If you were to ask a high school freshman what a concussion is, do you think they would be able to tell you? All I would’ve been able to tell you when I was a high school freshman is that a concussion is when you hit your head really hard. I had no idea really what the consequences of a concussion were and obviously I had a really naïve sense of what it actually is. Luckily that understanding has left me. But I ask….do you think other high school freshmen are different than I was? Sophomores? Juniors? Seniors? What about beyond that? Well hopefully this article can help shed light on what a concussion is and how it can affect your brain after the fact.
A concussion is a traumatic brain injury (TBI) that is characterized by an injury to the head or the body that causes the brain to shake inside of the skull. (Freshman me was partially correct.) If the concussion is severe enough it can cause you to lose consciousness but generally symptoms of a concussion include confusion, slurred speech, sensitivity to light and noise, sluggishness etc. The causes for a concussion are the injuries that result from physical activity such as sports. The most common and famous sport when talking about concussions is football and many of us are aware of the controversy that surrounds it. But why would this be controversial? Well the repeated amount of concussions from football, boxing whatever the activity may be can cause Chronic traumatic encephalopathy (CTE) which is basically a neurodegenerative disorder that is a continuation from repeated concussions that can permanently cause brain damage and worsen the symptoms and premature death. There are an estimated 2-4 million concussions per year in the United States. An article in the Neurosurgery journal discusses the biochemical processes resulting from a traumatic brain injury. It all starts with a high influx of ions into the area affected. This results in overactive cellular responses that kick energy metabolism into overdrive. This can cause damage to the cytoskeleton of the cell and affect the axons that are responsible moving information between cells and within cells. This than can have altered neurotransmission where information is processed more slowly or at an abnormal rate due to the altered neurotransmission. Microglia and supporting neurons will be caused to be overactive and they will release cytokines and trophins that will increase brain inflammation. After all of these sequential events occur the cell or cells will die resulting in neurodegeneration. It is no secret that having repetitive traumatic brain injuries could cause severe brain damage.
This information I believe would be very beneficial to know for people who are involved with sports activities. Parents and players often do not understand the severity of concussions, which makes life difficult for care providers. People need to realize that these symptoms will go away eventually but proper treatment is vital because the risk of severe damage increases during the recovery period of an already in place concussion. This means time for rest and no stimulating activity including intense cognitive thought, which is conducive with schoolwork. Many different factors come into when dealing with a concussion. Teachers, parents, coaches, players etc. all need to come to a realization and a general consensus that concussions are not a topic to throw under the table. Sports and physical activity will not just go away, which means concussions, will not either. However a deeper understanding of what concussions are and how we can treat them
Is Alzheimer’s Disease (AD) Type III Diabetes?
Alzheimer’s disease (AD) is a disease associated with the destruction of brain cells resulting in the decline of cognitive functioning, memory, and social skills. The most common cause of AD is aging. There are approximately 36 million people worldwide who suffer from Alzheimer’s. Since AD is common and not entirely understood, it is important to better understand the processes regulating AD progression in order to develop more targeted treatments and interventions that can delay or prevent the disease.
Something I didn’t realize about Alzheimer’s disease (AD), until we talked about it in our Neurochemistry capstone class this week is that insulin has a compelling role in the progression of the disease. Obviously AD is multifactorial, since things like hyperphosphorylated tau and AB plaques are other problematic contributors to the disease. But interestingly, several studies have shown that overactivation of the P13-k/Akt/ mTOR signaling pathway is an early feature of AD.
Insulin is one of the key activators of this P13-k/Akt/ mTOR signaling pathway. While signaling through this pathway, it is crucial for the cell to maintain the proper activity level. Proper signaling through the P13-k/Akt/ mTOR signaling pathway allows for the beneficial processes resulting in DNA repair, cellular repair, translation of anti-stress proteins, and overall maintenance of healthy cell systems within the neurons of the brain.
Evidence is suggesting that insulin resistance is problematic occurrence within the neurons of people with AD. Insulin resistance does not allow the proper regulation of the P13-k/Akt/ mTOR signaling pathway because of sustained activation. This is a problem because insulin resistance in AD neurons has been associated with decreases in episodic and working memory, resulting in the symptoms of AD.
