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New Findings On Alzheimer Disease

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Last Updated: 17 October 2020

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General | Latest Info

As the most common form of Dementia and the sixth - leading cause of death in the US, Alzheimer's Disease is not foreign to Americans. Many in the US know someone battling a disease or disease that doctors are still continuing to understand. While the majority of previous research has been focused on treatment, researchers are beginning to shift their attention toward prevention. In recent virtual presentation in partnership between Alzheimers Associations Michigan chapter and Michigan Alzheimers Disease Research Center, Bruno Giordani, ph. D, professor in departments of psychiatry, neurology and psychology, discussed science behind Alzheimers Disease as well as the latest research from the most recent Alzheimers Association International Conference. According to Giordani, new research findings lead to an entire change in emphasis of research, as more evidence was released to support risk - reducing tactics over later treatment. Alzheimer's Disease involves memory loss, confusion and spatial difficulties, which all come down to the existence of amyloid plaques. Amyloid plaques, or hallmarks of Alzheimer's Disease, as Giordani calls them, are clumps of misshapen proteins that form between nerve cells and essentially act as roadblocks for memory. Cell death also occurs in specific areas of the brain, such as the hippocampus, which is critical for areas of cognition like memory and spatial navigation. Scientists are gaining better understanding of the course of Alzheimer's Disease, which progresses from prodromal or pre - clinical period to mild cognitive impairment and then Dementia. Knowledge of this path, as well as earlier tracking of amyloid, has given doctors the chance to work toward risk diagnosis and preventative medications, as opposed to later treatment of disease. Id usually tell you about all the exciting new amyloid drugs present at AAIC meeting; amyloid busters that we can apply to get rid of amyloid in the brain. Frankly, these have not worked out as expect, Giordani explain. Researchers are now attempting to disrupt the process even earlier, before amyloid plaques form and begin to disturb memory. In recent discussion with Giordani, he highlighted news that Biogen, American biotechnology company, completed submission to the US Food and Drug Administration for review of aducanumab, investigational treatment for Alzheimer's Disease that targets amyloid in the brain in hopes of reducing its buildup. If approve, aducanumab would become the first therapy to reduce clinical decline of Alzheimer's Disease and would also be the first therapy to demonstrate that removing amyloid beta results in better clinical outcomes, which could be significant news for Alzheimer's treatment. Researchers are also examining how parts of the body, other than the brain, may play a role in disease development. Studies have looked into the effect of various medications individuals are already taking, such as insulin, and are finding promising results. Study looking at inhaled insulin show some cognitive and amyloid - tau distribution improvements, but the type of inhaler seems to make a big difference. Other approaches include studying gingivitis and other markers of inflammation, which Giordani says may help track disease process earlier on as well.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

The hope for future drugs

Finding out if you or your loved one has Alzheimer's Disease can be difficult, confusing and scary. Fortunately, future is looking brighter as researchers and organizations like the Alzheimers Association work towards finding a cure. Learn more about disease, what preventative measures you can take, and current therapies being Study. First discovered by Dr. Alois Alzheimer in 1906, Alzheimer's Disease is a type of Dementia that causes issues with memory, thinking and behavior. Typically, symptoms develop and worsen over time, eventually becoming severe enough to interfere with daily tasks. There is not one single cause of Alzheimers, but risk factors include: age - people tend to develop Alzheimers at age 65 and older. Family history - if you have an immediate family member with a disease, youre more likely to develop it yourself. Genetics - Certain genes, like apolipoprotein E, are linked to Alzheimer's Disease. While there is currently no known cure for Alzheimer's Disease, there are medications or other treatments doctors can recommend in order to help ease symptoms and delay progression of the disease. At present, there are five Alzheimer's drugs approved by the US Food and Drug Administration to treat symptoms of the disease, but they do not treat its cause or progression. There are no known methods of preventing disease. However, researchers have focused on overall healthy lifestyle choices as a way to prevent decline, including: quitting smoking Regular exercise Cognitive training exercise Plant - base diet Consume antioxidants Interact socially we use Life Stations at Edgewood to help our residents spark old memories and create activities that encourage interest, movement and interaction. Make up of old gardening supplies, baby dolls and other items, these stations help residents revisit and retain memories while also inspiring new moments of joy. The next generation of drug therapies is under research, and they give some hope for the future of preventing and curing Alzheimer's Disease. The following are examples of medications being analyze:

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Alzheimer's prevention trials

