Alzheimer infection: there is always the right way to cure

Alzheimer infection is a type of dementia which influences moderately aged and more established individuals. It is a dynamic sickness that gradually executes the victimized people nerve cells in the mind.

Alzheimer is a somewhat complex ailment that is by all accounts created by a few impacts. Alzheimer is figured to be a lethal sickness; however the standard reason for death is typically another disease specially named as pneumonia which can grow as a difficulty in an individual as of now extremely debilitated by Alzheimer. Amid the early phases of Alzheimer there are individuals who will have the capacity to adapt exceptionally well to the sickness however as time advances, the later stages may demonstrate very much as the seriousness of the condition takes its toll and sufferers are once in a while not ready to do anything for themselves and get to be confined to bed.

Concentrating on the foremost side effects

Concentrate on that your cerebrum has an illness and it is dynamic so submit time to handle the issue and if nothing else lets moderate the sickness. Our studies as www.newspsychology.com prove, for Alzheimer ailment there is right now no cure. The reason and change of Alzheimer's sickness is not well seen, but rather is connected with plaques and tangles in the mind. Notice is a mind issue named for German doctor Alois Alzheimer. In its most basic structure, it happens in individuals more than 65 years of age despite the fact that a less pervasive early onset shape exists in their own form. The character played by the foremost guardian is often taken by the accomplice or a decent relative.

Consolidated medications

Consolidating in the meantime with other AD medications may be more compelling than any single treatment. Additionally, different medicines may help control behavioural side effects, for example, restlessness, fomentation, meandering, tension, and misery. 

Alzheimer Disease – read and knows more about!

Memory misfortune is typical. While it may be ordinary to turn into a bit absent minded as we age, genuine memory misfortune is not typical. About 18 million individuals worldwide is a victim of the disease named Alzheimer.

Any serious loss of memory, for example, which connected with Alzheimer or different types of dementia, is not ordinary under any condition. There are some medication and non-tranquilize medicines that give incidentally alleviation to both behavioural and cognitive manifestations of Alzheimer's disease. Alzheimer's ailment is a gathering issue including the parts that control thought, memory, and dialect. Alzheimer's sickness is getting to be sadly normal. It is assessed in a much right way now.

Cognitive decrease in seniority

Accoriding to our research at www.newspsychology.com, around 4.5 million Americans have Alzheimer Disease. Cognitive decrease in seniority has been depicted all through history. Be that as it may, it was not until the early piece of the 20th century that an accumulation of cerebrum cell variations from the norm was particularly distinguished by a German doctor, Alois Alzheimer, for whom the fear sickness was known. The primary fact to recollect before taking any of these Alzheimer's meds, is to enlighten your specialist concerning some other pharmaceutical that you are as of now taking, and whatever other wellbeing issues that you may have. The way that this medication works, is that it serves to direct the movement of Glutamate in the cerebrum.

Vital intense cell reinforcement

The most intense cell reinforcement is thought to be OPC's, experimentally known as Oligomeric Proanthocyanidins. OPC's are found in the skin and seed of grapes, furthermore found in pine bark. Generally, OPC's found in pine bark are called Pycnogenol and those found in grapes are called OPC. It is the most widely recognized sort of dementia, representing approximately seventy percent of diagnosed cases, and it knows no boundaries, being spread crosswise over distinctive societies and influencing both guys and females in equivalent measure.

Emotional neglect in children linked to increased stroke risk later in life

The results from a new study by neurological researchers from the Rush Alzheimer's Disease Center at Rush University Medical Center suggest that people who were emotionally neglected as children may have a higher risk of stroke in later adulthood.

"Studies have shown that children who were neglected emotionally in childhood are at an increased risk of a slew of psychiatric disorders. However, our study is one of few that looked at an association between emotional neglect and stroke," said study author Robert S. Wilson, PhD, a neuropsychologist at Rush.

The findings are published in the September 19, online issue of Neurology, the medical journal of the American Academy of Neurology.

For the study, 1,040 participants in the Memory and Aging Project who did not have dementia and were 55 years of age or older took a survey measuring physical and emotional abuse before the age of 18. The retrospective survey questions focused on whether the participant felt loved by their parents or caregiver when they were younger, were made to feel afraid or intimidated and whether they were punished with a belt or other object. Questions about parental divorce and the family's financial needs were also included.

