Is Ad Just An Exaggeration Of Normal Aging
Normal aging is associated with brain changes such as tissue loss and degeneration of the synapse, which is the part of the nerve cell that is involved in passing an electrical or chemical signal to another nerve cell. Plaques and sometimes tangles are known to develop in cognitively normal older adults. These changes occur more frequently and severely in people with advanced vascular disease, suggesting that reduced blood flow to brain cells may be important in the development of AD. Many cognitively normal older adults show no NFTs, suggesting that AD is more than just normal aging of the brain.
The loss of brain cells that produce acetylcholine, a neurotransmitter that is active in the transmission of nerve impulses was an early finding in AD research. It led to the development of the cholinesterase-inhibiting drugs such as donepezil . Unfortunately, these medications are symptomatic treatments at best and often achieve only a limited benefit. The loss of these particular brain cells, therefore, is thought by many to be an effect rather than a cause of AD. In support of that idea is the finding that cell loss includes not only cholinergic cells but other cell types as well. Other neurotransmitters such as serotonin are also reduced in AD.
Emotion And Behavior Treatments
The emotional and behavioral changes linked with Alzheimers disease can be challenging to manage. People may increasingly experience irritability, anxiety, depression, restlessness, sleep problems, and other difficulties.
Treating the underlying causes of these changes can be helpful. Some may be side effects of medications, discomfort from other medical conditions, or problems with hearing or vision.
Identifying what triggered these behaviors and avoiding or changing these things can help people deal with the changes. Triggers may include changing environments, new caregivers, or being asked to bathe or change clothes.
It is often possible to change the environment to resolve obstacles and boost the persons comfort, security, and peace of mind.
The Alzheimers Association offer a list of helpful coping tips for caregivers.
In some cases, a doctor may recommend medications for these symptoms, such as:
- antidepressants, for low mood
develops due to the death of brain cells. It is a neurodegenerative condition, which means that the brain cell death happens over time.
In a person with Alzheimers, the brain tissue has fewer and fewer nerve cells and connections, and tiny deposits, known as plaques and tangles, build up on the nerve tissue.
Plaques develop between the dying brain cells. They are made from a protein known as beta-amyloid. The tangles, meanwhile, occur within the nerve cells. They are made from another protein, called tau.
How Is Alzheimers Diagnosed And Treated
Doctors may ask questions about health, conduct cognitive tests, and carry out standard medical tests to determine whether to diagnose a person with Alzheimers disease. If a doctor thinks a person may have Alzheimers, they may refer the person to a specialist, such as a neurologist, for further assessment. Specialists may conduct additional tests, such as brain scans or lab tests of spinal fluid, to help make a diagnosis. These tests measure signs of the disease, such as changes in brain size or levels of certain proteins.
There is currently no cure for Alzheimers, though there are several medicines approved by the U.S. Food and Drug Administration that can help manage some symptoms of the disease along with coping strategies to manage behavioral symptoms. In 2021, FDA provided accelerated approval for a new medication, aducanumab, that targets the protein beta-amyloid, which accumulates abnormally in the brains of people with Alzheimers. The new medication helps to reduce amyloid deposits, but has not yet been shown to affect clinical symptoms or outcomes, such as progression of cognitive decline or dementia.
Most medicines work best for people in the early or middle stages of Alzheimers. Researchers are exploring other drug therapies and nondrug interventions to delay or prevent the disease as well as treat its symptoms.
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We May Finally Know What Causes Alzheimers And How To Stop It
Alzheimers disease has destroyed neurons in the right-hand brain above
Jessica Wilson/Science Photo Library
AFTER decades of disappointment, we may have a new lead on fighting Alzheimers disease. Compelling evidence that the condition is caused by a bacterium involved in gum disease could prove a game-changer in tackling one of medicines biggest mysteries, and lead to effective treatments or even a vaccine.
As populations have aged, dementia has skyrocketed to become the fifth biggest cause of death worldwide. Alzheimers constitutes some 70 per cent of these cases , yet we dont know what causes it. The condition, which results in progressive loss of memory and cognitive function, usually over a decade or so, is devastating both to those who have it and to their loved ones.
