Ive Talked To An Editor Recently From One Of The Top Ten Journals And She Said The Field Is Exploding And I Told Her: With Every Explosion Theres A Lot Of Dust Being Generated And We Have To Wait Until That Is Settled And See What Good Data Remains
He also begged the question: Do certain genes render people more likely to be affected by infections? Itzahki and other researchers have found that people with the ApoE4 gene, the largest genetic risk factor of Alzheimers, who have HSV-1 in the brain are 12 times more likely to develop Alzheimers than those with neither the disease or the virus.
But the biological mechanisms that may explain such phenomena remains unknown, according to Itzahki, though she suggested that as ApoE4 may be less efficient at competing with HSV-1 to enter cells in our body than other types of ApoE proteins.
In the case of periodontitis, Cortexymes team found that gingipains produced by Porphyromonas gingivalis had a penchant for damaging ApoE4 proteins, which Dominy said, may explain why carriers of the mutant gene are at a higher risk for developing Alzheimers.;
What To Do If You Think Your Loved One Has An Infection
Advocate for him. Inform the doctor, and begin by explaining what his normal behavior, mood, and cognitive functioning are. Be sure to explain any changes to the physician, as well as if he has a history of frequent urinary tract infections, for example.
If an antibiotic is prescribed, be sure to administer the whole course that is prescribed, even if your loved one appears to be feeling better. Sometimes, doctors might recommend additional treatments, such as an inhaler or nebulizer for an upper respiratory infection. If your loved one is resistive to whatever kind of treatment that is prescribed, notify the physician again so that an alternative treatment can be considered.
How C Albicans Affects The Brain Memory
Dr. Corry and colleagues tested several doses of C. albicans in a mouse model of the infection. They were trying to find a dose that would be high enough to affect the brain, but not high enough to cause debilitating disease.
Finally, the scientists decided to inject a dose of 25,000 yeasts in the rodents bloodstream. Dr. Corry and the team were surprised to discover that the fungus penetrated the blood-brain barrier.
The blood-brain barrier is a mechanism that protects the brain from pathogens that may exist in the blood. The barrier separates the brains capillaries, or blood vessels, from the brains cells and tissue.
C. albicans crossed this barrier and affected the brains immune cells. We thought that yeast would not enter the brain, but it , comments Dr. Corry.
In the brain, the yeast triggered the activity of microglia, a resident type of immune cell, he explains, adding, he cells became very active, eating and digesting the yeast. They also produced a number of molecules that mediated an inflammatory response, leading to the capture of the yeasts inside a granule-type structure inside the brain.
The researchers called this structure fungus-induced glial granuloma, or FIGG. The scientists also noticed that, as FIGGs formed, amyloid precursor proteins and molecules of a protein called amyloid beta developed around the yeast cells.
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Gum Disease And Alzheimers
Periodontitis, commonly known as gum disease, affects about 40 percent of American adults 30 years or older. Its also a risk factor for cognitive decline and Alzheimers. The bacteria that is the main culprit of the disease, Porphyromonas gingivalis, is present in the brains of more than 90 percent of people with Alzheimers.;
Recent findings suggest that the bacteria may trigger an antibacterial response from beta-amyloid as well as impair the function of tau, a protein thought to play a role in regulating the communication between brain cells.;
In a study published this month, researchers observed that, after they infected human brain neurons with Porphyromonas gingivalis bacteria, the bacteria reproduced and created toxins called gingipains. According to Stephen Dominy, an author of the study and the co-founder and chief scientific officer of biopharmaceutical company Cortexyme, a quarter of the brain cells died subsequently and the surviving;neurons developed pathologies linked to Alzheimers, such as the breaking down of tau.;
Dominy and other researchers also found in a study last year that Porphyromonas gingivalis may stimulate the production of beta-amyloid 42 peptide, a type of beta-amyloid. The peptides killed the bacteria, he explained, by binding onto and damaging its membrane.;
And, the theory is supported by a growing body of research to suggest that beta-amyloid may be a natural defense mechanism of the brain.;;
Large Study Links Gum Disease With Dementia
The mouth is home to about 700 species of bacteria, including those that can cause periodontal disease. A recent analysis led by NIA scientists suggests that bacteria that cause gum disease are also associated with the development of Alzheimers disease and related dementias, especially vascular dementia. The results were reported in the Journal of Alzheimers Disease.
Gum disease results from infection of the oral tissues holding teeth in place. Bleeding gums, loose teeth, and even tooth loss are the main effects of this disease. Bacteria and the inflammatory molecules they make can travel from infections in the mouth through the bloodstream to the brain. Previous lab studies have suggested that this is one mechanism influencing the cascade of events that leads to dementia, but large studies with people have not been conducted to confirm this relationship.