Over a period of three and a half years, 257 people in the study died, of which 192 had a brain autopsy to look for signs of stroke. Forty of the participants had evidence of a stroke based on their medical history or an examination. A total of 89 people had signs of a stroke based on the autopsy results.

The study found that the risk of stroke was nearly three times higher in those people who reported a moderately high level of childhood emotional neglect than those who reported a moderately low level. The results stayed the same after considering factors such as diabetes, physical activity, smoking, anxiety and heart problems.

"Interestingly, the autopsy showed emotional neglect was associated with the presence of cerebral infarctions," said Dr. David A. Bennett, director of the Rush Alzheimer's Disease Center and co-author of the study. "The results add to a growing body of evidence suggesting that early life factors such as traumatic childhood experiences influence the development of physical illness and common chronic conditions of old age."

Wilson noted that a limitation of the study is that neglect was reported from memory many years after occurrence, so participants may not have remembered events accurately.

The study was supported by the National Institutes of Health and the Illinois Department of Public Health.


Journal Reference:

  1. Robert S. Wilson, Patricia A. Boyle, Steven R. Levine, Lei Yu, Sophia E. Anagnos, Aron S. Buchman, Julie A. Schneider, and David A. Bennett. Emotional neglect in childhood and cerebral infarction in older age. Neurology, September 19, 2012 DOI: 10.1212/WNL.0b013e31826e25bd

Test can help make diagnosis of Creutzfeldt-Jakob disease

A new guideline released by the American Academy of Neurology may help doctors in making the diagnosis of Creutzfeldt-Jakob disease. The guideline is published in the September 19, 2012, online issue of Neurology®, the medical journal of the American Academy of Neurology.

Creutzfeldt-Jakob disease is a rare, always fatal brain disorder that involves quickly progressing dementia. New cases appear in about one person per million each year worldwide and confirming the diagnosis is challenging. People with the disease can have a wide range of symptoms. Many other conditions can cause similar symptoms, and with some of these conditions the dementia can be treated.

The guideline focused only on the diagnosis of sporadic Creutzfeldt-Jakob disease.

While several tests are available to help diagnose sporadic Creutzfeldt-Jakob disease, a brain biopsy is the most accurate test that can be performed on a person living with the disease. Brain biopsy is potentially dangerous.

The guideline examined the diagnostic accuracy of testing for a protein called 14-3-3 in the spinal fluid. The guideline authors reviewed all of the available evidence on the test, which included samples of 1,849 people with suspected sporadic Creutzfeldt-Jakob disease from nine studies.

They found that in cases where doctors strongly suspect Creutzfeldt-Jakob to be the cause of the dementia, the test can be helpful in reducing the uncertainty of the diagnosis. However, the test is not accurate enough to diagnose the disease with certainty or to rule it out completely. The test has a sensitivity of about 92 percent and a specificity of about 80 percent. Sensitivity is the percentage of patients with the disease who have a positive test result, and specificity is the percentage of patients who do not have the disease and who are correctly identified as having a negative test result.

The guideline determined that the 14-3-3 protein test can be useful when the probability of the person having Creutzfeldt-Jakob disease is between 20 percent and 90 percent.

"This means that if the physician considers the likelihood of Creutzfeldt-Jakob disease to be extremely low or extremely high, then testing for 14-3-3 protein would not be useful regardless of the result," said guideline author Taim Muayqil, MBBS, FRCPC, of King Saud University in Riyadh, Saudi Arabia, and a member of the American Academy of Neurology.

Muayqil noted that only doctors experienced in diagnosing dementia should determine whether the 14-3-3 protein test is needed and how results should be interpreted.


Journal Reference:

  1. Taim Muayqil, Gary Gronseth, and Richard Camicioli. Evidence-based guideline: Diagnostic accuracy of CSF 14-3-3 protein in sporadic Creutzfeldt-Jakob disease: Report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology, 2012 DOI: 10.1212/WNL.0b013e31826d5fc3

Alzheimer’s disease in men linked to low levels of hormone IGF-1

— Low serum levels of insulin-like growth factor-1 (IGF-1) and insulin-like growth factor binding protein-3 (IGFBP-3) are associated with Alzheimer's Disease in men, but not women, according to a recent study accepted for publication in The Endocrine Society's Journal of Clinical Endocrinology & Metabolism (JCEM).