The World Alzheimer's Report 2015 reveals that 46. 8 million people worldwide were living with dementia in 2015, and the total global societal cost of dementia was estimated to be US $818 billion. Alzheimer's Disease is the most common dementia type and may account for 60 - 70% of dementia cases. Ads typically present progressive memory decline initially, which is accompanied or followed by other cognitive dysfunctions, such as visuospatial abnormalities, navigation difficulties, executive problems, and language disturbance. These cognitive impairments further affect daily life activities, and many behavioral psychological symptoms of dementia usually occur during the disease course. Pathological evidence regarding AD shows that degeneration in cholinergic neuron - rich regions, namely nucleus basalis of Meynert, frontal cortex, anterior cingulate cortex, and posterior cingulate cortex, is associated with memory loss, agitation, and apathy. Acetylcholine has been shown to be highly correlated with memory function, including memory encoding, consolidation, storage, and retrieval process. Currently, at least three cholinesterase inhibitors approved by the US Food and Drug Administration are being used to treat AD, with some clinical improvement in cognition and global function. However, AChEIs can only improve cognitive symptoms of AD for certain periods but cannot modify disease course. The real causes of AD are still unclear. Two pathological hallmarks of AD exist, in terms of senile plaques, which consist of Amyloid fibrils composed of Amyloid - beta peptide and neurofibrillary tangles consisting of hyperphosphorylated tau protein. Another essential finding is brain atrophy, particularly in the hippocampus. The proposition that accumulation is a central event in AD pathogenesis was initially proposed by three independent groups in 1991. All mutant genes of hereditary, Autosomal, and Dominant familial AD, including Amyloid precursor protein, presenilin 1, and presenilin 2, encode major proteins involved in Amyloid metabolism. Patients with trisomy 21 have APP gene locations with more Amyloid accumulation and high AD risk in late life because they have one more copy of APP gene, which results in increased Amyloid production. Previous studies have shown that cerebral deposition of fibrils can occur decades before an individual shows clinical symptoms. Molecular imaging studies such as those using Amyloid positron emission tomography have shown that deposition reaches plateau before brain atrophy can be identified from structural magnetic resonance imaging and cognitive symptoms. The Amyloid hypothesis has been the mainstream explanation for AD pathogenesis for decades, but all prior Clinical Trials involving Amyloid burden reduction fail. Tau accumulation, which might be a consequence of neuronal damage, was proposed to begin between AD Clinical symptom development and accumulation. Neurofibrillary tangles and quantitative neuronal loss, but not Amyloid plaques, have been found to correlate with disease severity and dementia duration. Moreover, PET studies have shown that spatial patterns of tau tracer binding are closely linked to neurodegeneration patterns and clinical presentation in patients with AD. Recently, biomarkers of Amyloid, tau, and neurodegeneration were used for precisely diagnosing AD. Furthermore, brains of patients with AD exhibit evidence of sustained inflammation.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Summary

In 1901, Karl Deter, railway worker, admitted his fifty - one - year old wife, Auguste, to a psychiatric institution with symptoms of memory loss, confusion, violent outbursts, and inability to use language. According to Karl, Auguste symptoms began to emerge in the late 1890s and were quite uncommon for person he had come to know. She had become increasingly fearful and anxious and would sometimes scream loudly for several hours. Her condition became so overwhelming and debilitating that her family could no longer manage her care. For the next five years, until she passed away, Auguste remained at the institution and was observed by German psychiatrist, Alois Alzheimer. After her death, Alzheimer performed histological studies on Auguste Deters brain tissue. In the process, he discovered two abnormalities: Large abnormal clumps had formed between neurons, and ropelike tangles had formed inside neurons. Calling these abnormalities peculiar Disease of cortex, Alzheimer presented his findings at a 1906 psychiatric conference in Germany, marking the first documented case of what is now known as Alzheimer's Disease. Over the next five years, eleven similar cases were Report in medical journals. Today, more than one hundred years later, there are approximately 35. 6 million people suffer from Alzheimer's Disease worldwide. To the shock of many, 2010 World Alzheimer's Report project that this number will almost double to 65. 7 million cases by 2030 and will more than triple to 115. 4 million cases by 2050. Alzheimer's Disease is categorized as an incurable, degenerative neurological disorder. In popular language, Alzheimer's Disease is commonly used interchangeably with the term Dementia, but they are not the same. Dementia is a general term used to describe decline in cognitive abilities and can be associated with a number of different neurological or psychiatric diseases. An important distinction, Alzheimer's Disease is the most common cause of Dementia, accounting for 60% to 80% of all Dementia diagnose. It is primarily characterized by loss of short - term memory as well as impairments in other cognitive functions such as language, problem solving, attention, and orientation. As disease progress, severe mood swings and unprovoked aggression are common. Eventually, patient lose almost all language ability and motor function. For most definitive diagnosis, scientists use postmortem analysis of brain tissue. Tissue abnormalities first defined by Alzheimer's as clumps and tangles among neurons in the cortex are more specifically defined as amyloid plaques and neurofibrillary tangles. Plaques are deposits of protein called beta - amyloid, which scientists believe is one of the earliest signs of the disease process. Over time, buildup of this protein in the brains of Alzheimer's patients eventually disrupts effective communication between neurons. Scientists hypothesize that these amyloid accumulations can themselves trigger formation of neurofibrillary tangles, which are made of different protein called p - tau and have a distinct stringlike appearance. Like plaques, these tangles also interfere with neurons, but they do so by accumulating inside of them in large amounts and eventually killing them.


