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New Study Shows Link between Blood Vessel Disease and Alzheimer’s

Study Suggests Possibility of New Risk Factors for Alzheimer’s disease

Though not definitive, a new study recently published in The Lancet Neurology, offers some hope that we might have another tool in our efforts to prevent or diminish the impact of Alzheimer’s dementia.

The study, conducted at Chicago’s Rush University Medical Center, involved analysis of data from post-mortem examinations of the brain cells of 1,143 individuals. The analysis found a link between blood vessel disease and Alzheimer’s, specifically atherosclerosis and arteriosclerosis. The study’s authors stress that at this point, they can only state that there is a link but not the nature of it. For this, more research is needed. Nevertheless, the findings do open up the possibilities of new prevention strategies.

 Alzheimer's disease

Atherosclerosis is when layers of fat enter the vessels, causing a build-up of plaque. Arteriosclerosis is a thickening of the blood vessels. Both are referred to as cardiovascular disease. We have known that stroke is a causative factor in developing dementia but a possible link between blood vessel disease and Alzheimer’s has not been researched. The Chicago study titled, “Relation of Cerebral Vessel Disease to Alzheimer’s Disease Dementia and Cognitive Function in Elderly People; a Cross-sectional Study,” implies that there is such a link.

Scientists examined the brain autopsy data for indicators of Alzheimer’s and of blood vessel disease in the brain. Of the 1,143 deceased individuals, half were over the age of 88 when they died, 42 percent had Alzheimer’s, 35 percent were stricken with arteriosclerosis and 39 percent with atherosclerosis. The research showed that as blood vessel disease worsened, the risk of Alzheimer’s rose. Scientists also found that patients with atherosclerosis demonstrated more severe cognitive dysfunction, especially in the areas of visuospatial abilities, semantic and episodic memory and speed of perception. The presence of APOE ε4, a gene known to be a risk factor for Alzheimer’s, was not compromised in the study.

Clearly, this is a very good beginning and with more research into how blood vessel disease is contributing to Alzheimer’s, we may have yet another way to identify patients at risk and be able to implement earlier and more effective treatment strategies.


Michael Mullan at The New College Of Florida

Watch Michael Mullan Speaking at The New College Of Florida :

Alzheimer’s Disease Patients May Soon Have Two New Drugs in Their Treatment Plan

Two new drugs, memantine and cholinesterase inhibitors, have recently been approved by the FDA for use in treating Alzheimer’s patients. Both drugs address the problem of cognitive dysfunction which is very significant in Alzheimer’s disease.

Clinical trials

Clinical trials are an approved and safe way to measure the safety and effectiveness of new drugs. Under this carefully monitored regiment, new drugs are introduced to patients and the outcomes can be measured in a controlled environment, noting their impact on the disease and patient. Clinical trials provide the only mechanism for developing new drug protocols and moving them to market, thereby coming closer and closer to disease prevention.

Average approach to Alzheimer’s disease therapy

Each Alzheimer’s patient receives an individualized treatment plan, depending upon the doctor’s recommendations following a careful assessment and measurement of relevant factors, such as:

• An overall health appraisal and collection of the patient’s medical history
• Measurement of the disease’s progression thus far
• Identifying what drug and treatment therapies are tolerable to the patient
• Assessing the patient’s prospects into the future
• The wishes of the patient or of his guardians

Cognitive function is seriously impacted by Alzheimer’s disease

One of the most serious and debilitating outcomes of Alzheimer’s is that the patient loses the ability to access memory and learn new concepts. This is due to brain cell death and the destruction of the synapses, the connectors, between cells which worsens as the disease advances. Medications available today on the market cannot reverse this damage caused to the cells and synapses. The best they can offer is a lessening of the symptoms and slight improvement in mental outlook of the patient.

Neurotransmitters are key to neuron communication

The two new drugs, cholinesterase inhibitors and memantine both act on neurotransmitters. In the brain of an Alzheimer’s patient, neuron communication is hindered by damaged synapses. Cholinesterase inhibitors decelerate the process that is the cause of neurotransmitter damage. Memantine addresses glutamate, which when attached to the cell’s surface creates a condition whereby calcium is able to enter the cell. Alzheimer’s disease results in overproduction of glutamate, leading to higher levels of calcium and cell destruction. Memantine will limit the amount of calcium going into the cells.

How to Avoid Alzheimer’s Disease

The cognitive decline of an Alzheimer’s disease sufferer is heart-rending to family and friends. This disease is debilitating and as yet, has no certain cure. Although there is also no concrete way of predicting how Alzheimer’s will progress, recent studies show that lifestyle changes may play a significant role in deterring the disease. Preventing the onset of the disease requires therapeutic lifestyle modification early in life thereby reducing risk factors associated with the disease?

The Research

Several studies have been made in which it was concluded that lifestyle changes and social enhancement do indeed play a role in the prevention of Alzheimer’s disease. The Finnish Geriatric Study to Prevent Cognitive Impairment and Disability (FINGER) conducted one such study with astounding results. All the participants selected for the study were at risk for developing Alzheimer’s due to factors like age and heart health not being optimal. Participants were given basic healthcare across the board.

Only half of the participants were given a complete lifestyle make-over and a social support system that included cognitive training, control of risk factors and social activities. When the study ended after two years, these participants were in much better health than their peers who did not benefit from an improved lifestyle and social support. These individuals not only made significant improvement in their chances of avoiding Alzheimer’s disease but also drastically enhanced their quality of life – a win-win situation.

