Alzheimer’s Is Caused By

How Common Is Alzheimers Disease

Alzheimers disease is the most common cause of dementia . Alzheimers disease is the sixth leading cause of death in the United States.

One in 10 people older than 65 and nearly half of people older than 85 have Alzheimers disease. Alzheimers disease can also affect people in their 40s. The percentage of people who have Alzheimers disease rises every decade beyond the age of 60. According to the Alzheimer’s Association, with the aging of the population and without successful treatment, there will be 14 million Americans and 106 million people worldwide with Alzheimers disease by 2050.

What To Do If You Suspect Alzheimers Disease

Getting checked by your healthcare provider can help determine if the symptoms you are experiencing are related to Alzheimers disease, or a more treatable conditions such as a vitamin deficiency or a side effect from medication. Early and accurate diagnosis also provides opportunities for you and your family to consider financial planning, develop advance directives, enroll in clinical trials, and anticipate care needs.

Alzheimers Disease Risk Factors

5.2.1. Aging

The most important risk factor in AD is aging. Younger individuals rarely have this disease, and most AD cases have a late onset that starts after 65 years of age . Aging is a complex and irreversible process that occurs through multiple organs and cell systems with a reduction in the brain volume and weight, a loss of synapses, and ventricles enlargement in specific areas accompanied by SP deposition and NFT. Moreover, several conditions might emerge during aging such as glucose hypometabolism, cholesterol dyshomeostasis, mitochondria dysfunction, depression, and cognitive decline. These changes also appear in normal aging, which makes it difficult to distinguish the cases in early AD . AD can be divided based on age of onset into early-onset AD , the rare form with around 16% of cases, in which most of them are familial AD characterized by having more than one member in more than one generation with AD, and ranges from 3060 or 65 years. The second type is the late-onset AD , which is more common with age of onset above 65 years. Both types may occur in people who have a family with a positive history of AD and families with a late-onset disease .

5.2.2. Genetics

Herein, we discuss the strong genetic risk factors in AD.

• Amyloid Precursor Protein

• Presenilin-1 and Presenilin-2

• Apolipoprotein E

• ATP Binding Cassette Transporter A1

• Clusterin Gene and Bridging Integrator 1

• Evolutionarily Conserved Signaling Intermediate in Toll pathway

• Estrogen Receptor Gene

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Medications For Cognitive Symptoms

No disease-modifying drugs are available for Alzheimers disease, but some options may reduce the symptoms and help improve quality of life.

Drugs called cholinesterase inhibitors can ease cognitive symptoms, including memory loss, confusion, altered thought processes, and judgment problems. They improve neural communication across the brain and slow the progress of these symptoms.

Three common drugs with Food and Drug Administration approval to treat these symptoms of Alzheimers disease are:

• donepezil , to treat all stages
• galantamine , to treat mild-to-moderate stages
• rivastigmine , to treat mild-to-moderate stages

Another drug, called memantine , has approval to treat moderate-to-severe Alzheimers disease. A combination of memantine and donepezil is also available.

The Role Of Plaques And Tangles

Scientists arent completely sure about why neurons die and tissue shrinks in the brains of people with Alzheimers disease, but they strongly suspect that amyloid plaques and tau tangles are the cause.

The thinking is that plaques form when pieces of a protein called beta-amyloid clump together. Researchers are beginning to think that groups of a few pieces of beta-amyloid, rather than plaques, may cause the worst damage by blocking the chemical signals neurons use to communicate.

In healthy brain tissue, tau protects the transport systems that supply cells with nutrients and other important substances. But when tau forms tangles, cells cant get the essentials they need and begin to die, according to the Alzheimers Association.

However, there is new controversy surrounding the role of beta-amyloid in Alzheimers, so more research is needed on the subject.

