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 alpha secretase the soybean peptides exist in the extracellular space I know themselves metabolized impose no problem and now sinus disease part of this process of APP cleavage becomes in pad which results in progressive neuronal loss in selected parts of the cortex before we take a more detailed look at the mechanism underlying this neuronal death let's examine the gross anatomical changes which take place outside his disease. Sorry the macroscopic changes and out Simon's include cerebral atrophy with narrowing of the Jari M. whiting the sulky as well as dilation of ventricles which occurs secondary to those former changes structures of the medial temporal lobe principally the hippocampal I and they make a lie or involved early in the disease I'm become severely atrophied in the later stages of the structures such as the frontal and parietal lobes eyes when a subcortical nuclei are also involved in the stages of the disease. Let's now look at some specific changes which take place on the molecular level in brains affected without sinus disease the pathological hallmark about Simon's is the accumulation of amyloid beta and tau proteins and the mechanism underlying this build up is known as the amyloid energetic pathway as mentioned earlier a normal healthy neuron will degrade old amyloid precursor proteins in its membrane and replace them with new ones the by product of this degradation produces harmless soluble peptides however in outside his disease a different enzyme called beta secretase cleaves APP into an insoluble peptide known as amyloid beta. Individual amyloid beta peptides I could get together to form to lodge a toxic molecules known as amyloid pizza and make amends and amyloid beta plaques the oligomers coolest neuronal apoptosis by increasing the neurons probability to calcium and the plaques disrupt neuronal signaling by accumulating in the extracellular space plaques can also accumulates on cerebral blood vessels in a process known as cerebral amyloid on gypsy which increases the likelihood of small cerebral hemorrhages another protein called tau also contributes to its neuronal death an outside miss in health insurance tau protein forms part of the cell's microtubules button outside Mister sees top accounts for sorely needed by the effects of amyloid beta and accumulates to form new referee tangles within the neurons affected brain areas. As a very quick recap of the pathogenesis about Simon's you should know that APP is pathologically cleaved by Peter secretase forming exercise insoluble amyloid-beta and they commit some plaques and secondly to this top protein undergoes phosphorylation and accumulates into intracellular neurofibrillary tangles. So now I want to briefly talk about an important structure involved in learning and processing the memories and how it's after fee throughout sinus disease can lead to impaired memory. The diagram shown here illustrates the complex anatomy of a structure located in the major temporal lobe the hippocampal formation. 

The hippocampal formation has 3 components the dentate gyrus the hippocampus proper and the secular. The hippocampus proper is the S. shape shop structure which is outlined in red on the diagram. Long term potentiation is thought to be a very important mechanism by which memories are formed a high-frequency activity at sign-ups is within the hippocampal formation results in a long-lasting increase in synaptic strength between those neurons involved in the sinuses in other words lots of firing of postsynaptic neurons caused by stimulation by presynaptic neurons increases the efficiency of signed up to transmission of future impulses through the selective loss of neurons of the hippocampal formation as is the case and outside Mr sees one of the classical clinical features about Simon's impaired a prosthetic memory is manifested. Let us now go over some of the important clinical features of the sinus the clinical features about Simon's are cumulative and temporal which means more survey symptomatology because as cortical atrophy progresses over time. The symptoms can be divided with respect to the stage of the disease but for simplicity, I should describe the symptoms in general. Empat episodic memory affects the patient's ability to line retain and process new information this impairment is progressive I know new Boston's with time. In contrast patients, distant memory is often preserved until the late stages of the disease. Language tends to become diminished with time specifically with respect to what finding however personality tends to remain unaffected other common clinical features about Simon include apraxia which is the reduced ability to carry out the skill by truck to the T. 

I can I see a the failure to recognize objects people places and impaired executive function for example empowerment organizing and planning some late features about Simon's include extreme apathy myoclonus which may be accompanied by seizures and dysplasia which predisposed to complications such as pneumonia which is itself often a terminal event. How sinus disease can be classified into familial and sporadic forms familiar about Simon's is associated with mutations in amyloid precursor protein present in more than percent into and is always an early onset disease starting between 30 to 40 years of age. For many about Simon's comprises just 5 to 10 percent of all cases. Now sporadic outside is far more common comprising the remaining 90 to 95 percent of cases and it is the result of interactions between genes and environment homozygous expression of apolipoprotein E. Absalom full which is audio is associated with an increased likelihood of developing sporting house I miss the vast majority of sporadic outside Mr these occurs in those over the age of 65. The single greatest risk factor for developing separate accounts Simas is increasing age other factors such as homozygosity for apolipoprotein E. apps on for vascular faxes such is increased blood pressure diabetes dyslipidemia and decreased physical activity also satiated with the development of sporadic house I miss the disease. In summary, out sinus disease can be classified as familial or sporadic risk factors for developing the familial form include inheritance of mutated 8 PP presenting one presented into jeans and risk factors for developing the sporadic form include increasing H. and expression of the apolipoprotein E. Absalom for Idaho. 

Regardless of etiology, the pathogenesis about Simon's involves exercise and I'm willing to be taxation and intracellular tau in neurofibrillary tangles these changes a toxic to neurons and in pandering signaling manifesting clinically as the features discussed area. Subscribe to certain brand hope for more videos to help explain the mysteries of the brain.