Symptoms

Memory problems are typically one of the first signs of cognitive impairment related to Alzheimer's disease. Some people with memory problems have a condition called mild cognitive impairment. In MCI, people have more memory problems than normal for their age, but their symptoms do not interfere with their everyday lives. Movement difficulties and problems with sense of smell have also been linked to MCI. Older people with MCI are at greater risk for developing Alzheimers, but not all of them do. Some may even go back to normal cognition. First symptoms of Alzheimers vary from person to person. For many, decline in non - memory aspects of cognition, such as word - finding, vision / spatial issues, and impaired reasoning or judgment, may signal very early stages of Alzheimers disease. Researchers are studying biomarkers to detect early changes in the brains of people with MCI and in cognitively normal people who may be at greater risk for Alzheimers. Studies indicate that such early detection is possible, but more research is needed before these techniques can be used routinely to diagnose Alzheimer's disease in everyday medical practice.


What Causes Alzheimers Disease?

Doctors use several methods and tools to help determine whether a person who has memory problems has possible Alzheimers dementia or probable Alzheimers dementia. Ask person and family member or friend questions about overall health, use of prescription and over - counter medicines, diet, past medical problems, ability to carry out daily activities, and changes in behavior and personality. Conduct tests of memory, problem solving, attention, counting, and language. Carry out standard medical tests, such as blood and urine tests, to identify other possible causes of problem Perform brain scans, such as computed tomography, magnetic resonance imaging, or positron emission tomography, to rule out other possible causes for symptoms. These tests may be repeated to give doctors information about how persons memory and other cognitive functions are changing over time. Alzheimer's Disease can be definitely diagnosed only after death, by linking clinical measures with examination of brain tissue in autopsy. People with memory and thinking concerns should talk to their doctor to find out whether their symptoms are due to Alzheimers or another cause, such as stroke, tumor, Parkinsons Disease, sleep disturbances, side effects of medication, infection, or non - Alzheimers dementia. Some of these conditions may be treatable and possibly reversible. If diagnosis is Alzheimers, beginning treatment early in the disease process may help preserve daily functioning for some time, even though the underlying disease process cannot be stopped or reverse. Early diagnosis also helps families plan for the future. They can take care of financial and legal matters, address potential safety issues, learn about living arrangements, and develop support networks. In addition, early diagnosis gives people greater opportunities to participate in clinical trials that are testing possible new treatments for Alzheimer's Disease or other research studies.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

From mouse to man

In current research, which features in Nature Communications, scientists measure neuronal death key process underlying symptoms of Dementia in mouse models of Alzheimers Disease, as well as in people with MCI and those with Alzheimers Disease. They measure how many neurons have died using protein called HMGB1, which dying neurons release. They measured levels of this protein in fluid surrounding the spinal cord of 26 people with MCI and 73 people with Alzheimer's Disease. Researchers also carried out an innovative new test, using a new biomarker called pSer46 - MARCKS to detect dying neurons at different stages of disease in the brains of Alzheimers Disease MODEL mice and people with MCI. Neuronal death is obviously very important in the development of Alzheimers but is notoriously difficult to detect in real time because dying cells cannot be stained using chemical or immunohistological methods, explains lead author of the study, Hikari Tanaka. Researchers were surprised to find that neurons die much earlier than they expect. In fact, participants with MCI had more neuronal deaths than those with Alzheimer's Disease.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Trapped YAP