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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

Research And Statistics: How Many People Have Alzheimers

More than six million people in the United States are living with Alzheimers, and 1 in 3 seniors dies with Alzheimers or another dementia, according to the Alzheimers Association

As the number of older Americans rises, reflecting advances in medicine and the aging of the baby boomers, the number of people with Alzheimers is expected to more than double to as many as 13 million by 2050, barring any significant medical breakthroughs.

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Summary Of Alzheimers Causes

How do we make sense of all these different theories? One approach is to view AD as a final common pathway reached by many different routes. AD may be a type of brain destruction that can eventually occur with aging but may be accelerated by:

• diminished blood flow,
• excess accumulation of abnormal brain proteins,

Amyloid: Still An Important Piece Of The Alzheimer’s Puzzle

The initial 1907 report of Dr. Aloysius Alzheimer described senile plaques, later recognized as containing beta amyloid. These plaques, along with neurofibrillary tangles, are hallmarks of AD.

The Amyloid Cascade Hypothesis proposes that deposition of beta amyloid in the brain triggers the formation of amyloid plaques and neurofibrillary tangles . This theory fits with evidence from mice studies.

It also fits with genetic findings that I’ll discuss later in this article. However, brain injury can trigger the formation of senile plaques, raising the possibility that these plaques are an effect rather than a cause of some more basic disease process in AD. Furthermore, the connection between plaques and the development of NFTs is not yet fully understood. There is an additional concern about the ACH: The theory’s prediction that reducing brain amyloid might improve cognitive performance or diminish the risk of AD has been tested with trials of medications that do indeed reduce amyloid in the blood and brain. So far, clinical trial results have been negative for many of these medications and the small number of positive findings have been of limited magnitude.

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What Are The Stages Of Alzheimers

Alzheimers disease slowly gets worse over time. People with this disease progress at different rates and in several stages. Symptoms may get worse and then improve, but until an effective treatment for the disease itself is found, the persons ability will continue to decline over the course of the disease.

Early-stage Alzheimers is when a person begins to experience memory loss and other cognitive difficulties, though the symptoms appear gradual to the person and their family. Alzheimers disease is often diagnosed at this stage.

During middle-stage Alzheimers, damage occurs in areas of the brain that control language, reasoning, sensory processing, and conscious thought. People at this stage may have more confusion and trouble recognizing family and friends.

In late-stage Alzheimers, a person cannot communicate, is completely dependent on others for care, and may be in bed most or all the time as the body shuts down.

How long a person can live with Alzheimers disease varies. A person may live as few as three or four years if he or she is older than 80 when diagnosed, to as long as 10 or more years if the person is younger. Older adults with Alzheimers disease need to know their end-of-life care options and express their wishes to caregivers as early as possible after a diagnosis, before their thinking and speaking abilities fail.

How To Talk To A Loved One About Signs Of Alzheimers Disease

Scientists have identified a condition called mild cognitive impairment that for some people is a harbinger of Alzheimers dementia. MCI involves problems with memory or mental function that are noticeable to the person affected but not serious enough to interfere with everyday life.

Men and women who have MCI may be at higher risk of developing Alzheimers or other forms of dementia than individuals who dont. But MCI doesnt always progress some people even get their cognitive abilities back. Researchers are trying to figure out why, notes the Mayo Clinic.

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Diagnosis Of Alzheimer Disease

• Safety and supportive measures

• Drugs that may improve mental function

Treatment of Alzheimer disease involves general measures to provide safety and support, as for all dementias. Also, certain drugs can help for a while. The person with Alzheimer disease, family members, other caregivers, and the health care practitioners involved should discuss and decide on the best strategy for that person.

Pain and any other disorders or health problems are treated. Such treatment may help maintain function in people with dementia.

Scientists Propose New Mechanism Driving Alzheimer’s Disease

WEDNESDAY, Oct. 5, 2022 — Amyloid-beta plaques have long been linked to Alzheimer’s disease, with some scientists theorizing that the plaques actually cause the degenerative brain disease.