IGF-1 and IGFBP-3 are involved in longevity and could be beneficial to cognition, especially in Alzheimer's disease where experimental studies have shown that IGF-1 opposes the main pathological processes of Alzheimer's disease. The current study investigated the relationship between IGF-1 and IGFBP-3 serum levels and cognitive impairment, including Alzheimer's disease.

"At this time, no curative treatment is available for Alzheimer's disease so focus on modifiable associated factors is of major importance," said Emmanuelle Duron, MD, PhD, of Broca Hospital in Paris, France and lead author of the study. "Our research shows a possible usefulness of IGF-1 in Alzheimer's disease treatment, especially in early stages."

In this multicentric cross-sectional study, researchers measured IGF-1 and IGFBP-3 serum levels in 694 elderly subjects (218 men and 476 women). Of the study participants, 481 had memory complaints and were diagnosed with Alzheimer's disease or mild cognitive impairment. Duron and her colleagues found that IGF-1 and IGFBP-3 serum levels were significantly associated with cognitive status in men, but not in women.

"Our cross-sectional association does not mean a causal relationship," notes Duron. "Our results justify a longitudinal study to evaluate whether circulating IGF-1/IGFBP-3 are predictive of cognitive decline according to gender."

Other researchers working on the study include: Benoit Funalot, Nadege Brunel, Cecile Viollet, Jacques Epelbaum and Yves le Bouc of Institut National de la Santé et de la Recherche Médicale (INSERM) in Paris France; Joel Coste and Laurent Quinquis of Hotel Dieu in Paris, France; Joel Belmin of Charles Foix Hospital in Seine, France; Pierre Jouanny of Centre Hospitalo in Amiens, France; Florence Pasquier of Hopital Roger Salengro in Lille, France; Jean-Marc Treluyer of France Unite de Recherche Clinique in Paris, France; and Olivier Hanon of Broca Hospital in Paris, France.


Journal Reference:

  1. Duron E, Funalot B, Brunel N, Coste J, Quinquis L, Viollet C, Belmin J, Jouanny P, Pasquier F, Treluyer JM, Epelbaum J, le Bouc Y, Hanon O. Insulin-Like Growth Factor-I and Insulin-Like Growth Factor Binding Protein-3 in Alzheimer's Disease. J Clin Endocrinol Metab., 2012 Sep 26

Common RNA pathway found in ALS and dementia

Two proteins previously found to contribute to ALS, also known as Lou Gehrig's disease, have divergent roles. But a new study, led by researchers at the Department of Cellular and Molecular Medicine at the University of California, San Diego School of Medicine, shows that a common pathway links them.

The discovery reveals a small set of target genes that could be used to measure the health of motor neurons, and provides a useful tool for development of new pharmaceuticals to treat the devastating disorder, which currently has no treatment or cure.

Funded in part by the National Institutes of Health and the California Institute for Regenerative Medicine (CIRM), the study will be published in the advance online edition of Nature Neuroscience on September 30.

ALS is an adult-onset neurodegenerative disorder characterized by premature degeneration of motor neurons, resulting in a progressive, fatal paralysis in patients.

The two proteins that contribute to the disease — FUS/TLS and TDP-43 — bind to ribonucleic acid (RNA), intermediate molecules that translate genetic information from DNA to proteins. In normal cells, both TDP-43 and FUS/TLS are found in the nucleus where they help maintain proper levels of RNA. In the majority of ALS patients, however, these proteins instead accumulate in the cell's cytoplasm — the liquid that separates the nucleus from the outer membrane, and thus are excluded from the nucleus, which prevents them from performing their normal duties.

Since the proteins are in the wrong location in the cell, they are unable to perform their normal function, according to the study's lead authors, Kasey R. Hutt, Clotilde Lagier-Tourenne and Magdalini Polymenidou. "In diseased motor neurons where TDP-43 is cleared from the nucleus and forms cytoplasmic aggregates," the authors wrote, "we saw lower protein levels of three genes regulated by TDP-43 and FUS/TLS. We predicted that this, based on our mouse studies, and found the same results in neurons derived from human embryonic stem cells."

