Alzheimer
[ Los J ] Lyrics
Jump to: Overall Meaning ↴ Line by Line Meaning ↴
Los momentos que mencionas se me esconden tras las sombras
Y no logro recordar
Son tantas voces tantos rostros que no paran de gritar
De gritar
Con el tiempo hay tanto que memorizar
Y no te aferres a estos huesos secos de tanto llorar
Cada mirada cada historia tiene un fin
Es tu mirada que se posa en mi
Y no se ni quien seras
Si tu nombre yo llegara a recordar
Pensando en ti no voy a estar nunca mas
Relampagos que caen y estallan
Oigo tu voz y no se calla
Sicatrices que se van pero no se si volvera
Cada mirada cada historia tiene un fin
Pues la nuestra se termina aqui
Es tu mirada que se posa en mi
Y no se ni quien seras
Si tu nombre yo llegara a recordar
Pensando en ti no voy a estar nunca mas
Cada mirada cada historia tiene un fin
Es tu mirada que se posa en mi
Y no se ni quien seras
Si tu nombre yo llegara a recordar
Pensando en ti no voy a estar nunca mas
The song "Alzheimer" by Los J is a poignant reflection on memory loss and the ravages of time. The opening lines set the tone by imploring the listener to stop talking about the past, as the memories mentioned are lost in the shadows, unable to be recalled. The singer acknowledges the difficulty in remembering amidst the multitude of voices and faces that clamor for attention. The repetition of the phrase "de gritar" emphasizes the overwhelming nature of these memories and the frustration that comes with trying to hold onto them.
The chorus highlights the ephemeral nature of life, with each look and story having a definite end. The singer recognizes that their time with the person they are singing to is coming to a close, and that they may never remember their name. The image of lightning bolts and scars hint at the pain and trauma that may be associated with this loss, and the haunting presence of the person in question, whose voice cannot be silenced.
Overall, the song captures the heartbreak and confusion of Alzheimer's disease and memory loss. The lyrics are evocative and moving, and the somber melody accentuates the theme of loss and fading memories.
Line by Line Meaning
Deja, de hablar
Stop talking
Los momentos que mencionas se me esconden tras las sombras
The moments you talk about hide behind shadows and I can't remember them
Y no logro recordar
And I can't remember
Son tantas voces tantos rostros que no paran de gritar
There are so many voices and faces that keep screaming
De gritar
Screaming
Con el tiempo hay tanto que memorizar
With time, there is so much to memorize
Y no te aferres a estos huesos secos de tanto llorar
And don't hold on to these dry bones from crying so much
Cada mirada cada historia tiene un fin
Every look, every story has an end
Pues la nuestra se termina aqui
And ours ends here
Es tu mirada que se posa en mi
It's your gaze that rests on me
Y no se ni quien seras
And I don't even know who you are
Si tu nombre yo llegara a recordar
If I were to remember your name
Pensando en ti no voy a estar nunca mas
Thinking of you, I will never be again
Relampagos que caen y estallan
Lightning strikes and explodes
Oigo tu voz y no se calla
I hear your voice and it doesn't stop
Sicatrices que se van pero no se si volvera
Scars that go away but I don't know if they'll come back
Cada mirada cada historia tiene un fin
Every look, every story has an end
Es tu mirada que se posa en mi
It's your gaze that rests on me
Y no se ni quien seras
And I don't even know who you are
Si tu nombre yo llegara a recordar
If I were to remember your name
Pensando en ti no voy a estar nunca mas
Thinking of you, I will never be again
Cada mirada cada historia tiene un fin
Every look, every story has an end
Es tu mirada que se posa en mi
It's your gaze that rests on me
Y no se ni quien seras
And I don't even know who you are
Si tu nombre yo llegara a recordar
If I were to remember your name
Pensando en ti no voy a estar nunca mas
Thinking of you, I will never be again
Contributed by Leah H. Suggest a correction in the comments below.
Steve Woody
For those interested, I made a full transcript of this video. Hope this helps someone else out, especially those writing papers! I double checked everything, but please let me know if I missed anything.
"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 can be caused by a variety of diseases. Alzheimer's disease, now referred to as Alzheimer disease is the most common cause of dementia. Alzheimer 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, leads to the symptoms characteristic of dementia. although the cause of Alzheimer disease isn't completely understood, two major players that are often cited in its progression are plaques in tangles.