The condition often involves the accumulation of two types of proteins called amyloid and tau in the brain. As these are among the earliest physical signs of the disease, the leading hypothesis since 1984 has been that the condition is caused by the defective control of these proteins, especially amyloid, which accumulates to form large, sticky plaques in the brain.
The bulk of research into understanding and treating Alzheimers has centred on this amyloid hypothesis. Huge sums of money have been invested in experiments involving mice genetically modified to produce amyloid, and in developing drugs that block or destroy amyloid proteins, or sometimes degraded tangles of tau.
Down Syndrome And Alzheimers Disease
People with Down syndrome have a third copy of chromosome 21, instead of the usual two copies. This genetic change causes a collection of characteristics, including intellectual disability and some common physical traits.The APP gene that leads to the production of the beta-amyloid protein present in Alzheimers plaques is located on chromosome 21. This means that people with Down syndrome make one and a half times the amount of APP and, as a consequence, more beta-amyloid. This appears to be the cause of the earlier appearance of the brain changes typical of Alzheimers disease in people with Down syndrome.
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Signs And Symptoms Of Early
Symptoms are generally mild to start, but become more noticeable as the disease progresses. The person may begin having difficulty with:
- Memory Losing items like keys around the house, forgetting a friends name or a recent conversation, getting lost in a familiar place.
- Speech Repeating oneself or struggling to follow a conversation.
- Visual Perception Difficulty seeing things in three dimensions and judging distances.
- Concentrating, Organizing, or Planning Struggling to make decisions, solve problems, or complete multistep tasks, like cooking a meal.
- Orientation Getting confused about where they are or the time or date.
- Mood Feeling anxious, depressed, or irritable.
Can I Get Alzheimers Disease If Im Younger Than 65
Even though Alzheimers disease most commonly affects people older than 65, it can develop and cause symptoms in younger people.
When that happens, its referred to as early-onset Alzheimers disease or younger-onset Alzheimers disease. This condition can strike when someone is even in their 40s and 50s, which can make getting an accurate diagnosis difficult as we mainly think of the disease happening in someone older.
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What Can Lead To Alzheimer’s Disease
There are a few things that may make people more likely to get Alzheimerâs. So far, research has linked the disease with:
- Age. Your risk for Alzheimer’s goes up as you get older. For most people, it starts going up after age 65.
- Gender. Women get the disease more often than men.
- Family history. People who have a parent or sibling with Alzheimerâs are more likely to get it themselves.
- Down syndrome. Itâs not clear why, but people with this disorder often get Alzheimer’s disease in their 30s and 40s.
- Head injury. Some studies have shown a link between Alzheimer’s disease and a major head injury.
- Other factors. High cholesterol levels and high blood pressure may also raise your risk.
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Alternative And Complementary Therapies
Despite the growing number of herbal remedies, dietary supplements, and medical foods aimed at people with Alzheimers, there is no scientific proof that any of these products work.
For instance, some people with Alzheimers consume coconut oil based on the theory that the caprylic acid in the oil can provide energy to brain cells that are no longer able to metabolize glucose. But there has been no research confirming that this helps cognition.
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Neurofibrillary Tangles And Senile Plaques
Plaques are dense, mostly insoluble deposits of protein and cellular material outside and around the neurons. Plaques are made of beta-amyloid , a protein fragment snipped from a larger protein called amyloid precursor protein . These fragments clump together and are mixed with other molecules, neurons, and non-nerve cells .
In AD, plaques develop in the hippocampus, a structure deep in the brain that helps to encode memories, and in other areas of the cerebral cortex that are used in thinking and making decisions. Plaques may begin to develop as early as the fifth decade of life. Whether Ab plaques themselves cause AD or whether they are a by-product of the AD process is still unknown. It is known that changes in APP structure can cause a rare, inherited form of AD.