So how does this relate to diabetes? Well Type I Diabetes (T1D) is associated with hyperglycemia because the beta cells of the pancreas that produce insulin are destroyed by the person’s own body, resulting in decreased insulin action. Type II Diabetes (T2D) is associated with insulin resistance in peripheral tissues due to low insulin receptor expression and activity. Like T2D, AD can be associated with insulin resistance, but in this case confined to the neurons of the brain. In this way, AD could be considered Type III Diabetes. With this in mind, future research should consider treatments for AD that can minimize the impacts of insulin resistance in the brain.
Maternal Autoimmunity and Its Implications in Autism
Autism spectrum disorder (ASD) is a neurodevelopmental disorder that is known to impair a child’s communication, social behavior, and contribute to the characteristic repetitive behaviors. Like many neurological impairments, ASD has many possible contributing factors to the disorder. In our studies this week during our Neurochemistry course, the paper we discussed outlined prenatal viral infections, zinc deficiency, abnormal melatonin synthesis, maternal diabetes, prenatal stress, toxins, and parental age as possible environmental factors that influence the development of autism.
The risk factor that I found particularly interesting to the story is maternal autoimmunity. This also relates to the age of the mother in children with autism because the majority of autoimmune disorders arise when someone is 30 years of age or older. Autoimmunity is an immune response of the body that attacks and destroys the body itself. A couple of examples of autoimmune disorders are type I diabetes mellitus, myasthenia gravis, and lupus. (Not all types of maternal autoimmunity will result in the development of ASD)
Why an autoimmune disorder is problematic for fetal neural development is that even maternal autoantibodies are able to cross the placental barrier. The placenta normally provides a selective barrier that allows immune factors and molecules for nutrition to transfer to the developing fetus, while restricting the passage of other potentially harmful molecules like pathogens. While it is a positive that the placenta allows the mother to give some passive immunity to the fetus during development, this same process is a negative for the baby when their mothers exhibit autoimmunity. A normal maternal IgG will provide the baby with protective immunity from the mother’s environmental exposures until it is able to have an immune response on its own. Unfortunately, auto reactive IgGs from the mother will also be cross the placental barrier, recognizing self-proteins and possibly interfere with fetal development.
Another interesting fact about fetal development is that the blood brain barrier of the fetus is not fully developed for the majority of gestation. For mothers, their own blood brain barrier is important because it normally restricts auto reactive IgG from the CNS. Since fetal protein reactive IgGs are able to cross the placental barrier during gestation, these IgGs may have access to the developing brain of the fetus that does not have the fully developed blood brain barrier to protect itself. It is therefore possible that fetal protein reactive IgGs of the mother that have access to the fetal brain could interfere with CNS development of the baby and result in neurodevelopmental disorders like autism. Several studies have reported that fetal brain reactive antibodies are more commonly found in the circulation of mothers of children with certain subsets of ASD.
Better understanding of autoimmune disorders and especially fetal brain reactive antibodies will be important for considering the mechanisms that fetal exposure to maternal autoantibodies have in the development of ASD.
Treatments for the Cause or the Symptom?
Parkinson’s disease….. A very tough disease to deal with. It seems the more you know about this disease the less you do actually know. Upon learning about PD I found myself asking more questions than I had to start. Lets see what you think…..
Parkinson’s Disease is a progressive disorder that affects the movement of person suffering with the disease. Around 1 million people in the United states suffer from Parkinson’s Disease and each year, around 60,000 new cases are diagnosed. The disease is characterized as a loss of dopamine neurotransmission in the human brain. This results in all of the symptoms characterized with PD such as, tremors, slowed movement, rigid muscles, impaired posture and balance, speech difficulties etc. These symptoms come at the cost of decreased dopamine neurotransmission that fuels the neurons and connections in your brain.
The current treatments for Parkinson’s disease are mainly to treat the symptoms of the disease. L-Dopa or levodopa is an amino acid that is a precursor to neurotransmitters dopamine, norepinephrine and epinephrine. It is able to cross the blood brain barrier and subsequently be converted into dopamine. Early studies showed that L-DOPA can cause sever side effects such as nausea and vomiting. These side effects were occurring because the L-DOPA was being converted into dopamine before it was crossing the blood brain barrier. So researchers added inhibitors of dopa-decarboxylase, which is the enzyme responsible for converted levodopa into dopamine; these inhibitors are called carbidopa and benserazide. L-DOPA medication provides relief to the tremors and shakiness symptoms of Parkinson’s disease. However, long-term use of the drug is shown to induce dyskinesia for 80% of patients that use levodopa. Dyskinesia is a disorder characterized by involuntary muscle movement. As patients progress with the treatment of levodopa the drug effects begin to wear off several hours of some or all doses of the medication. The reasons these motor fluctuations occur is unclear but is thought to be because of uneven changes in the basal ganglia circuitry resulting in the depletion of both dopamine and the drug treatment. Treatment of levodopa-induced dyskinesia is difficult but treatments used for the disease or dopamine agonists and neurosurgery. The main problems with both Parkinson’s disease and LID are the depletion of dopamine or the lack of dopamine circulating throughout the brain.