In 2011, this team of UC San Diego scientists discovered that more than one-third of the genes in the brains of mice are direct targets of TDP-43, affecting the functions of these genes. In the new study, they compared the impact of the FUS/TLS protein to that of TDP-43, hoping to find a large target overlap.

"Surprisingly, instead we saw a relatively small overlap, and the common RNA targets genes contained exceptionally long introns, or non-coding segments. The set is composed of genes that are important for synapse function," said principal investigator Gene Yeo, PhD, assistant professor in the Department of Cellular and Molecular Medicine and the Institute for Genomic Medicine at UC San Diego and a visiting professor at the Molecular Engineering Laboratory in Singapore. "Loss of this common overlapping set of genes is evidence of a common pathway that appears to contribute to motor neuron degeneration."

In an effort to understand the normal function of these two RNA binding proteins, the scientists knocked down the proteins in brains of mice to mimic nuclear clearance, using antisense oligonucleotide technology developed in collaboration with ISIS Pharmaceuticals. The study resulted in a list of genes that are up or down regulated, and the researchers duplicated the findings in human cells.

"If we can somehow rescue the genes from down regulation, or being decreased by these proteins, it could point to a drug target for ALS to slow or halt degeneration of the motor neurons," said Yeo.

These proteins also look to be a central component in other neurodegenerative conditions. For example, accumulating abnormal TDP-43 and FUS/TLS in neuronal cytoplasm has been documented in frontotemporal lobar dementia, a neurological disorder that has been shown to be genetically and clinically linked to ALS, and which is the second most frequent cause of dementia after Alzheimer's disease.


Journal Reference:

  1. Clotilde Lagier-Tourenne, Magdalini Polymenidou, Kasey R Hutt, Anthony Q Vu, Michael Baughn, Stephanie C Huelga, Kevin M Clutario, Shuo-Chien Ling, Tiffany Y Liang, Curt Mazur, Edward Wancewicz, Aneeza S Kim, Andy Watt, Sue Freier, Geoffrey G Hicks, John Paul Donohue, Lily Shiue, C Frank Bennett, John Ravits, Don W Cleveland, Gene W Yeo. Divergent roles of ALS-linked proteins FUS/TLS and TDP-43 intersect in processing long pre-mRNAs. Nature Neuroscience, 2012; DOI: 10.1038/nn.3230

New human neurons from adult cells right there in the brain

This is a direct observation of neuronal reprogramming of PDGFR-sorted pericyte-derived cells from the adult human brain by continuous live imaging in culture. Note the change in morphology of a cell coexpressing Sox2 and Mash1 (blue arrow) during reprogramming. Postimaging immunocytochemistry for III-tubulin (white) confirms the neuronal identity of the reprogrammed cell at the end of live imaging. (Credit: Cell Stem Cell, a Cell Press Journal, Karow et al.)

Researchers have discovered a way to generate new human neurons from another type of adult cell found in our brains. The discovery, reported in the October 5th issue of Cell Stem Cell, a Cell Press publication, is one step toward cell-based therapies for the treatment of neurodegenerative diseases, such as Alzheimer's and Parkinson's.

"This work aims at converting cells that are present throughout the brain but themselves are not nerve cells into neurons," said Benedikt Berninger, now at the Johannes Gutenberg University Mainz. "The ultimate goal we have in mind is that this may one day enable us to induce such conversion within the brain itself and thus provide a novel strategy for repairing the injured or diseased brain."

The cells that made the leap from one identity to another are known as pericytes. Those cells, found in close association with the blood vessels, are important for keeping the blood-brain barrier intact and have been shown to participate in wound healing in other parts of the body.

"Now, we reason, if we could target these cells and entice them to make nerve cells, we could take advantage of this injury response," Berninger says.

Further testing showed that those newly converted neurons could produce electrical signals and reach out to other neurons, providing evidence that the converted cells could integrate into neural networks.

"While much needs to be learnt about adapting a direct neuronal reprogramming strategy to meaningful repair in vivo, our data provide strong support for the notion that neuronal reprogramming of cells of pericytic origin within the damaged brain may become a viable approach to replace degenerated neurons," the researchers write.

