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Memory disorders

 I was remembering it a German this is good but it might come but then those could be sick because I don't think about America what about the discrepancy Buxtehude but a man do you do we do have are causing some stuff but there was a lousy all up getting post much department loaded the local important that's so good to go but they can't lock up put it in all it was like it was going home is a  keep up cool publicly bonus ability to quickly get you could join up what could you react easily doing it would you look anywhere it was just that and if you want to watch because we knew that he got in the popular G. or with windows 8 you can get some looks we look but by using this link so now it is because of all the topic.  I am not disease what can look again what does this keep this going memory disorders V. both sustenance okay yes this is musically up with him and what he had to learning I'm learning about what head do okay unison capacity Hey yup joining ever to be awarde

Alzheimer's disease

  A century ago a German doctor called Alice outside spotted anomalies in brain sections from a patient with dementia.  Ever since people have been studying the strange plaques and tangles he saw in the hope that we could one day on the stand and kill what is now known outside his disease.  Insoluble deposits of a peptide called amyloid-beta A. B.   The phone when approaching.  Because the protein is sequentially clean by 2 and a beta and gamma secretase.  All the molecules are generated by this cleavage and may play a role in the disease but A. B. tech is the main culprit.  ABC tends to miss full become sticky eventually clumping together home saludable all the goodness.  Some of these aggregates into large insoluble fibrils the deposits in the brain plaques.  The.  In several forms of speech.  We don't know exactly which species is toxic research shows that the communication and plasticity sign up.  This could be what stops the brain from full.  The big memories.  New homes on th

Chronic nerve degenerative disease

Welcome to this awesome brand have video on outside his disease with the aid of some diagrams I'm going to describe the pathogenesis about Simon's resulting microscopic and macroscopic changes which take place and some of the clinical features which manifest with these changes.  Sir what is awesome is disease Alzheimer's disease is a chronic nerve degenerative disease of the cortex which begins insidiously as impairment of high cognitive function and progresses resulting deficits of memory visuospatial orientation judgment personality and language these changes typically occur over a 5 to 10 year.   First let's talk about the functioning of the house in your own in the part of the cell membrane of neurons which forms a sign ups there are numerous proteins called amyloid precursor proteins otherwise known as A. P. P. and as with all proteins old versions of a PPO degraded and new ones take their place 8 PP is normally broken down into soluble peptide spine enzyme called

Suffering from dementia

  Time is deceased was described for the first time in 1907 by the German psychiatrist Eloise as a timer.  In performing histopathologic studies of the brain of his patient Augustine suffering from dementia he brought to light the presence of 2 types of lesions in the brain.  Senile plaques and neurofibrillary tangles he reached the conclusion of a distinct disease of a cerebral cortex 100 years later thanks to current scientific techniques research has made a great leap and the understanding of the disease.  We know that the brain is made up of neurons and that these are interconnected to form a vast network.  These connections known as synapses enable the transmission of information from one neuron to another.  And now it's time for us to cease 10 to 15 years before the appearance of the symptoms to main lesions forms in the brain.  Senile plaques composed of amyloid-beta protein and neurofibrillary tangles composed of tau protein.  How is the senile plaque formed?  On the surfac

Defective tau proteins

  Time is deceased was described for the first time in 1907 by the German psychiatrist Eloise as a timer.  In performing histopathologic studies of the brain of his patient Augustine suffering from dementia he brought to light the presence of 2 types of lesions in the brain.  Senile plaques and neurofibrillary tangles he reached the conclusion of a distinct disease of a cerebral cortex 100 years later, thanks to current scientific techniques research has made a great leap and the understanding of the disease.  We know that the brain is made up of neurons and that these are interconnected to form a vast network.  These connections known as synapses enable the transmission of information from one neuron to another.  And now it's time for us to cease 10 to 15 years before the appearance of the symptoms to main lesions forms in the brain.  Senile plaques composed of amyloid-beta protein and neurofibrillary tangles composed of tau protein.  How is the senile plaque formed?  On the surfa

Hippocampus

 Hippocampus, which is known to encode a new protein called PGC-1α that acts as a strong synaptic activator in the hippocampus.  The fact of course remains there are many factors involved with stress and cognitive dysfunction including loss or disease of brain cells - but since we know this can happen more frequently then you might think people would assume it's related to the illness so doctors look for clues if they get an old wound on their scalp from being spanked/tossed around all day long?  Hippocampus in humans and other primates is associated with anxiety-like behavior. In addition to the hippocampal dysfunction that may be involved here, we are interested herein also in how impaired brain function relates directly or indirectly using a novel model of neurodegenerative diseases. We observed previously in Alzheimer's disease patients reduced cognitive performance on measures of attention span across two tests—the spatial working memory task and an executive function test

The disease comes on gradually

 With the growth of age, disease comes gradually and some of them become dominant. Family history and lifestyle are important.  This is a genetic condition that most often occurs after an accident or trauma to the head, especially when someone has died from this type of stroke. This can also happen if you are pregnant or suffering from traumatic damage such as your baby's birth.  The symptoms can include difficulty seeing, hearing, or thinking clearly, along with involuntary muscle spasms and mental confusion. 

Alzheimer's is a slow fatal disease

  What is Alzheimer's disease?  Alzheimer's is a slow fatal disease of the brain affecting one in 10 people over the age of 65.  No one is immune.  The disease comes on gradually as abnormal protein fragments called plaques and tangles accumulate in the brain and kill brain cells.  They start here in the hippocampus the part of the brain where memories are the first to form.  Over many years' time, the plaques and tangles slowly destroy the hippocampus and it becomes harder and harder to form new memories.  Simple recollections from a few hours or days ago but the rest of us might take for granted are just not there.  After that more plaques and tangles spread into different regions of the brain.  Ellen cells and compromising function wherever they go this is spreading around is what causes the different stages of Alzheimer's.  From the hippocampus, the disease spreads here to the region of the brain where the language is processed when that happens it gets tougher and