AVANCE - HELPS TO MAINTAIN MEMORY & BRAIN FUNCTIONS
10 years ago a team of researchers in Germany started to investigate innovative plant actives related to Brain Health and Mood. Evaluating hundreds of plants, one species showed superior benefits and we have developed a natural solution to harness this power in AVANCE.
Cognitive health is the ability to clearly think, learn, and remember. Functions such as motor skills, emotional responses, and sensory responses indicate a resilience to neuropathological damage. Genetic, environmental, and lifestyle factors are all thought to influence cognition and health.
Cognitive impairment is not an illness, but a description of someone's condition. It means they have trouble with things like memory or paying attention.
They might have trouble speaking or understanding. And they might have difficulty recognising people, places or things, and might find new places or situations overwhelming.
Dementia is the loss of cognitive functioning — thinking, remembering, and reasoning — to such an extent that it interferes with a person's daily life and activities. Some people with dementia cannot control their emotions, and their personalities may change.
The biggest risk factor for dementia is ageing. This means as a person gets older, their risk of developing dementia increases a lot. For people aged between 65 and 69, around 2 in every 100 people have dementia. A person's risk then increases as they age, roughly doubling every five years.
Dementia ranges in severity from the mildest stage, when it is just beginning to affect a person's functioning, to the most severe stage, when the person must depend completely on others for basic activities of living. There are several different forms of dementia, including Alzheimer’s disease. A person’s symptoms can vary depending on the type.
Alzheimer’s disease ,or AD, is a brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks. In most people with the disease — those with the late-onset type symptoms first appear in their mid-60s. Early-onset Alzheimer’s occurs between a person’s 30s and mid-60s and is very rare. Alzheimer’s disease is the most common cause of dementia among older adults.
The brain typically shrinks to some degree in healthy aging but, surprisingly, does not lose neurons in large numbers. In Alzheimer’s disease, however, damage is widespread, as many neurons stop functioning, loose connections with other neurons, and die. Alzheimer’s disrupts processes vital to neurons and their networks, including communication, metabolism, and repair. At first, Alzheimer’s disease typically destroys neurons and their connections in parts of the brain involved in memory, including the entorhinal cortex and hippocampus. It later affects areas in the cerebral cortex responsible for language, reasoning, and social behavior. Eventually, many other areas of the brain are damaged. Over time, a person with Alzheimer’s gradually loses his or her ability to live and function independently. Ultimately, the disease is fatal.
Many molecular and cellular changes take place in the brain of a person with Alzheimer’s disease. These changes can be observed in brain tissue under the microscope after death. Investigations are underway to determine which changes may cause Alzheimer’s and which may be a result of the disease.
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The beta-amyloid protein involved in Alzheimer’s comes in several different molecular forms that collect between neurons. It is formed from the breakdown of a larger protein, called amyloid precursor protein. One form, beta-amyloid 42, is thought to be especially toxic. In the Alzheimer’s brain, abnormal levels of this naturally occurring protein clump together to form plaques that collect between neurons and disrupt cell function. Research is ongoing to better understand how, and at what stage of the disease, the various forms of beta-amyloid influence Alzheimer’s.
Neurofibrillary tangles are abnormal accumulations of a protein called tau that collect inside neurons. In Alzheimer’s disease, abnormal chemical changes cause tau to detach from microtubules and stick to other tau molecules, forming threads that eventually join to form tangles inside neurons. These tangles block the neuron’s transport system, which harms the synaptic communication between neurons. Emerging evidence suggests that Alzheimer’s-related brain changes may result from a complex interplay among abnormal tau and beta-amyloid proteins and several other factors.
Research suggests that chronic inflammation may be caused by the buildup of glial cells normally meant to help keep the brain free of debris. One type of glial cell, microglia, engulfs and destroys waste and toxins in a healthy brain. In Alzheimer’s, microglia fail to clear away waste, debris, and protein collections, including beta-amyloid plaques.
People with dementia seldom have only Alzheimer’s-related changes in their brains. Any number of vascular issues—problems that affect blood vessels, such as beta-amyloid deposits in brain arteries, atherosclerosis (hardening of the arteries), and mini-strokes—may also be at play. Vascular problems may lead to reduced blood flow and oxygen to the brain, as well as a breakdown of the blood-brain barrier, which usually protects the brain from harmful agents while allowing in glucose and other necessary factors.
In Alzheimer’s disease, as neurons are injured and die throughout the brain, connections between networks of neurons may break down, and many brain regions begin to shrink. By the final stages of Alzheimer’s, this process—called brain atrophy—is widespread, causing significant loss of brain volume.
In Alzheimer’s disease, as neurons are injured and die throughout the brain, connections between networks of neurons may break down, and many brain regions begin to shrink. By the final stages of Alzheimer’s, this process—called brain atrophy—is widespread, causing significant loss of brain volume.
By inhibiting re-uptake of neurotransmitters, AVANCE positively influences multiple cognitive pathways.
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