Tangles are insoluble twisted fibers that build up inside the nerve cell. Although many older people develop some plaques and tangles, the brains of people with AD have them to a greater extent, especially in certain regions of the brain that are important in memory. There are likely to be significant age-related differences in the extent to which the presence of plaques and tangles are indicative of the presence of dementia.
SPs also accumulate primarily in association cortices and in the hippocampus. Plaques and tangles have relatively discrete and stereotypical patterns of laminar distribution in the cerebral cortex, which indicate predominant involvement of corticocortical connections.
What Are Some Complications Of Alzheimers Disease
Alzheimers disease is an irreversible form of dementia. The rate of progression differs between people: some people have it only in the last 5 years of their life, while others may have it for as long as 20 years. Alzheimers disease eventually leads to complete dependence and increasing frailty. This means a secondary illness, such as pneumonia, may eventually cause death.
Other complications of Alzheimers disease may include:
- an inability to complete daily tasks such as planning meals and managing money
- a tendency to wander from home
- personality changes such as anxiety, depression and irritability that make relationships more difficult
- delusions and hallucinations in advanced stages of the disease
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Research Into The Cause Of Vascular Dementia
Vascular dementia is the second most commonly diagnosed type of dementia, and may account for 15 – 20% of all cases. Vascular dementia is caused by chronic reduced blood flow to the brain, usually as a result of a stroke or series of strokes. It can often coexist with Alzheimer’s disease.
Stroke, small vessel disease, or a mixture of the two can cause vascular dementia. Most commonly there is a blockage of small blood vessels somewhere in the network of arteries that feeds the brain. Blockages may be caused by plaque build up on the inside of the artery wall, or by blood clots which have broken loose. Clots can form as a result of abnormal heart rhythms, or other heart abnormalities. Also, a weak patch on an artery wall can balloon outward and form an aneurysm, which can burst and deprive brain cells of oxygen.
It is estimated that about 50% of cases of vascular dementia result from high blood pressure, which can lead to a major stroke or a series of strokes and a build up of brain damage over time. Less common causes of vascular dementia are associated with autoimmune inflammatory diseases of the arteries such as lupus and temporal arteritis, which are treatable with drugs that suppress the immune system.
An inherited form of vascular dementia known as CADASIL is caused by a mutation on the Notch3 gene. This is a very rare form of dementia and only affects families carrying the Notch3 gene mutation.
What Are Some Risk Factors For Alzheimers Disease
Risk factors for the development of Alzheimers disease include:
- Age. Increasing age is the primary risk factor for developing Alzheimers disease.
- Genetics . There is a certain gene, apolipoprotein E that is associated with late-onset Alzheimers disease. Other genes have been associated with early-onset Alzheimers disease.
Researchers believe the presence of the last five risk factors mentioned above might reduce the clearance of amyloid protein from the brain, which then increases the risk of developing Alzheimers disease. In particular, the presence of a number of these risk factors at the same time and while the person is in his or her 50s is associated with a higher risk of Alzheimers disease.
There may be some ways to reduce the risk of mental decline. In general, living a healthy lifestyle protects the body from strokes and heart attacks and is believed to also protect the brain from cognitive decline. Scientists cant absolutely prove the cause and effect of the following factors, but studies have shown a positive association.
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Dementia Is Depressing But You Dont Have To Be Depressed
Dementia isnt a specific disease, but rather a general term to describe any decline in brain function that affects memory, language, and other cognitive abilities, and that is serious enough to interfere with daily life.
Alzheimers disease is the most common type of dementia, accounting for 60 to 80 percent of all dementia cases.
Living With Frontotemporal Dementia
This condition isnât life-threatening. But you should find a doctor who knows how to manage it as soon as possible. Speech experts, physical therapists, and nurses may be able to help, too.
You should also think about doing these things:
- Ask your doctor whether medications can help.
- Find a support group.
- Get a driving evaluation.
- Exercise and eat healthy foods.
- Create a plan for when your ability to live on your own and make decisions is impaired.