Scientists may also have discovered what causes neurons to die SO early in the disease process, suggesting that a protein called YAP is responsible. Previous genetic studies have found a link between YAP and Alzheimer's disease. Yap, which regulates neuronal death, was present in lower levels in people with MCI. Interestingly, researchers found missing YAP trapped inside clumps of beta - Amyloid deposits that have the most known association with Alzheimer's disease. This finding may change how scientists think about Alzheimer's disease. Popular opinion among scientists is that beta - Amyloid Protein is the first trigger for Alzheimer's disease, leading to death of neurons. They call this Amyloid hypothesis. However, these new findings suggest that loss of YAP Protein, which happens before Amyloid build up in the brain, might actually be the main cause of neuronal death. This discovery might change Amyloid hypothesis, says senior author Hitoshi Okazawa.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

A new treatment option?

Anti - amyloid aggregation agents hypothesis that aggregation leads to toxic oligomeres has driven research into studying compounds that could prevent this aggregation. The only aggregation inhibitor reaching phase III is synthetic glycosaminoglycan 3 - amino - 1propaneosulfonic acid. It is designed to interfere with the binding of glycosaminoglycanes and. Disappointing results of the North American phase III trial in year 2007 have led to the discontinuation of the European phase III trial. Nevertheless, 3APS will now be commercialized as a branded nutraceutical. However, recent data suggest that tramiprosate promotes abnormal aggregation of tau protein in neuronal cells. These results emphasize the importance of testing potential drugs for treatment of AD on both types of pathology. Another molecule undergoing testing is colostrinin, proline - rich polypeptide complex derived from sheep colostrum. Colostrinin inhibits aggregation and neurotoxicity in cellular assays and improves cognitive performance in animal models. Although the phase II trial demonstrated modest improvements in Mini Mental State Evaluation scores for patients with mild AD over a treatment period of 15 months, this beneficial effect was not sustained during the additional 15 months of continued treatment. Another compound named scyllo - inositol is able to stabilize oligomeric aggregates and inhibit toxicity in mouse hippocampus. An 18 - month, randomize, double - blind, placebo - control, dose - ranging, safety and efficacy study of oral scyllo - inositol in participants with mild to moderate AD has been carried out by Transition Therapeutics / Elan. Long - term follow - up class II Study in subjects with AD provides insufficient evidence to support or refute the benefit of ELND005. Primary Clinical efficacy outcomes were not significant. Safety and cerebrospinal fluid biomarker results will guide selection of optimal dose for future studies, which will target earlier stages of AD. Drugs interfering with metals, zinc and copper are both involved in the aggregation of A42. Several chelators of Zn / Cu have been shown to inhibit aggregation in vitro and in animal studies. Pbt2 is a second - generation 8 - OH quinoline metal - protein - attenuating compound that affects Cu2 + - mediate and Zn2 + - mediate toxic oligomerization recent phase IIA Study concluded that the safety profile is favorable for ongoing development of PBT2. Effect on putative biomarkers for AD in CSF but not in plasma suggests central effect of drug on metabolism. Cognitive efficacy was restricted to two measures of executive function. In post hoc analysis, cognitive, blood marker and CSF neurochemistry outcomes from the trial were subject to further analysis. Ranking responses to treatment after 12 weeks with placebo, PBT2 50 mg and PBT2 250 mg reveal that proportions of patients showing improvement were significantly greater in the PBT2 250 mg group than in the placebo group. These findings further encourage larger - scale testing of PBT2 for AD. It is generated through proteolytic processing of transmembrane peptide APP. Apps can be cloven by two competing proteases, Secretase and Secretase. Only cleavage by Secretase, followed by - Secretase cleavage, which in AD is the dominant pathway, will lead to production of A40 and A42.


Keeping tau from tangling

Methylene blue, known as phenothiazine, is evaluated in AD studies as a potential tau aggregation inhibitor. The problem with this drug is that urine is colored blue, resulting in lack of blinding. A Monotherapy trial with MB on mild and moderate AD has demonstrated some clinical benefit in moderate, but not mild AD. 82 However, methodology of study, as blinding is impossible, has been highly criticize. 83 methylene blues derivative TRx0237 which was studied in phase 3 failed finally to show efficacy, and based on analysis of results, new phase 2 / 3 study named LUCIDITY was started 1 year ago in subjects with mild AD with a lower dose of agent.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Sources

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

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