So what is the cause for this lack of dopamine Neurotransmission? Why do people get Parkinson’s Disease? Several factors point to genes. Specifically the SNCA gene which encodes for a-synuclein protein. A review article in the frontiers in molecular neuroscience journal discusses this very protein and why it is highly involved in Parkinson’s disease. In a general sense, a-synuclein is being turned on in a specific area on the protein called Serine 129 (S129) which is called hyperphosphorylation. This attributes to the formation of Lewy bodies which consequently, cause the cell to die and thus no dopamine present.
The article also goes into detail of different proteins that are related to the mechanism for the hyperphosphorylation of a-synuclein, such as polo-like kinase, casein kinases, and G protein coupled receptor kinase. However, more research needs to go into this mechanism in order to establish more of an understanding of this phenomenon. In addition to the hyperphosphorylation of a-synuclein, other factors such as the dysredulation of kinase proteins are attributed in the pathogenesis of PD. These kinases include proteins called LRRK2 and PINK1. Like the hyperphsophorylation of a-synuclein these are due to genetic factors and more research needs to be done.
Like I said, this disease is very complicated to understand. It seems like the more you know the less. Hoever, I reall think that this disease needs to be researched more and I believe eventually we can come up with an effective way to treat the causality of the disease not just the symptoms.
Removing Addiction From the Shadows
The American Society of Addiction Medicine describes addiction as a chronic disease of brain reward and motivation systems. Affected individuals do not have the ability to abstain, control, and recognize problems with one’s behavior.
Risk Factors
Environmental factors influence and individuals genetic risk factors which alone account for roughly half of the probability that someone will become addicted during their life time. This combination effect determines how likely addiction is to manifest in any individual. Although, studies have shown that life experiences such as education from parents can infact minimize risk. Other factors can increase risk such as experiencing a trauma, depression, and damaged social connections.
Current Research
Addictive drugs alter transmission within the brain. These drugs of abuse impact the complex signaling pathways involved with reward learning. Specifically, complex dopamine and glutamate signaling pathways are altered by changes to secondary signaling molecules such Calcium and cAMP.
Protein kinase ability is also decrease which are crucial for the phosphorylation and de-phosphorylation mechanisms necessary for proper synaptic plasticity. These drugs also dysregulate complex dopamine and glutamate signaling networks further affecting synaptic plasticity and function. All of which contributes to the progression of a healthy brain to an addicted state.
Harmful Attitudes Towards Addiction
This disease commonly carries negative stereotypes, misconceptions, and harsh judgement that create barriers to public awareness and treatment for affected individuals. Common beliefs persist in our society such that affected individuals lack the desire, willpower, and morals to simply choose to quit.
Addiction is a very complex disease that can happen before an individual realizes what is going on and often necessitates more than just pure will power to overcome. Recently, I even stumbled across a social media article with a direct message to individuals struggling with addiction to stop calling it a disease and labeling it as a ‘pity identity’.
One of the main stereotypes surrounding addiction is that it is a choice. In some cases, in a very basic sense may be true for some cases.
However, humans make mistakes and I do not believe that anyone experiments with a drug to intentionally become addicted. In many cases, it is a unintentional byproduct of medical care, and other environmental factors.
Medical issues such as chronic pain can lead to substance abuse problems. Opioid addiction often begins by taking pain medications given in a medical setting to manage a condition. People assume that medications received from a medical setting are safer to use than an illicit drug. However, individual biological risk factors can lead some individuals down the addiction pathway from something as simple managing back pain. One study found that up 80% of heroin addicts report their first opioid use was in the form of a prescription drug. It is a situational risk that everyone needs to be aware of to make informed decisions regarding their health.
It is a simple fact that certain individuals are just more susceptible than others for developing an addiction. Eluding the mechanisms driving addiction and underlying risk factors are essential for removing stigma, and providing better treatment and prevention.