 

Journal Reference:

  1. Marisa Karow, Rodrigo Sánchez, Christian Schichor, Giacomo Masserdotti, Felipe Ortega, Christophe Heinrich, Sergio Gascón, Muhammad A. Khan, D. Chichung Lie, Arianna Dellavalle, Giulio Cossu, Roland Goldbrunner, Magdalena Götz, Benedikt Berninger. Reprogramming of Pericyte-Derived Cells of the Adult Human Brain into Induced Neuronal Cells. Cell Stem Cell, 2012; 11 (4): 471 DOI: 10.1016/j.stem.2012.07.007

Home-based assessment tool for dementia screening

ClockReader is the actual test and is taken with a stylus and computer or tablet. The participant is given a specific time and instructed to draw a clock with numbers and the correct minute and hour hands. Once completed, the sketch is emailed to a clinician, who uses the ClockAnalyzer Application to score the test. The software checks for 13 traits. They include correct placement of numbers and hands without extra markings. People with cognitive impairment frequently draw clocks with missing or extra numbers. Digits are sometimes drawn outside of the clock. The time is often incorrect. (Credit: Georgia Institute of Technology)

With baby boomers approaching the age of 65 and new cases of Alzheimer's disease expected to increase by 50 percent by the year 2030, Georgia Tech researchers have created a tool that allows adults to screen themselves for early signs of dementia. The home-based computer software is patterned after the paper-and-pencil Clock Drawing Test, one of health care's most commonly used screening exams for cognitive impairment.

"Technology allows us to check our weight, blood-sugar levels and blood pressure, but not our own cognitive abilities," said project leader Ellen Yi-Luen Do. "Our ClockMe System helps older adults identify early signs of impairment, while allowing clinicians to quickly analyze the test results and gain valuable insight into the patient's thought processes."

ClockReader is the actual test and is taken with a stylus and computer or tablet. The participant is given a specific time and instructed to draw a clock with numbers and the correct minute and hour hands. Once completed, the sketch is emailed to a clinician, who uses the ClockAnalyzer Application to score the test. The software checks for 13 traits. They include correct placement of numbers and hands without extra markings. People with cognitive impairment frequently draw clocks with missing or extra numbers. Digits are sometimes drawn outside of the clock. The time is often incorrect.

In addition to scoring automatically and consistently, ClockAnalyzer records the duration of the test and the time between each stroke. The software also replays the drawing in real-time, allowing a clinician to watch the drawing being created to observe any behavior abnormality.

"The traditional paper-and-pencil test is usually overseen by a technician and later scored by a clinician, who scores the test based only on the finished drawing," said Do, a professor in Georgia Tech's Colleges of Computing and Architecture. "By looking at the sketch, the scorer is not able to decipher whether the person struggled to remember certain numbers while drawing the clock. The ClockMe system's timing software highlights those delays."

And, because they're saved electronically, the drawings can be used to easily compare a person's cognitive ability progress or regression over time. Do's research found that traditional tests are often filed in a folder and are rarely used for future comparison.

The ClockMe system was initially tested at the Emory Alzheimer's Disease Research Center in Atlanta, where it's currently being used in addition to the traditional paper-and-pencil test. Despite a lack of computer literacy, all of the elderly patients who used the software during the study said they had no problems with the pen-based, computer technology.

"For this reason, as well as the ability to send the drawings directly to clinicians for convenient scoring, we envision ClockMe as a viable tool for home-based screening," said Do. "America's health care costs are expected to soar as baby boomers become senior citizens. If a screening tool can be used at home, unnecessary trips to clinics can be eliminated and medical expenses can be saved."

Do and her colleagues are hoping to commercialize the project in the future. Their research was published in September's Journal of Ambient Intelligence and Smart Environments.

This project is supported by the National Science Foundation (NSF) (Award Number SHB-1117665).

New evidence on easing inflammation of brain cells for Alzheimer's disease

 New research proves the validity of one of the most promising approaches for combating Alzheimer's disease (AD) with medicines that treat not just some of the symptoms, but actually stop or prevent the disease itself, scientists are reporting.