The analysis revealed that older adults with signs of gum disease and mouth infections at baseline were more likely to develop Alzheimers during the study period. Among those 65 years or older, both Alzheimers diagnoses and deaths were associated with antibodies against the oral bacterium P. gingivalis, which can cluster with other bacteria such as Campylobacter rectus and Prevotella melaninogenica to further increase those risks.
This research was supported entirely by the NIA Intramural Research Program.
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Urinary Tract Infections And Dementia
Urinary tract infections are a type of infection common among older people. If a person with a memory impairment or dementia has a UTI, this can cause sudden and severe confusion known as delirium.
Urinary tract infections and dementia
Along with all our information on dementia, we have more advice to support you during coronavirus.
Why Study C Albicans And The Brain
Dr. Corry explains the motivation for the research, pointing to the link between fungi, respiratory infections, and dementia.
He says, An increasing number of clinical observations indicates that fungi are becoming a more common cause of upper airway allergic diseases such as asthma, as well as other conditions such as , a potentially life-threatening disease caused by the bodys response to an infection.
These observations, continues Dr. Corry, led us to investigate the possibility that fungus might produce a brain infection and, if so, the consequences of having that kind of infection.
The corresponding researcher also highlights the fact that sepsis and allergic respiratory infections caused by fungi have correlated with a higher risk of dementia in previous studies.
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Signs And Symptoms Of Alzheimer’s Disease
Alzheimer’s disease is a progressive condition, which means the symptoms develop gradually over many years and eventually become more severe. It affects multiple brain functions.
The first sign of Alzheimer’s disease is usually minor memory problems.
For example, this could be forgetting about recent conversations or events, and forgetting the names of places and objects.
As the condition develops, memory problems become more severe and further symptoms can develop, such as:
- confusion, disorientation and getting lost in familiar places
- difficulty planning or making decisions
- problems with speech and language
- problems moving around without assistance or performing self-care tasks
- personality changes, such as becoming aggressive, demanding and suspicious of others
- hallucinations; and delusions
- low mood;or anxiety
Read more about the symptoms of Alzheimer’s disease.
Does A Virus Cause Alzheimers
Q.I know that some viruses live permanently inside us, but only make trouble now and then. I even heard recently that they might be a cause of Alzheimer’s disease. Why do they sometimes cause disease, and can we keep that from happening?
A. We live all of our lives with various microorganisms on us and inside us. One example is the herpes family of viruses. Out of more than a hundred herpesviruses, there are nine that infect humans. Once we get infected with these viruses usually early in life they remain with us, “asleep” inside some of our cells. But periodically, they “wake up” , start producing multiple copies of themselves, and infect other cells. That’s what’s happening when a cold sore suddenly forms on your lip.
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The Alzheimer Disease Field And Infectious Hypothesis
The answer likely stems from the composition of the AD field. Though expanding and diversifying, most AD researchers are not microbiologists or virologists. Typically, they are neuroscientists, biochemists, neuropathologists, neuropsychologists, and pharmacologists. There is a distinct lack of overlap between the disciplines that is sometimes hard to bridge in terms of forming collaborations or productive dialogue. The number of individuals who work on AD and identify as a microbiologist or virologist is extremely small.
The longstanding support for A research is overwhelming, despite high failure rates for therapeutics centered on A modulation . NIH funding for AD research as of this articles writing sits at $2.3 billion, a funding level reflective of the imminent health concern AD represents. Of the NIH AD funding, a negligible amount is used to investigate pathogens in AD . However, the recent announcement of special interest by the National Institute on Aging for grants examining a potential connection between pathogens and AD represents an important step in increased funding in this area .
For those with greater interest in specific aspects of the infectious hypothesis, we would direct you to more comprehensive reviews written by Dr. Ruth Itzhaki, who frequently publishes scientific reviews on the topic.
Choose The Proper Care
Due to the increased risk with dementia and infections, you may want to consider help in caring for your loved one with dementia. Many families want to give their loved one the best but simply cannot do it all on their own.
Dementia requires a watchful eye as it progresses, and the risk is great. Look into our dementia care;for an approach that centers on your loved ones best interest.
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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.
Compatibility Of An Infectious Etiology With The Epidemiology Of Other Alzheimer’s Disease Risk Factors
Many potential risk factors have been implicated in the complex epidemiology of AD and related dementias; not all are widely accepted. For example, claims that cigarette smoking is linked to AD remain controversial . Nonetheless, for any risk factor generally associated with AD, questions can be raised as to whether the factor is compatible with the infectious etiology for AD and related dementias. Although an exhaustive review of such correlates is not presented out here, a brief consideration of 2 groups of risk factors is offered. The first is a set of AD risk factors associated with infant and childhood characteristics, including lower socioeconomic status and poverty, minority status , and lower educational attainment and poorer educational performance . This set of risk factors and the economic gradient it represents are also associated with an increased risk of several categories of early-acquired infections, such as tuberculosis, sexually transmitted infections , and H. pylori . Although this compatibility is noted, these childhood social and ethnic gradients also might be associated with putative noninfectious causes of AD, such as head trauma .