Type III Diabetes: Alzheimer’s Disease
Many may wonder the rationale behind this title, and indeed it seems a strange connection to make. But the truth of Alzheimer’s disease lies in insulin receptors, and eventually insulin resistance. These receptors are, of course, localized to the brain, and not the pancreas (as in the case of diabetes as we know it). To understand the idea of Alzheimer’s as an insulin disorder, we must initially observe and understand the properties of the receptor on a cell.
Insulin is, at its very simplest, a growth factor. This means, in short, that it promotes cell longevity and proliferation. Growth factors could lead to a plethora of anti-aging medicines. And just so, we can also realize that an enormous risk factor for Alzheimer’s disease is aging. Certainly, if aging is happening, insulin reception is not (or at least not as well as it normally does). This is the first connection of Alzheimer’s with insulin resistance.
But if that were the only connection, it would likely be coincidence. We must delve deeper into the causes of Alzheimer’s, or at least the causes doctors have identified thus far. The beta-amyloid plaque has been used as the sure-sign of Alzheimer’s for decades. This is an aggregation of protein that essentially clogs up neurons and eventually causes their degeneration. But what could these beta-amyloids have to do with insulin resistance? The answer lies in competition.
Many body receptors have a certain ligand/molecule they like to bind to, but nothing is perfect, and other molecules can also bind instead. It has been proposed that beta-amyloid plaques can bind to insulin receptors on neurons and essentially cause them to not recognize when insulin is actually present. This leads to the opposite effect of the insulin “growth factor” and instead causes the cell to degenerate. Even further, since the cell is recognizing that many of these receptors are full of binding molecules, it “decouples” the receptors from the membrane, making insulin signaling even more difficult.
In reverse, studies have indicated that low levels of insulin reception cause levels of beta-amyloid plaques to increase, exacerbating the problem. There is still no consensus on whether low insulin reception initially creates high levels of beta-amyloid, and this feedback causes lower levels of insulin reception, or whether high levels of beta-amyloid begin the process. Either way, this emphasizes the “insulin resistance” that is so common with diabetes.
All of this culminates in the treatment for Alzheimer’s. A newly-prescribed medicine is intranasal insulin spray. By introducing the molecule to the nasal membranes, it quickly makes its way into the brain, increasing insulin levels. These increased levels might be able to “push” the beta-amyloid plaques out of the insulin receptors and allow normal binding and signaling to occur. Whether this is actually the case is unknown, but the medicine shows promising results.
Is this just one more reason to eat a healthy diet and exercise frequently? Perhaps. But in the end, the choice is our own. We must simply realize that our actions today have an effect on us for the rest of our lives.
Drug Addiction: The Scope of the Problem and It’s Effects on the Brain
In the United States there has been much discussion about drug use over the past several decades. Of course this all started with the War on Drugs which was first mentioned by President Richard Nixon in 1971. However, the United States has been combating drugs since the Harrison Narcotics Act of 1914. This ultimately led up to the formation of the Bureau of Narcotics in 1930. Since then there has been many new drug laws being put on the books. Ultimately the drug scare arose in the Comprehensive Drug Abuse Prevention and Control Act of 1970. This led to the first mandatory minimums and some people would argue to the rapid rise of incarceration in the United States. That is a topic for another post.
In the modern day and age it is estimated in 2013 that approximately 24.6 million Americans (9.4% of the population) had used drugs in the past month, according to the National Institute on Drug Abuse. This was an increase from the 8.3% of the population in 2002. However, one important thing to note is that the National Institute on Drug Abuse estimates that the number of people that are dependent on drugs is decreasing. Even if this is the case it is still important to understand what is occurring in the brain and how someone can get help if they need it.
First it is probably best to explain what occurs in the normal brain. In the normal brain there are dopamine receptors and glutamate receptors located on medium spiny neurons. Medium spiny neurons are GABAergic inhibitory neurons that comprise about 95% of all neurons in the striatum/basal ganglia. The receptors discussed above bind dopamine and glutamate, respectively. These molecules when released bind to their respective receptor and cause downstream signaling that can lead to memory formation, motivated behavior, reward learning consolidation, and synaptic remodeling. It is important to remember that this is a natural process and occurs every day.
