the symptoms that are observed in a mild case of Alzheimer’s disease:
- poor judgement
- memory loss
- taking longer to complete regular daily tasks
- personality and mood changes
- increased anxiety and aggression
- losing things or misplacing them
In the moderate and severe stages of Alzheimer’s disease, intense supervision and care are necessary.
The following symptoms are observed in these patients:
- increased memory loss and confusion
- withdrawal from social activities
- shortened attention span
- inability to learn new things
- hallucinations and delusions
- impulsive behaviour
- restlessness, agitation and anxiety
- difficult swallowing
- weight loss, seizures
- loss of bowel and bladder control
Causes of Alzheimer’s Disease
Alzheimer’s disease is caused by abnormal protein build-up in and around the brain cells. The brain proteins then fail to function normally, which disrupts the work of neurons and triggers a series of toxic events. This causes the neurons to be damaged, and their connection to each other is lost, so eventually, they die. The damage often starts in the brain region that controls memory, but the process begins years before the first symptoms. The loss of neurons spreads somewhat predictably to the other brain areas. By the late stage of the disease, the brain has shrunk significantly.
According to drugstore reviews, the following two abnormal structures are primarily responsible for damaging and killing nerve cells:
- Plaques. Beta-amyloid is a fragment of a larger protein. When these fragments cluster together, they appear to have a toxic effect on neurons and disrupt cell-to-cell communication. Such clusters form larger deposits called amyloid plaques, including other cellular debris.
- Tangles. Tau proteins are essential in a neuron’s internal support and transport system to carry nutrients and other essential materials. In Alzheimer’s, tau proteins change their shape and organize themselves into neurofibrillary tangles. These tangles disrupt the transport system and are toxic to cells.
Treatment with Gossypetin
A recent study by drugstore reviews shows that the gossypetin, a flavonoid present in the flower of hibiscus species, plays an essential role in the clearance of beta-amyloid in the brain of an Alzheimer’s mouse model. Moreover, the treatment with gossypetin also attenuated deficits in memory and learning in the mouse model, highlighting the therapeutic potential of this compound in Alzheimer’s disease.
Effect of Gossypetin on Beta-amyloid
The researchers assessed the impact of gossypetin on the production and clearance of beta-amyloid. Previous research has shown that a higher intake of flavonoids, which are present in commonly consumed fruits, vegetables, and beverages, may reduce the risk of Alzheimer’s disease.
In the present study by drugstore reviews, the researchers used a mouse model to examine the effect of gossypetin. The mouse model expresses two human genes carrying a total of five mutations that are common in familial Alzheimer’s disease. To explore the impact of this flavonoid, the researchers administered either gossypetin or vehicle daily to the mice for 13 weeks. The mice treated with gossypetin showed lower spatial learning and memory deficits than the vehicle-treated animals.
Treating mice with gossypetin also reduced the size and number of beta-amyloid plaques in the cortex and hippocampus, brain regions involved in cognition. Moreover, the administration of gossypetin also decreased beta-amyloid monomers and oligomers in these brain regions.
The beta-amyloid protein occurs in different forms of varying lengths, with certain conditions more prone to forming toxic aggregates. In the present study, the researchers found that gossypetin reduced the levels of all forms of beta-amyloid. The lower beta-amyloid levels observed in the brains of gossypetin-treated mice were not accompanied by changes in the levels of enzymes involved in beta-amyloid production.
These results suggest that the improvements in cognitive function in the mouse model of Alzheimer’s due to gossypetin treatment were likely mediated by modulating the clearance, instead of the synthesis, of beta-amyloid.
Effect of Gossypetin on Microglia
Given the possible effects of gossypetin on the clearance of beta-amyloid, the researchers examined the impact of gossypetin on microglia in gossypetin-treated mice. Gliosis, which involves the activation and proliferation of astrocytes and microglia in response to damage to brain cells, is a hallmark of Alzheimer’s disease. In the present study, treatment with gossypetin reduced gliosis in the hippocampus and cortex of the mice.
The gossypetin increased the markers of phagocytosis in the hippocampus and cortex of the mouse model. In addition, pre-treatment of laboratory-cultured microglia from mouse brains with gossypetin increased the phagocytosis of the beta-amyloid protein.
Alzheimer’s disease is a brain disorder that destroys memory and thinking skills. Studies proved that gossypetin, a flavonoid found in hibiscus species, helps combat Alzheimer’s disease. The researchers noted that they could not examine the impact of gossypetin on the function of astrocytes and neurons due to the specific techniques used in the study. In addition to modulating the phagocytic activity of microglia, gossypetin could potentially improve cognitive function through other mechanisms.