01-27-2013, 07:39 AM
(This post was last modified: 05-04-2015, 12:28 AM by Administrator.)
Doctors who study or treat Alzheimer's disease and its early clinical stages (mild cognitive impairment, MCI) are focused on the obvious problems with short-term memory. However, a new study suggests that people with later development of Alzheimer's disease can have problems much earlier, in the processing of semantic information or data based on previous knowledge, which could have great significance in the manner in which these patients are functioning in everyday life.
First Indications of Cognitive Problems
Terry Goldberg, PhD, a professor of psychiatry and behaviorism in the Hofstra North Shore-LIJ School of Medicine at Hofstra University and director of department for neurocognition in the Alzheimer's Disease and Memory Disorders Center at the Feinstein Institute for Medical Research in in Manhasset, New York, said that doctors have noticed a variety of cognitive disorders in patients with Mild Cognitive Impairment, but they were not systematically studied. A large number of experts noted that some of the patients find even the simplest tasks extremely confusing. In this latest study, which was published in monthly American Journal of Psychiatry, cleverly designed tests are used to analyze the ability of individuals for the processing of semantic information.
Do people with Mild Cognitive Impairment have problems in accessing certain types of prior acquired knowledge? Are there any obvious semantic problems which have not been observed? The answer is yes.
The Experiment
To test the system is semantic processing, dr Goldberg and his colleagues needed a task that does not include a verbal response. That would be confusing, and the results would be more difficult to interpret. They decided to use size to test a person's ability to use semantic information to make a conclusion on two opposed definitions. Doctor Goldberg explained: "If someone is asked what is more, the key or ant, he will respond more slowly than if you ask him what is larger, a house or a key." The greater the difference in size between the two things, the more quickly will the person, being healthy or not , recognize the difference and respond.
The study included 25 patients with mild cognitive impairment (MCI), 27 with Alzheimer's disease and 70 people with no cognitive problems. They found that there are significant differences between healthy controls and patients with Mild Cognitive Impairment and Alzheimer's disease. Doctor Goldberg concluded that the results indicate problems in the processing of semantic information. It is mostly seen when the patients with mild cognitive disorder and Alzheimer's disease cope with the task with small differences in size.
Then they made the task more complicated by showing patients the images of little ants and big houses or big ants and small houses. This time the patients with mild cognitive disorder and with Alzheimer's disease solved the first part of the test without any problems - when they were asked what is bigger, they chose a house, not an ant. But if the pictures did not reflect reality - a big ant looked like a little house - they were confused, answered incorrectly, or they took longer to respond.
Patients with mild cognitive impairment were somewhere between those of healthy and those with Alzheimer's disease. "When the decision was difficult, the reaction time was slower."
Would Damage to The Semantic System Influence The Everyday Functions?
To answer this question, researchers have turned to UCSD scale to evaluate the use of skills, the tool which is used in patients with mild cognitive disorder and Alzheimer's disease and in patients with schizophrenia, to determine the functional deficiencies. The test examines the ability of a person to perform complex checks or to organize a trip to the zoo for a cold day.
It's a good way to check whether someone has a problem with the semantic knowledge. Semantic processing takes place in the left temporal lobe. "The semantic system is organized as a network that reflects the various types of relationships and associations," said the researchers in the study. "Semantic data and knowledge are acquired in the larger intervals, often through a large number of repetitions, and do not reflect what has been recently adopted."
Doctor Goldberg says that this discovery is very important because it might be possible to strengthen by training the connections that arise in semantic processing. "This suggests that patients are getting slow due to semantic and not episodic memory," said Goldberg. Patients will be observed further in order to determine whether the deteriorating semantic problems worsen as the disease progresses.
Within additional article, David P. Salmon, Ph.D., from Department of Neuroscience at the University of California, said that "deficiencies in semantic memory, that this study demonstrated, confirm the suspicion that in patients with mild cognitive impairment of an anamnestic type, happens a slight cognitive impairment. Since the task did not require problematic remembering and reproduction of certain words or linguistic structures, it can be concluded that these shortcomings reflect the early and gradual loss of the integrity of semantic knowledge. "
He added that "This study proves that the deterioration of semantic memory in patients with mild cognitive impairment can contribute to the reduced ability to perform everyday activities."
Institute for Medical Research Feinstein
The Institute for Medical Research Feinstein, based in Manhasset, New York, many leading international scientists are engaged in areas such as Parkinson's disease, Alzheimer's disease, psychiatric disorders, rheumatoid arthritis, lupus, sepsis, genetics, pulmonary hypertension, leukemia, neuroimmunology, and medical chemistry. The institute, which is part of the North Shore Health System , belongs to the top 5% of all state institutes according to scholarships awarded to research centers for health care.