How to Start Making Changes

Try to adapt your lifestyle to make as many of the following changes as possible:
• Decide on a daily exercise regime: Consult a physician to ensure that it is suitable to your current health status.
• Eat healthy: In recent years the so-called Mediterranean diet has become associated with optimum health and considerably lower risk of cognitive decline. It consists of fresh ingredients like vegetables, fish and uses olive oil as the main source of fat. Avoid processed foods, excessive sugar, salt and saturated fats.
• If you smoke, stop. Damaging the brain vessels in any way increases inflammation and the risk of Alzheimer’s as well as many other serious health threats.
• Get enough sleep: Sleep is good for learning and memory and lack of it can seriously impact on your mental functions.
• Take supplements, but not to excess: Deficiencies in Folate and Vitamin B12 have been proven to increase the risk of Alzheimer’s. However, nothing has been conclusively proven in studies conducted on the effects of other vitamins, minerals and fatty acids.
• Finally, avoid impact to your head if possible: It is a known fact that Traumatic Brain Injury (TBI) increases the likelihood of Alzheimer’s. Accidents happen but taking precautions like wearing protective headgear when engaging in sports and investing in anti-slip mats around the home is an excellent practice.

While we cannot as yet cure the disease, it is possible to lower the risk with a lifestyle overhaul. Remember the sooner you adopt a healthier lifestyle, the more likely it is to be an effective preventative measure. Programs like Sci-Brain  that is developed to primarily address an objective way to optimize cognitive outcome based on reducing risk factors associated with Alzheimer’s disease based on Research at the Roskamp Institute.

A Fascinating Alzheimer’s Research – Sleep and Glymphatic System / Dr. Michael Mullan

images (4)What does the new study on the role of sleep in the removal of toxic waste from the brain show?

The new study from scientists at the University of Rochester has shown that sleep has a different effect on the removal of potentially toxic waste products from our brain compared to the waking state. In the rest of the body, a system called the lymphatic system removes waste accumulated from most cell types. This system, which consists of an interconnected network of tubes and lymph nodes, allows the passage of toxins in lymph back into the blood circulation. From here, most toxins from metabolic processes are destroyed in the liver or are otherwise disposed of by the body. However, the brain lacks a lymphatic system that is separate from the vasculature. Instead, cerebrospinal fluid passes from the large stores in the brain (ventricles) where it is made and passes around the arteries which provide blood to the whole brain. Much of the waste produced in the brain mixes with this cerebrospinal fluid (CSF) and passes around the outside of veins which leave the brain allowing the waste product to pass out of the brain also. This system has been called the glymphatic system and using new techniques, has now come under intense scrutiny from neuroscientists.

What is the main finding from the new study?

The new study suggests that during sleep, a much larger volume of CSF passes around the arteries and that consequently, there is a greater movement of waste products out of the brain. The researchers saw a very dramatic decrease in the influx of CSF around the arteries and into the brain when a mouse was awoken from a sleep state. Interestingly, researchers saw something similar when mice were anesthetized and therefore, unconscious. Again, there was a much greater influx of CSF around blood vessels and into the brain when the mice were unconscious. Interestingly, in order to explain why there was more CSF in the brain during sleep, the researchers showed that there was more space available to be occupied by CSF in the sleeping state. There seemed to be as much as a 60% increase in the space between brain cells during sleep allowing, the researchers suggest, more CSF to enter the brain during that time.

What is the significance of these findings for Alzheimer’s disease?

Previous studies have shown that the accumulation of the small protein amyloid in the brain is associated with damage to neurons if its accumulation goes unchecked. Previous studies have also shown that amyloid is cleared by the glymphatic system. In other words, neurons in the brain make amyloid but, these are normally taken out of the brain along the veins and harmlessly dealt with outside of the brain. The researchers showed that amyloid is cleared much more efficiently from the brain during sleep which is consistent with their findings of increased glymphatic flow during sleep. Essentially, the same finding was found during anesthesia that amyloid was cleared more rapidly from the brain. The scientists went on to show that certain brain neurotransmitters, particularly adrenaline [or norepinephrine (NE)] was responsible for reducing the amount of space available to CSF influx. They showed that by blocking receptors for adrenaline or NE, they could mimic in waking animals the increased clearance of CSF that was observed in the sleeping state.

What are the broad implications for this research for our understanding of sleep?

The reasons why all higher organisms have a need for sleep has been much debated over the centuries. It is well known that humans or animals deprived of sleep will eventually die. Fatal familial insomnia, an inherited disease caused by mutations in the prion gene leads to delirium, hallucinations, and subsequently death. Sleep may have many functions including the requirement for integration of new information acquired during the waking state. These new findings, however, suggest a more basic need for sleep (as even advanced Alzheimer cases who acquire no new memories still require sleep). The suggestion is that sleep is linked to the ability of the brain to allow additional high levels of CSF to enter and bathe the neurons and other cells in  fluid which can absorb many toxic substances including, importantly, amyloid. Future studies may look at ways to artificially manipulate the system to increase the clearance of amyloid from the brain, thus preventing its accumulation and toxic damage to neurons.

Read more about Alzheimer’s research by Michael Mullan