Our Research on Neurodegenerative Disease
Basics of neuroscience
The brain is composed of 86 billion neurons whose survival and proper functioning depend on oxygen and glucose provided through blood circulation. When the spines on the dendrites of the neurons receive signals from other neurons, they generate electrical charges. This charge is transmitted to “nerve terminals” where chemical neurotransmitters are released, cross the synapse (the gap between neurons), and bind to the surface of another neuron. The electrical impulse is then transmitted through the axon to the nerve terminal. This is the process through which the brain sends and receives information to other neurons, muscles, or organs. Proper brain functioning largely depends on the strength of a nerve signal and is strictly controlled by the number of synapses and shape of dendritic spines. Changes in these variables are the basis of various cognitive functions of the brain such as learning, memory, emotional control, and executive functions. Accordingly, the ability of the brain or neurons to change the strength of synapses in response to stimuli is termed “synaptic plasticity”.
Effects of Aging
As we age, blood flow to the brain can decrease, and the body’s immune system can prolong or increase inflammatory responses triggered by injury or disease. These changes result in the shrinkage of parts of the brain and decreased neuronal communication, which is important for learning and emotional control among other functions.
Reduction of Synapses
As shown in the figure above, aged neurons have fewer dendritic spines, which also have deformed morphology. These features manifest as diminished synaptic function and plasticity, which result in reduced electrophysiological and brain activities.
Brain Deterioration and Cognitive Dysfunction
“Brain degeneration” describes the symptoms that occur when brain functions decline but does not necessarily describe a particular disease. In the past few years, the term “brain degeneration” has entered widespread usage in Hong Kong, leaving “dementia” or “Alzheimer’s disease” to more specifically refer to patients with a given disease. Meanwhile, the gradual decline in memory and learning, which affects a person’s daily functioning, is termed “cognitive impairment,” which is only one of many manifestations of brain degeneration (others include motor dysfunction).
Diminished Synaptic Functions
According to the latest neuroscience research findings, synaptic plasticity decreases along with impaired synaptic functioning in the early stage of brain degeneration. Brain function is regulated by the strength of the signal transmitted between neurons. The strength of these signals depends on the functional regulation of synapses, and synaptic function is affected by the number and shape of dendritic spines on neurons. “Long-term potentiation” is the electrophysiological response that indicates synaptic plasticity upon stimulation. Accordingly, long-term potentiation is significantly reduced in experimental models of cognitive impairment.
Increase of Amyloid-beta Oligomers
The causes of brain degeneration and reduced synaptic plasticity are not fully understood. Nevertheless, they are known to be related to aging, genetics, and environmental factors. One of the most well-known causative agents of Alzheimer’s disease is soluble amyloid-beta (Aβ) oligomers. Current neuroscience research shows that Aβ oligomers inhibit synaptic plasticity and reduce the electrophysiological response of neurons and thus the long-term potentiation effect, thereby impairing brain activity.
When the amount of Aβ oligomers continues to increase, they tend to aggregate and form plaques in brain tissue. The latest findings indicate that Aβ plaques are already visible in the brain scans of 20–40% of elderly people with normal cognitive abilities. Therefore, by the time a person outwardly shows reduced cognitive and memory abilities, a large quantity of Aβ has already accumulated in the brain and neuronal cells have been damaged. This results in the shrinking of brain tissue. When a person is clinically diagnosed as having Alzheimer’s disease, Aβ accumulation, brain cell damage, and tissue shrinkage have already peaked, and cognitive and memory abilities are significantly affected. This impaired brain function eventually worsens and affects other body functions. Thus, the nature of Alzheimer’s disease leaves a narrow window of opportunity for treatment. Given the delay between the onset of Alzheimer’s disease and the appearance of symptoms, it is important for people to be aware of the importance of early prevention, delaying the occurrence of symptoms, and maintaining physical and mental health. Based on our understanding of Alzheimer’s disease, a method that effectively reshapes synaptic plasticity and enhances functioning could improve cognitive and memory abilities. Cogniherbs® target the root causes of synaptic plasticity impairment. Cogniherbs® have been demonstrated to effectively improve the neurotransmission of synapses in an experimental model of cognitive dysfunction, reverse the effects of brain degeneration factors, and increase brain activity, thereby reducing brain degeneration.
The most common cognitive disorders are related to Alzheimer’s disease, vascular dementia, frontotemporal dementia, Lewy body dementia, and Parkinson’s disease-related dementia.