Now when drugs of abuse enter the body they alter dopamine and glutamate neurotransmission. The primary receptor targeted is the dopamine receptor because of its primary role in the reward system and their interaction with glutamate receptors to signal reward learning. Underlying regulatory mechanisms of these receptors become altered and ultimately lead to functional and structural neuroplasticity. Basically, what I am saying is that drugs can alter the behavior and function of the receptors to promote the addictive state. This ultimately can lead to hyper-synaptic remodeling, overwhelming reward learning, and uncontrollable drug-seeking and drug-taking. This leads to a never ending cycle that can cause an addict to have uncontrollable urges to obtain and take drugs. Inevitably this may lead to such a reliance on the drug that the addict may ultimately die to the body’s dependence on it. One important thing to note is that since the drug causes structural and functional alterations to the brain, withdrawals can be severe and going “cold turkey” may actually do more harm than good.
If you know anyone that is addicted please reach out to help them to prevent these scenarios. Get them help and be there for them as support to make it through the process.
Understanding the Causes for Autism
Autism spectrum Disorder (ASD) is a mental health disorder that is characterized with the difficulty with social skills, repetitive behaviors, and most forms of communication and uniqueness of strengths. Autism is a disease that has many different forms that are in a range of severity, which is why it is called autism spectrum disorder. The different forms of autism are the result of different combinations of genetic and environmental factors. It is currently accepted that ASD is contracted through polygenic inheritance, meaning that there are multiple genes that can contribute to the formation of the disorder. The disorder is usually diagnosed between 14 months and by age 3. Diagnosing ASD can be very difficult because there is no physical medical test such as a blood screening to validate the presence of the disorder. Diagnosing takes two steps of Developmental Screening and Comprehensive Diagnostic Evaluation. These steps include evaluating their behaviors and progression through development. ASD can include associated neurological disorders such as mood disorders and systemic disorders such as immune dysfunction and GI tract problems. The symptoms of autism are usually lifelong but can be managed to reduce symptoms and improve skills and abilities.
A review Article in the Frontiers of Psychiatry journal discuses more on the factors linked to ASD. Although the polygenic genetic inheritance is predominately responsible for the development of autism it does explain the whole story. The review article discusses the many different environmental factors such as immune system abnormalities and Zinc deficiency. The picture below expresses all of the difficulties and risk factors of Autism.
Immune system abnormalities are linked to prenatal stress, prenatal viral infection, and parental age at the time of pregnancy. During prenatal stress the mother releases corticotrophins from her adrenal gland, which can pass through the placenta and cross the blood brain barrier causing inflammation in the fetus’ hippocampus. Parental age is associated with the increase rick of autoimmune disorders around the age of 30 years old which can affect the fetus and cause immune system abnormalities.
Zinc deficiencies are said to be caused by prenatal malnutrition, heavy metal poisoning, and maternal diabetes. Zinc is a very important molecule that regulates many different functions in the body and is a structural component in the body. Thus, indicating that a deficiency of Zinc could be related to immune deficiency and increase risk of infections.
Although the causes and rick factors for autism have been displayed, the underlying causes and specific biological abnormalities are k=not well known. Many people throughout the world suffer from Autism. Families struggle with finding and adapting to their family member that suffers from the disorder. I believe that more research and more people should investigate the causes and mechanisms that are responsible for autism spectrum disorder.
Parkinson’s Disease and How You Can Make a Difference
What is Parkinson’s
Roughly one million people in the US alone are living with Parkinson’s Disease (PD). It is a neurodegenerative disorder that slowly takes away an individuals ability to coordinate muscle movement. Although not directly fatal, the loss of motor control and other non-motor symptoms tremendously reduce quality and expected length of life. Research is ongoing to elucidate the underlying molecular mechanisms that lead to PD. As with many diseases affecting the brain, no cure yet exists. However, some treatments are available to manage symptoms. Raising awareness and public support is a critical component to ensure progress continues towards better outcomes for those living with PD.
Early Signs and Symptoms
- Tremor or Shaking
- Small Hand Writing
- Loss of Smell
- Trouble Sleeping
- Trouble Moving or Walking
- Constipation
- Softening of Voice
- Dizziness
- Muscle Stiffness
- Slowing of Movement
- Loss of Balance
What Happens In The Brain
The substantia nigra is a structure located in the mid brain that contains dopamine producing neurons involved in controlled/planned movement, reward seeking, and addiction. Symptoms of PD are the result of the progressive malfunction and death of these neurons.
Much of the research done on PD has implicated the hallmark protein alpha-synuclein (a-syn). It has a poorly characterized function, but may be important for synaptic function and dopamine release. In diseased brains abnormally high levels of phosphorylated a-syn create aggregates that generate toxic protein inclusions known as Lewy Bodies. The dysregulated a-syn is a main component of the disease, but whether it is the cause, or result of PD remains a mystery.
