Dementia isn't technically a disease

 Dementia isn't technically a disease but more of a way to describe a set of symptoms like poor memory and difficulty learning new information which can make it really hard to function independently. Usually, dementia is caused by some sort of damage to the cells in the brain which could be caused by a variety of diseases. Alzheimer's disease now referred to as Alzheimer's disease is the most common cause of dementia Alzheimer's disease is considered a neurodegenerative disease meaning it causes the degeneration or loss of neurons in the brain particularly in the cortex. This as you might expect we see the symptoms characteristic of dementia. Although the cause of Alzheimer's disease isn't completely understood 2 major players that are often cited in its progression are plaques and tangles. All right so here we've got the cell membrane of inner on in the brain in the membrane you've got this molecule called amyloid precursor protein or APP one end of this guy's in the cell and the other ends outside the cell are thought that this guy helps the neuron grow and repair itself after an injury. Since A. P. P. is a protein just like other proteins it gets used and over time it gets broken down and recycled. Normally it gets chopped up by an enzyme called alpha-secretase and its body gamma-secretase. This chopped up peptide soluble and goes away and everything's all good. If another enzyme beta-secretase teams up with gamma-secretase instead then we've got a problem and this leftover fragment isn't soluble and creates a monomer called amyloid-beta. These monomers tend to be chemically sticky and bond together just outside the neurons and form what is called beta-amyloid plaques these clumps of lots of these monomers. These plaques can potentially get between the neurons which can get in the way of the neuron to neuron signaling if the brain cells can't signal and relay information then brain functions like memory can be seriously impaired. It's also thought that these plaques can start-up an immune response and because the information which might damage surrounding neurons. Amyloid plaque can also deposit around blood vessels in the brain called amyloid Angie apathy which weakens the walls of the blood vessels and increases the risk of hemorrhage or rupture and blood loss. Here's an image of amyloid plaque on histology these clumps are buildups of beta-amyloid and this is happening outside the cells. Another big part of Alzheimer's disease though are tangling and these are actually found inside the cell as opposed to the beta-amyloid plaques. Just like other cells neurons are held together by their side skeleton which is partly made up of microtubules these track like structures that essentially act like a minecart shipping nutrients and molecules along the length of the cell a special protein called tau make sure that these tracks don't break apart kind of like railway ties. Although again it's not completely understood it's not that the beta-amyloid plaque build-up outside the neuron initiates pathways inside the neuron that leads to activation of kinase an enzyme that transfers phosphate groups to the tau protein. 

The top protein then changes shape stop supporting the microtubules and clumps up with other tau proteins and gets tangled and leads to the other characteristic finding of Alzheimer's disease neurofibrillary tangles. Neurons with tangles in non-functioning microtubules can't signal as well and sometimes end up undergoing pop ptosis or programmed cell death here's an image of histology showing these neurofibrillary tangles form inside the neurons. As neurons die large scale changes start to take place in the brain for one the brain atrophy use or shrink in the Giro get narrower which are the characteristic ridges of the brain as those get narrower the sulky which are the groups between the jaggery get wider with atrophy the ventricles are fluid-filled cavities in the brain gets larger as well. 

So that's a path of physiology part but why does this happen some people and not others well Alzheimer's disease can be split into 2 groups sporadic and familial. Alex used to describe the late-onset type where the exact cause isn't very well defined and it's probably a combination of genetic and environmental risk factors. Informatik accounts for the vast majority of cases. With sporadic Alzheimer's the risk increases significantly with age affecting around 1 percent of people between ages 55 and 50 percent of people over the age of 85. In fact a gene that's been identified as possibly contributing to an increased risk of Alzheimer's disease is the E. 4 allele of April life of protein E. Jean or APOE E. 4. Researchers have shown that the risk of developing Alzheimer's disease increases for patients that inherit one E. 4 allele and increases even more for patients who inherited 2 E. 4 alleles one from each parent. April like a protein E. helps break down beta-amyloid but the E. 4 allele seems to be less effective than the other alleles like the APOE 2 allele meaning patients are more likely to develop beta-amyloid plaques. Familial Alzheimer disease on the other hand is used to describe cases where some dominant gene was inherited that speeds up the progression of the disease so sometimes familial Alzheimer's disease is referred to as early-onset Alzheimer's. Familial accounts for about 5 to 10 percent of cases I could be caused by several gene mutations first mutations in the P. S. E. N. one R. P. S. E. N. 2 genes on chromosome 14 or chromosome one respectively have been linked to early-onset Alzheimer's these genes encode for presenilin one and presenilin 2 both protein subunits of gamma secretase. Cations in these PSTN wonder PSE into Jean's can change the location or gamma-secretase chops A. P. P. producing different length of beta amyloid molecules we seem to be better at clumping up in forming plaques. Another no genetic cause of Alzheimer's is trisomy 21 or down syndrome which involves an extra copy of chromosome 21.

It turns out that the gene responsible for producing APP is located on chromosome 21 which means that people with down syndrome have an extra 8 P. P. Jean M. presumably increased expression of APP potentially increasing the amount of amyloid plaque build-up. For this reason, familial Alzheimer's disease often progresses by age 40 in patients with down syndrome. Symptoms of Alzheimer's disease worsens as plaques and tangles build up and damage to the neurons accumulates. In the early stages, symptoms might not even be detectable as it progresses though patients lose short-term memory like for example, they might not be able to remember what they had for breakfast that morning. They then progressed to loss of motor skills making things like eating difficult without help. Also, language becomes affected making it more difficult to communicate. Eventually, they lose long term memory like forgetting the name of their spouse or even that they're married in the first place. And they progressively become more disoriented which can be dangerous because they might wander from home and get lost. In the late stages, they become bedridden and the most common cause of death is actually infection like pneumonia. Diagnosis of Alzheimer's disease is really tough because the only way to definitively show that a person had Alzheimer's is by performing a brain biopsy after autopsy. Usually, a clinician will therefore make a diagnosis after excluding other causes of dementia. Currently, there isn't any cure for Alzheimer's disease some medications exist but the benefits are small and there haven't been any medications that clearly and definitively halt the progression of Alzheimer's.