But a new study suggests that the plaques are actually a symptom of what’s going on in the brain, rather than the cause of Alzheimer’s.

Instead, decreasing levels of the “normal,” water-soluble form of amyloid-beta is the real culprit behind Alzheimer’s, a research team argues in the Journal of Alzheimers Disease.

“The paradox is that so many of us accrue plaques in our brains as we age, and yet so few of us with plaques go on to develop dementia, said lead researcher Dr. Alberto Espay. He’s director and endowed chair of the Center for Parkinson’s Disease and Movement Disorders at the University of Cincinnati Neuroscience Institute.

“Yet the plaques remain the center of our attention as it relates to biomarker development and therapeutic strategies,” Espay said in a university news release.

The team’s previous research had found that regardless of plaque buildup in the brain, people with high levels of soluble amyloid-beta kept their brain health. On the other hand, those with low levels of the protein were more likely to have cognitive impairment.

The researchers think soluble amyloid-beta levels decrease because the normal protein, exposed to stressors, starts transforming into abnormal amyloid plaques.

More information

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Research Into The Genetics Of Dementia

Genes carry patterns for the many proteins that form our bodies. Proteins are the essential building blocks of life – forming cells, organs, and enzymes which help the body to function. Once they are made, proteins can be folded into different structures and shapes to fulfil their many functions. Genes are found in every cell in the body in packages of twisted DNA called chromosomes. Half of these chromosomes are inherited from each parent – providing the basis for genetic inheritance. Genes explain why family resemblances occur and why some diseases can run in families.

There is still much we don’t know about the role of genes in Alzheimer’s disease and other dementias, but researchers continue to study this area. In most cases, dementia occurs sporadically, is not directly caused by a single gene and has no clear pattern of family inheritance. However, in a minority of cases, Alzheimer’s disease and some other types of dementia can be directly caused by an inherited gene mutation. The table below summarises some of the genes that have been found to cause or be involved in dementia. Each type is discussed in more detail under the relevant section below.

Bad Bacteria And Other Microbes

It might seem surprising that a mouth bacterium has been implicated in Alzheimers disease . But it wouldnt be the first time an illness has turned out to have an unexpected infectious origin.

The iconic case is stomach ulcers, once thought to be caused by stress or excess acid, and treated with acid-lowering medications. Then Australian doctor Barry Marshall showed that a stomach bacterium called Helicobacter pylori was behind them, a feat that won him a Nobel prize.

Streptococcus bacteria, which cause tonsillitis and strep throat, are suspected of triggering obsessive-compulsive disorder in children. The thinking is that the immune systems attack on the bacteria cross-reacts with certain human proteins, causing an autoimmune attack against the persons own brain tissue.

Bacteria arent the only ones under suspicion. There are indications that a virus is behind some cases of obesity. And one study has found that people with antibodies to a single-celled brain parasite called Toxoplasma gondii, which is spread in cat faeces, are more likely to develop schizophrenia. Some people think up to a third of cases could be caused by infection with T. gondii.

But not all purported links bear fruit. Twenty years ago, there was great excitement when a bacterium that can cause pneumonia lung infections was found in the blood vessel plaques that cause heart disease. But giving people antibiotics to kill this bug didnt help reduce heart attacks. Clare Wilson

More on these topics:

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The Basics Of Alzheimers Disease

Scientists are conducting studies to learn more about plaques, tangles, and other biological features of Alzheimers disease. Advances in brain imaging techniques allow researchers to see the development and spread of abnormal amyloid and tau proteins in the living brain, as well as changes in brain structure and function. Scientists are also exploring the very earliest steps in the disease process by studying changes in the brain and body fluids that can be detected years before Alzheimers symptoms appear. Findings from these studies will help in understanding the causes of Alzheimers and make diagnosis easier.