A Major Step Toward Developing The Vaccine For Alzheimer's Disease
A team of researchers from the Center for Research CHU (France, Centre Hospitalier Universitaire) at the University of Laval in Quebec and pharmacological company GlaxoSmithKline (GSK) has found a way to stimulate the natural defense mechanisms of the brain in people who suffer from Alzheimer's disease. This is an important achievement, and its details have been published in the online edition of the journal Proceedings of the National Academy of Sciences. This research opened the door to the development of effective treatment for Alzheimer's disease and toward finding an efficient vaccine.
____________________________________________________________
---- Article by BojanaL----
____________________________________________________________
Treatment for Alzheimer disease:
Modern medicine and well established healthcare system prolonged the average length of the human life. Old age is associated with numerous neurodegenerative disorders; most typical is Alzheimer’s disease. Risk for developing Alzheimer’s disease is increasing with the age. It is estimated that 10% of people over the age of 65, and 50% of those over 85 suffers from Alzheimer’s disease. Most cases develop sporadically and just 1-5 % of Alzheimer’s cases are genetically inherited.
Alzheimer’s disorder is first described in 1906. Post mortem brain analysis and blood markers provided more information on this pathological brain disorder over the past 100 years, but exact trigger for the disease and successful treatment method are still lacking. Alzheimer’s disorder is characterized by brain shrinkage, loss of neuronal connections and disrupted blood brain barrier. Several theories about disorder genesis exist: cholinergic theory, where lack of acetylcholine triggers disorder, herpes simplex virus induced disorder, age related impaired myeline breakage or oxidative stress as a cause of neurodegeneration…Most probable are ones associated with altered metabolism of amyloid precursor protein and tau protein. Amyloid precursor protein is building part of neuronal synapses and essential ingredient of various cell membranes in the body. Proteolitic degradation of amyloid precursor protein results in formation of the fibrial protein - beta amiloid that is found in brain plaques, typical for Alzheimer’s disorder. Beta amiloid alters calcium ion homeostasis (resulting in apoptosis), inhibits enzymatic activity and prevents glucose utilization. Tau protein is essential for development of neuronal polarity; it promotes neuronal microtubule assembly and enhances axonal dynamics. When tau protein is hyperphosphorilated, it becomes insoluble and forms inclusions known as neurofibrillary tangles. Those tangles are associated with neuronal degeneration. Alzheimer’s disease can be diagnosed using couple of techniques: brain imaging (computed tomography or magnetic imaging), through neuropsychological tests or by blood analysis (couple known markers exist). Current treatments are focused on the main attributes of Alzheimer’s disease: dementia (memory loss), depression and cognitive impairments. Medication used is just slowing down the progression of neurodegeneration but it can’t prevent disease. Typical mechanism of action is focused on proteolysis of amyloid precursor protein; latest drugs could prevent proteolysis or bind to already formed beta amyloid prior its aggregation and eliminate it. Other drugs affect distribution of beta amiloid through the brain or decrease the rate of neuroinflammation. Alzheimer’s disease is one of the most common neurodegenerative disorders associated with old age and one of the most expensive to be treated because patients demand special care due to physically, physiologically and socially altered behavior.
Latest discoveries in the stem cells field could move Alzheimer’s treatment in completely new direction. Scientists from the University Of California, Irvine developed new line of stem cells - choroid plexus epithelial cells (CPECs) using human and mouse embryonic cells. Choroid plexus is part of the brain ventricles where cerebrospinal fluid is produced. This liquid is important for cleaning the waste products and metabolites that could damage the brain function. 500 milliliters of cerebrospinal fluid is produced each day, and it is renewed 4 times a day to ensure efficient detoxification of the neuronal tissue. CPECs are forming important blood - cerebrospinal fluid barrier. Neurodegenerative disorders are associated with dysfunctional CPECs and inefficient removal of the waste material (like beta amiloid) from the cerebrospinal fluid. Scientists were familiar with the role and importance of CPECs cells, but until now they couldn’t find the way to produce those cells in vitro. Embryonic cells are pluripotent and different transcription factors determine their cellular faith (direction of their differentiation). After discovering that brain morphogenic factor 4 (BMF4) is responsible for differentiation of the neuronal progenitor cells into CPECs, researchers applied BMF4 to produce sufficient amount of CPECs. Both human and mouse neuronal progenitor cells used in the experiment matured successfully into CPECs after BMF4 was applied. Developed CPECs act just like naturally produced cells; they could integrate in choroid plexus epithelium and form secretory vesicles. Neurological disorders associated with the accumulation of the peptides, proteins and other metabolites that alter normal function of the brain could be treated using CPECs. Scientists are hoping that this approach will be especially helpful in Alzheimer’s and Huntington’s disease as well in treatment of pediatric neurodegenerative disorders.