The elevated levels of phosphorylated a-syn in diseased brains led researchers to investigate the role that kinase activity plays in the development of PD.
Dysregulation of kinase activity can induce or result in mitochondrial dysfunction, oxidative stress, autophagy, and inflammation. This altered activity can in turn create the high levels of phosphorylated a-syn and increase the likelihood of cell death. It is probable that some of the altered kinase activity initiates the disease pathway and others continue the progression of PD. Determining what causes the altered kinase activity and the role they play in the development and progression could provide future targets for prevention and therapy.
What You Can Do
Supporting organizations such as the National Parkinson’s Foundation, American Parkinson’s Disease Association (APDA), and The Michael J. Fox Foundation, is crucial to support those affected and move research forward. These websites have great information regarding the disease and on how anyone can contribute. This includes tips on how to get involved with community fundraising, organize your own fundraising event, and more. They also have wonderful resources to provide support in any way possible to caregivers, families, and individuals currently dealing with PD. I encourage you to visit the websites to find out how you can find support, get involved, and raise awareness for Parkinson’s Disease.
Alzheimers Disease-and How to Minimize Your Risk
Alzheimer’s disease (AD) is a progressive and irreversible brain disorder affecting about 5 million Americans according to the Centers for Disease and Control (CDC). This equates to about one person developing the disease every 66 seconds. It is also the 6th leading cause of death right behind strokes, accidents, chronic lung disease, cancer, and heart disease.
What is Alzheimer’s?
Put simply it is the progressive death of brain cells leading to a gradual decline in cognitive function and brain shrinkage. Beta-amyloid plaques and hyper-phosphorylated tau proteins are the culprits driving neuronal cell death. They contribute to the formation of toxic neurofibrillary tangles (NFT’s) associated with the disease. However, why these proteins build up, become hyper-phosphorylated, and generate NFT’s is not well understood. Research has pointed to the dysregulation of the PI3k/Akt/mTOR (PI3) pathway as a potential player in the etiology of AD.
The PI3 pathway is an intercellular signaling mechanism important for several physiological functions such as cell cycle regulation. Dysregulation of this pathway occurs in some individuals with age and has been shown to have down-stream effects leading to the disease. Losing the ability to properly regulate this pathway promotes beta-amyloid formation and a reduced ability to get rid of it. The increased beta-amyloid levels in turn upregulate the level of PI3k signaling creating a vicious cycle. On top of that, it also increases the activity of the kinase responsible for phosphorylating tau. Which is a protein that helps stabilize the membrane of neurons.
The overactive PI3k signaling also increases levels of FOXO, a transcription factor important for proper protein metabolism, stress responses, and DNA repair. The hyper-phosphorylated tau and beta-amyloid plaques eventually lead to the trademark NFT’s and toxic cellular environments. These mechanisms progress to the point of cell death and lead to the associated dementia.
What are the Symptoms?
The symptoms present themselves as a slow decline in cognitive abilities. The first things typically noticed are forgetfulness and confusion. At first mild forgetfulness and confusion are noticed which progresses to more severe memory loss, especially with regards to recent memories. Besides memory, marked declines in thinking, reasoning, planning, and making proper judgments are present themselves. Emotional effects such as depression, mood swings, wandering, and delusions are also experienced. These things can also hurt the ability to properly care for current health problems. It can also make the individual susceptible to things such as falls, malnutrition, and bed sores. Eventually living assistance for all aspects of daily care is necessary.
Who is at Risk?
Aging is the main risk factor for about 95% of AD cases. One in nine people over the age of 65 have AD and it is present in nearly one-third of people over 85. Family history is another strong risk factor if you have a parent, brother, or sister with the disease. Most researchers agree that a combination of genetics, environmental factors, and unhealthy lifestyle contribute to AD risk.
How To Minimize Your Risk
A healthy life style is generally your best defense against any human affliction. This is also the best known way to avoid AD and other types of dementia. Research has found that strategies to promote healthy aging also lower AD risk. This includes things such as adequate sleep, proper diet, exercising (both body and mind), and avoiding tobacco.
Some current studies are finding benefits to brain training video games as a way to increase/maintain cognitive function and lower AD risk. Ongoing research such as this is promising and moving the field forward. However, much more needs to be done for finding a cure, improving treatments, and preventing the disease.