One of the great mysteries of Alzheimers disease is why it largely affects older adults. Research on normal brain aging is exploring this question. For example, scientists are learning how age-related changes in the brain may harm neurons and affect other types of brain cells to contribute to Alzheimers damage. These age-related changes include atrophy of certain parts of the brain, inflammation, blood vessel damage, production of unstable molecules called free radicals, and mitochondrial dysfunction .

Disproportionate Impact On Women

Globally, dementia has a disproportionate impact on women. Sixty-five percent of total deaths due to dementia are women, and disability-adjusted life years due to dementia are roughly 60% higher in women than in men. Additionally, women providethe majority of informal care for people living with dementia, accounting for 70% of carer hours.

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Medications To Treat The Underlying Alzheimer’s Disease Process

Aducanumab is the first disease-modifying therapy approved by the FDA to treat Alzheimers disease. The medication helps to reduce amyloid deposits in the brain and may help slow the progression of Alzheimers, although it has not yet been shown to affect clinical outcomes such as progression of cognitive decline or dementia. A doctor or specialist will likely perform tests, such as a PET scan or analysis of cerebrospinal fluid, to look for evidence of amyloid plaques and help decide if the treatment is right for the patient.

Aducanumab was approved through the FDAs Accelerated Approval Program. This process requires an additional study after approval to confirm the anticipated clinical benefit. If the follow-up trial fails to verify clinical benefit, the FDA may withdraw approval of the drug. Results of the phase 4 clinical trial for aducanumab are expected to be available by early 2030.

Several other disease-modifying medications are being tested in people with mild cognitive impairment or early Alzheimers as potential treatments.

Common Forms Of Dementia

There are many different forms of dementia. Alzheimer’s disease is the most common form and may contribute to 60-70% of cases. Other major forms include vascular dementia, dementia with Lewy bodies , and a group of diseases that contribute to frontotemporal dementia . Dementia may also develop after a stroke or in the context of certain infections such as HIV, harmful use of alcohol, repetitivephysical injuries to the brain or nutritional deficiencies. The boundaries between different forms of dementia are indistinct and mixed forms often co-exist.

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What Newer Medications Are Under Study

All currently approved medications target Alzheimers disease after it develops. Scientists are currently researching ways to stop or slow the progress of Alzheimers disease before it starts.

Some of the drugs in late-stage investigation are called monoclonal antibodies. These drugs target the amyloid protein that builds up in brain cells. They work by attaching to the amyloid proteins as they float in the brain and remove them, before they form into the plaques and tangles that interfere with the brains ability to properly function.

These drugs are still in clinical trials and are several years away from Food and Drug Administration approval in the United States. Early results have been mixed, with some trials showing no improvement in brain function others showing a slight improvement . Despite the mixed results, researchers are excited about this new potential method to modify the disease process.

Shocking Study Finds Decreased Proteins Not Amyloid Plaques Cause Alzheimers Disease

The prevailing theory is that Alzheimers disease is caused by the buildup of amyloid plaques in the brain. However, new research finds that it is actually caused by a decline in levels of a specific protein.

New research on patients with mutations published in the Journal of Alzheimers Disease.

Contrary to a prevailing theory that has been recently called into question, new research from the University of Cincinnati bolsters a hypothesis that Alzheimers disease is caused by a decline in levels of a specific protein.

UC researchers led by Alberto Espay, MD, and Andrea Sturchio, MD, in collaboration with the Karolinska Institute in Sweden, published the research on October 4, 2022, in the Journal of Alzheimers Disease.

Questioning the dominant hypothesis

This research study was focused on a protein called amyloid-beta. The protein normally carries out its functions in the brain in a form that is soluble, meaning that it is dissolvable in water. However, it sometimes hardens into clumps, known as amyloid plaques.

I think this is probably the best proof that reducing the level of the soluble form of the protein can be toxic. When done, patients have gotten worse. Andrea Sturchio, MD

Research results

Andrea Sturchio, MD. Credit: Provided

Even in this group of patients thought to have the highest risk of Alzheimers disease, the scientists observed similar results as the study of the general population.

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