First Indications of Cognitive Problems
Terry Goldberg, PhD, a professor of psychiatry and behaviorism in the Hofstra North Shore-LIJ School of Medicine at Hofstra University and director of department for neurocognition in the Alzheimer's Disease and Memory Disorders Center at the Feinstein Institute for Medical Research in in Manhasset, New York, said that doctors have noticed a variety of cognitive disorders in patients with Mild Cognitive Impairment, but they were not systematically studied. A large number of experts noted that some of the patients find even the simplest tasks extremely confusing. In this latest study, which was published in monthly American Journal of Psychiatry, cleverly designed tests are used to analyze the ability of individuals for the processing of semantic information.
Do people with Mild Cognitive Impairment have problems in accessing certain types of prior acquired knowledge? Are there any obvious semantic problems which have not been observed? The answer is yes.
The Experiment
To test the system is semantic processing, dr Goldberg and his colleagues needed a task that does not include a verbal response. That would be confusing, and the results would be more difficult to interpret. They decided to use size to test a person's ability to use semantic information to make a conclusion on two opposed definitions. Doctor Goldberg explained: "If someone is asked what is more, the key or ant, he will respond more slowly than if you ask him what is larger, a house or a key." The greater the difference in size between the two things, the more quickly will the person, being healthy or not , recognize the difference and respond.
The study included 25 patients with mild cognitive impairment (MCI), 27 with Alzheimer's disease and 70 people with no cognitive problems. They found that there are significant differences between healthy controls and patients with Mild Cognitive Impairment and Alzheimer's disease. Doctor Goldberg concluded that the results indicate problems in the processing of semantic information. It is mostly seen when the patients with mild cognitive disorder and Alzheimer's disease cope with the task with small differences in size.
Then they made the task more complicated by showing patients the images of little ants and big houses or big ants and small houses. This time the patients with mild cognitive disorder and with Alzheimer's disease solved the first part of the test without any problems - when they were asked what is bigger, they chose a house, not an ant. But if the pictures did not reflect reality - a big ant looked like a little house - they were confused, answered incorrectly, or they took longer to respond.
Patients with mild cognitive impairment were somewhere between those of healthy and those with Alzheimer's disease. "When the decision was difficult, the reaction time was slower."
Would Damage to The Semantic System Influence The Everyday Functions?
To answer this question, researchers have turned to UCSD scale to evaluate the use of skills, the tool which is used in patients with mild cognitive disorder and Alzheimer's disease and in patients with schizophrenia, to determine the functional deficiencies. The test examines the ability of a person to perform complex checks or to organize a trip to the zoo for a cold day.
It's a good way to check whether someone has a problem with the semantic knowledge. Semantic processing takes place in the left temporal lobe. "The semantic system is organized as a network that reflects the various types of relationships and associations," said the researchers in the study. "Semantic data and knowledge are acquired in the larger intervals, often through a large number of repetitions, and do not reflect what has been recently adopted."
Doctor Goldberg says that this discovery is very important because it might be possible to strengthen by training the connections that arise in semantic processing. "This suggests that patients are getting slow due to semantic and not episodic memory," said Goldberg. Patients will be observed further in order to determine whether the deteriorating semantic problems worsen as the disease progresses.
Within additional article, David P. Salmon, Ph.D., from Department of Neuroscience at the University of California, said that "deficiencies in semantic memory, that this study demonstrated, confirm the suspicion that in patients with mild cognitive impairment of an anamnestic type, happens a slight cognitive impairment. Since the task did not require problematic remembering and reproduction of certain words or linguistic structures, it can be concluded that these shortcomings reflect the early and gradual loss of the integrity of semantic knowledge. "
He added that "This study proves that the deterioration of semantic memory in patients with mild cognitive impairment can contribute to the reduced ability to perform everyday activities."
Institute for Medical Research Feinstein
The Institute for Medical Research Feinstein, based in Manhasset, New York, many leading international scientists are engaged in areas such as Parkinson's disease, Alzheimer's disease, psychiatric disorders, rheumatoid arthritis, lupus, sepsis, genetics, pulmonary hypertension, leukemia, neuroimmunology, and medical chemistry. The institute, which is part of the North Shore Health System , belongs to the top 5% of all state institutes according to scholarships awarded to research centers for health care.