The study, in the journal ACS Medicinal Chemistry Letters, also identifies a potential new oral drug that the scientists say could lead the way.

Wenhui Hu and colleagues point out that existing drugs for AD provide only "minimal" relief of memory loss and other symptoms, creating an urgent need for new medicines that actually combat the underlying destruction of brain cells. Research suggests that inflammation of nerve cells in the brain is a key part of that process. One medicine, Minozac, is in clinical trials. But Hu says Minozac still has more space to improve its efficacy. So the scientists sifted through compounds with a molecular architecture similar to Minozac in an effort to find more active substances.

The report describes success in doing so. They discovered one compound that appeared especially effective in relieving nerve inflammation and in improving learning and memory in lab mice widely used in AD research. "In general, this study not only proves that countering neuroinflammation is indeed a potential therapeutic strategy for Alzheimer's disease, but also provides a good lead compound with efficacy comparable to donepezil [an existing AD medicine] for further oral anti-AD drug discovery and development," the report states.


Journal Reference:

  1. Wei Zhou, Guifa Zhong, Xiurong Rao, Hui Xie, Shaogao Zeng, Tianyan Chi, Libo Zou, Donghai Wu, Wenhui Hu. Identification of Aminopyridazine-Derived Antineuroinflammatory Agents Effective in an Alzheimer's Mouse Model. ACS Medicinal Chemistry Letters, 2012; : 120913133048003 DOI: 10.1021/ml3001769

A molecular scissor related to Alzheimer’s disease

The enzyme meprin is located at the cell wall (lined-up white balls). The enzyme binds a protein (red) within its active site cleft (light blue) to cleave it. (Credit: Christoph Becker-Pauly & Xavier Gomis-Rüth)

An international research team led by the Spanish National Research Council (CSIC) and researchers from Kiel University revealed the atomic‐level structure of the human peptidase enzyme meprin β (beta). The enzyme is related to inflammation, cancer and Alzheimer's Disease and is involved in cellular proliferation and differentiation. The knowledge of the enzyme structure will allow for the development of a new medication type different from those known up to now.

The study was published in the current issue of the Proceedings of the National Academy of Sciences.

"Now that we know how meprin β looks, how it works and how it relates to diseases, we can search for substances that stop its enzyme activities when they become harmful," explains Xavier Gomis-Rüth, researcher at the Molecular Biology Institute of Barcelona, who led the project. Meprin β is an enzyme that is anchored in the outer wall of cells. Its normal function in the human metabolism is to cut off certain proteins, e.g. growth factors, that are also anchored in the cell wall. In this way meprin β releases protein fragments into the environment surrounding the cells — a natural and normal process, as long as it occurs at a certain intensity. However, under specific circumstances, meprin β may function abnormally, and, for example, releases too many protein fragments. The protein pieces than overdo their natural task in the cell surroundings, causing disorder in the human body. Such disorder typically occurs when inflammation, cancer or Alzheimer's Disease get started.

In their study, the scientists found out that meprin β consists of two identical molecules building a dimeric structure with a cleft in the middle. "We also discovered that the active site cleft is something like the scissor of the enzyme, the actual place where the proteins are cleaved," explains Christoph Becker-Pauly, researcher at the Institute of Biochemistry at Kiel University, and principle investigator of the Kiel Collaborative Research Center 877 „Proteolysis as a Regulatory Event in Pathophysiology." Molecular biologist Gomes-Rüth points out to the next research goal: "We now need to find a substance that fits right into the cleft and will thus block the cleaving activity of meprin β." Such a substance could be the key to new therapeutical drugs against inflammation, cancer or Alzheimer's Disease.

The research has been carried out in collaboration with scientists from Max Planck Institute for Biochemistry and Johannes Gutenberg University Mainz (Germany) as well as University of Bern (Switzerland).

 

Journal Reference:

  1. J. L. Arolas, C. Broder, T. Jefferson, T. Guevara, E. E. Sterchi, W. Bode, W. Stocker, C. Becker-Pauly, F. X. Gomis-Ruth. Structural basis for the sheddase function of human meprin   metalloproteinase at the plasma membrane. Proceedings of the National Academy of Sciences, 2012; 109 (40): 16131 DOI: 10.1073/pnas.1211076109