Alzheimer's 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

 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

 Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a long evolution whose clinical symptoms appear late in life. However, in the last years, the paradigm of AD has changed. In the past, researchers thought AD was an age-related disorder that begins during the aging process. Today we know that the onset of the disease occurs between 15 (for the genetic) and 20–30 years (for the sporadic) before any clinical symptom appears.  There is no preventive or curative therapy for the disease and the lack of knowledge of when the disease begins greatly complicates the work of the physicians. Another added handicap is that neither do we know why the disease begins. In this sense, there are several hypotheses trying to explain the beginning of AD. These hypotheses may not be exclusive, and they may well overlap and take place at the same time. We can divide the hypotheses into three groups: The hypotheses based on protein deposits. This group includes the beta-amyloid (Aβ)