A Major Step Toward Developing The Vaccine For Alzheimer's Disease
A team of researchers from the Center for Research CHU (France, Centre Hospitalier Universitaire) at the University of Laval in Quebec and pharmacological company GlaxoSmithKline (GSK) has found a way to stimulate the natural defense mechanisms of the brain in people who suffer from Alzheimer's disease. This is an important achievement, and its details have been published in the online edition of the journal Proceedings of the National Academy of Sciences. This research opened the door to the development of effective treatment for Alzheimer's disease and toward finding an efficient vaccine.
____________________________________________________________
---- Article by BojanaL----
____________________________________________________________
Treatment for Alzheimer disease:
Modern medicine and well established healthcare system prolonged the average length of the human life. Old age is associated with numerous neurodegenerative disorders; most typical is Alzheimer’s disease. Risk for developing Alzheimer’s disease is increasing with the age. It is estimated that 10% of people over the age of 65, and 50% of those over 85 suffers from Alzheimer’s disease. Most cases develop sporadically and just 1-5 % of Alzheimer’s cases are genetically inherited.
Alzheimer’s disorder is first described in 1906. Post mortem brain analysis and blood markers provided more information on this pathological brain disorder over the past 100 years, but exact trigger for the disease and successful treatment method are still lacking. Alzheimer’s disorder is characterized by brain shrinkage, loss of neuronal connections and disrupted blood brain barrier. Several theories about disorder genesis exist: cholinergic theory, where lack of acetylcholine triggers disorder, herpes simplex virus induced disorder, age related impaired myeline breakage or oxidative stress as a cause of neurodegeneration…Most probable are ones associated with altered metabolism of amyloid precursor protein and tau protein. Amyloid precursor protein is building part of neuronal synapses and essential ingredient of various cell membranes in the body. Proteolitic degradation of amyloid precursor protein results in formation of the fibrial protein - beta amiloid that is found in brain plaques, typical for Alzheimer’s disorder. Beta amiloid alters calcium ion homeostasis (resulting in apoptosis), inhibits enzymatic activity and prevents glucose utilization. Tau protein is essential for development of neuronal polarity; it promotes neuronal microtubule assembly and enhances axonal dynamics. When tau protein is hyperphosphorilated, it becomes insoluble and forms inclusions known as neurofibrillary tangles. Those tangles are associated with neuronal degeneration. Alzheimer’s disease can be diagnosed using couple of techniques: brain imaging (computed tomography or magnetic imaging), through neuropsychological tests or by blood analysis (couple known markers exist). Current treatments are focused on the main attributes of Alzheimer’s disease: dementia (memory loss), depression and cognitive impairments. Medication used is just slowing down the progression of neurodegeneration but it can’t prevent disease. Typical mechanism of action is focused on proteolysis of amyloid precursor protein; latest drugs could prevent proteolysis or bind to already formed beta amyloid prior its aggregation and eliminate it. Other drugs affect distribution of beta amiloid through the brain or decrease the rate of neuroinflammation. Alzheimer’s disease is one of the most common neurodegenerative disorders associated with old age and one of the most expensive to be treated because patients demand special care due to physically, physiologically and socially altered behavior.
Latest discoveries in the stem cells field could move Alzheimer’s treatment in completely new direction. Scientists from the University Of California, Irvine developed new line of stem cells - choroid plexus epithelial cells (CPECs) using human and mouse embryonic cells. Choroid plexus is part of the brain ventricles where cerebrospinal fluid is produced. This liquid is important for cleaning the waste products and metabolites that could damage the brain function. 500 milliliters of cerebrospinal fluid is produced each day, and it is renewed 4 times a day to ensure efficient detoxification of the neuronal tissue. CPECs are forming important blood - cerebrospinal fluid barrier. Neurodegenerative disorders are associated with dysfunctional CPECs and inefficient removal of the waste material (like beta amiloid) from the cerebrospinal fluid. Scientists were familiar with the role and importance of CPECs cells, but until now they couldn’t find the way to produce those cells in vitro. Embryonic cells are pluripotent and different transcription factors determine their cellular faith (direction of their differentiation). After discovering that brain morphogenic factor 4 (BMF4) is responsible for differentiation of the neuronal progenitor cells into CPECs, researchers applied BMF4 to produce sufficient amount of CPECs. Both human and mouse neuronal progenitor cells used in the experiment matured successfully into CPECs after BMF4 was applied. Developed CPECs act just like naturally produced cells; they could integrate in choroid plexus epithelium and form secretory vesicles. Neurological disorders associated with the accumulation of the peptides, proteins and other metabolites that alter normal function of the brain could be treated using CPECs. Scientists are hoping that this approach will be especially helpful in Alzheimer’s and Huntington’s disease as well in treatment of pediatric neurodegenerative disorders.
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