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Oral Bacteria May Be Responsible For Alzheimers Disease
Alzheimers disease is the leading cause of dementia. It progressively worsens multiple aspects of health over time, from short-term memory loss to behavioral changes to loss of bodily functions. The actual cause of Alzheimers is currently unknown. One widely-accepted hypothesis proposes that Alzheimers is caused by the accumulation of misfolded proteins in the brain. Unfortunately, many drugs targeting misfolded proteins perform poorly in clinical trials, hinting that this hypothesis might be wrong. Misfolded proteins might be another side effect, not the cause.
Researchers recently published a new line of evidence supporting a hypothesis that Alzheimers might be a result of an infection by oral bacteria P. gingivalis. The bacteria produces toxins called gingipains that are found to accumulate in the brain of Alzheimers patients. The gingipains degrade human proteins, giving rise to the infamous misfolded proteins. The researchers also developed chemical compounds that could neutralize gingipains. Mice injected with gingipains developed degenerate brain cells, while mice that were pretreated with neutralizing compounds beforehand maintained healthy brain cells.
Managing Correspondent: Veerasak Srisuknimit
Dementia And Infections: Understanding The Connection
Chronic illness can affect your;life in many ways ranging from annoying to life-threatening. Recognizing illness early;on in yourself or a loved one may allow;for a better quality of life and even more time to live.
One such illness is Dementia. Not many conditions devastate a family quite like this one.
Arming yourself with information may help you combat the effects of this disease. Dementia and infections interplay with one another, and learning this information can save a loved ones life.
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Who Is Affected By Utis And How Are They Treated
Women are more commonly affected by them than men. Around half of women will need treatment for at least one UTI during their lifetime.
If treated with the right antibiotics, UTIs normally cause no further problems and the infection soon passes. Though complications are uncommon, they can be serious and include kidney damage and blood poisoning, which can be fatal.
Compatibility Of Central Nervous System Alzheimer’s Disease Pathology With Infections
AD neurohistopathology is characterized by the simultaneous presence of neuronal degeneration, intraneuronal neurofibrillary tangles and neuropil threads, and extracellular -amyloid plaques within particular regions of the brain. Neurofibrillary tangles and neuropil threads reside inside nerve cell bodies and dendritic processes, respectively, and arise as the result of tau hyperphosphorylation, which causes tau to accumulate and aggregate into insoluble fibrils . A plaques, on the other hand, accumulate in extracellular spaces as the result of gradual deposition and accumulation of specific A peptides . Plaque-forming A peptides are derived from the stepwise cleavage of APP, an integral membrane glycoprotein. APP is first cleaved by – and -secretase into N– and carboxyl terminal fragments . Next, the carboxyl terminal fragments are cleaved by -secretase into 39 to 42 amino acid residue long A peptides, of which the 42 and 40 amino acid residue long peptides primarily constitute the AD A plaques .
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Frontiers In Aging Neuroscience
University of Texas Health Science Center at Houston, United States
University of Texas Health Science Center at Houston, United States
The editor and reviewers’ affiliations are the latest provided on their Loop research profiles and may not reflect their situation at the time of review.
Treatment With Antifungal Agents
Clinical trials with antifungal compounds were proposed by Alonso et al. . Voriconazole, fluconazole, flucytosine and amphotericin B deoxycholate are antifungals with good CNS permeability that may be suitable for this purpose. In some cases, it may be beneficial to combine such treatments with neurosurgery, as noted in a recent review by Goralska et al. . Combined therapies should also be considered for AD patients exhibiting signs of a multifungal infectious burden .
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The Amyloid And Infection Theories Converge
There is a world in which both theories are right. As Being Patient considered earlier this year, these two theories might not be inherently contradictory: Mounting research points to the possibility that amyloid, a key biomarker Alzheimers thus thought by many to be the cause, may actually form the villainous clumps in order to protect the brain from infection. However, the relationship between beta-amyloid clumps and Alzheimers is not so straightforward.;
The Nature article discusses the research of both Rudolph Tanzi, a neurogeneticist at Massachusetts General Hospital, who found that the formation of amyloid plaques is a response to the presence of viruses, and who so named the theory the Antimicrobial Protection Hypothesis; and the research of Yueming Li, a chemical biologist at Memorial Sloan Kettering Cancer Center, who co-authored a study that found that when a virus enters the brain, a protein called IFITM3 activates and increases beta-amyloid production. This increase in beta-amyloid production grows more severe with age, corresponding neatly to Alzheimers.
However, the researchers are yet to find causation. Tanzi says that definitively observing the process of infection to amyloid response to Alzheimers, end to end, wont come anytime soon: He told Nature, We havent seen a smoking gun.