If youâre caring for someone with FTD, you can:
- Explain to others what to expect when theyâre with your loved one.
- Connect with other caregivers through caregiver support groups.
- Find respite caregivers who can step in when you need a break.
- Take care of your own physical and mental health by eating well, getting enough sleep, exercising, and spending time doing things you like to do.
Doctors are learning more about this kind of dementia, which may lead to better diagnosis and care.
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Lecanemab The One Recent Exception
How will our findings affect drug development and clinical trials for Alzheimers disease? Until the recent trial with lecanemab, an antibody drug that reduces plaques, all the drug trials in Alzheimers disease have failed.
Some drugs were designed to reduce the levels of amyloid-beta 42, based on the rationale that if levels of the normal protein are reduced, patients will accumulate fewer plaques. Unfortunately, these drugs often made the patients condition worse.
Lecanemab was recently reported to have a small but significant effect in reducing cognitive decline. According to previous studies, this drug increases the levels of amyloid-beta 42 in the CSF. This is, again, in line with our hypothesis, namely that the increase of the normal amyloid protein can be beneficial.
We will know more when the results of the lecanemab trial are published. At the moment, all we have is a press release from the makers of the drug.
We think that it will be important for future trials to focus on the levels of amyloid-beta 42, and whether it is beneficial to increase and restore its levels to normal values instead of targeting it for removal. This could be achieved using proteins similar to amyloid-beta 42 so-called protein analogues but that clump together less than the natural ones.
This active protein replacement approach might become a promising new avenue of treatment for Alzheimers and other protein aggregation diseases, such as Parkinsons and motor neuron disease.
Signs And Symptoms Of Later
As the disease becomes more advanced, symptoms above become more pronounced. According to the Alzheimers Society, people may also experience:
- Delusions For instance, believing, without reason, that someone is stealing from them
- Uncharacteristic Behavior Exhibiting aggression or agitation, calling out, or having disturbed sleep patterns
- Difficulty Walking and Talking Becoming bedridden or wheelchair-bound and requiring round-the-clock care to help with eating, drinking, and toileting
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How Does Alzheimer’s Start And Progress
Alzheimer’s disease tends to develop slowly and gradually worsens over several years. Eventually, Alzheimer’s disease affects most areas of your brain. Memory, thinking, judgment, language, problem-solving, personality and movement can all be affected by the disease.
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What Neurotransmitters Play A Role In Alzheimers Disease
Two neurotransmitters involved in memory and learningcalled acetylcholine and glutamateappear to play a role in Alzheimers disease. On the one hand, plaques appear to stimulate the production of chemicals that break down ACH, leading to their depletion. On the other, the progressive death of brain cells triggers the overproduction of glutamate, which overexcites brain cells and eventually kills them.
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Amyloid Hypothesis Versus Tau Hypothesis
A central but controversial issue in the pathogenesis of AD is the relationship between amyloid deposition and NFT formation. Evidence shows that abnormal amyloid metabolism plays a key pathogenic role. At high concentrations, the fibrillar form of Ab has been shown to be neurotoxic to cultured neurons.
Cultured cortical and hippocampal neurons treated with Ab protein exhibit changes characteristic of apoptosis , including nuclear chromatin condensation, plasma membrane blebbing, and internucleosomal DNA fragmentation. The fibrillar form of Ab has also been shown to alter the phosphorylation state of tau protein.
The identification of several point mutations within the APP gene in some patients with early-onset familial AD and the development of transgenic mice exhibiting cognitive changes and SPs also incriminate Ab in AD. The apolipoprotein E E4 allele, which has been linked with significantly increased risk for developing AD, may promote inability to suppress production of amyloid, increased production of amyloid, or impaired clearance of amyloid with collection outside of the neuron.
Autopsies have shown that patients with 1 or 2 copies of the APOE E4 allele tend to have more amyloid. Additional evidence comes from recent experimental data supporting the role of presenilins in Ab metabolism, as well as findings of abnormal production of Ab protein in presenilin-mutation familial Alzheimer disease.