All right, so here we've got this cell membrane of a neuron 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 end’s outside the cell. It's thought that this guy helps the neuron grow and repair itself after an injury. since APP’s a protein just like other proteins, it gets used and overtime it gets broken down and recycled. Normally, it gets chopped up by an enzyme called Alpha secretase and its buddy, Gamma secretase. This chopped up peptide is soluble and goes away and everything is all good. if another enzyme, beta secretase, teams up with gamma secretase instead then we've got a problem. 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 are 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 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 cause inflammation which might damage surrounding neurons.
Amyloid plaque can also deposit around blood vessels in the brain called amyloid angiopathy, 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 disease are tangles, 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 cytoskeleton 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 makes sure that these tracks don't break apart, kind of like railway ties. Although again it's not completely understood, it's thought that the beta amyloid plaque buildup outside the neuron initiates pathways inside the neuron that lead to activation of kinase an enzyme that transfers phosphate groups to the Tau protein. The Tau protein then changes shape, stops supporting the microtubules, and clumps up with other Tau proteins and gets tangled and leads to the other characteristic finding of Alzheimer disease, neurofibrillary tangles.
Neurons with tangles in non-functioning microtubules can't signal as well and sometimes end up undergoing apoptosis, or programmed cell death. Here's an image of Histology showing these neurofibrillary tangles formed inside the neuron. As neurons die, large scale changes start to take place in the brain. For one, the brain atrophies, or shrinks, and the Gyri get narrower (which are the characteristic ridges of the brain). As those get narrower the Sulci, which are the groups between the Gyri, get wider. With atrophy the ventricles, or fluid filled cavities in the brain, get larger as well.
So, that's the pathophysiology part, but why does this happen in some people and not others? well Alzheimer disease can be split into two groups sporadic and familial. Sporadic is used to describe the late onset type where the exact cause isn't very well defined and is probably a combination of genetic and environmental risk factors. And sporadic accounts for the vast majority of cases. With sporadic Alzheimer's, the risk increases significantly with age affecting around 1% of people between ages 60-65 and 50% of people over the age of 85. In fact, a gene that's been identified as possibly contributing to an increased risk of Alzheimer disease is the e4 allele of apolipoprotein E gene or APOE e4. Researchers have shown that the risk of developing Alzheimer disease increases for patients that inherit one e4 allele and increases even more for patients who inherited two e4 alleles, one from each parent. Apolipoprotein E helps breakdown beta amyloid, but the E4 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% of cases and could be caused by several gene mutations. First, mutations in the PSEN-1 or PSEN-2 genes on chromosome 14 or chromosome 1, respectively, had been linked to early-onset Alzheimer's. These genes encode for presenilin 1 and presenilin 2, both protein subunits of gamma secretase. Mutations in these PSEN-1 or PSEN-2 genes can change the location where gamma secretase chops APP, producing different length beta amyloid molecules, which seem to be better at clumping up and forming plaques.
Another known 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 APP gene and presumably increased expression of APP, potentially increasing the amount of amyloid plaque buildup. For this reason, familial Alzheimer disease often progresses by age 40 in patients with Down Syndrome.
Symptoms of Alzheimer disease worsen as plaques and tangles buildup 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 progress to a 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 1st 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 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 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."
Hat Kid Has Peace and Tranquility
Stage 1: Pre-diagnosis (Psuedodementia)
Occurs 10-15 years before actual diagnosis.
Stage 2: Mild Memory Loss (Basic Forgetfulness)
Noticeable.
Most likely diagnosed.
Symptoms:
Memory lapses become much more frequent. Can still interact and hold up social skills. Still able to drive. Forgets some names, might forget keys.
Stage 3: Mild-Moderate Memory Loss (Noticeable Memory difficulties)
much worse decline than stage 1 and 2.
Symptoms:
Trouble remembering information that was just read minutes ago.
Experience challenges in social situations.
Forgetful of words, names, and the denial that something is wrong.
Stage 4: Moderate Memory Loss (More than memory loss)
Steep decline from stage 3.
Symptoms:
Confusions about what day it is or where they are.
risk of wandering off alone or getting lost.
restlessness at night could occur, or sleepiness during the day.
Difficulty choosing appropriate clothing for weather.
Physical Symptoms:
Reduced motor abilities, may stumble on feet.
They will still remember major details of their life, such as where they live, or the person they are married to.
Stage 5: Moderate-Severe Memory Loss (Decreased Independence)
First stage where patient is not capable of living independently. They might need to go to the hospital, or be assigned a caretaker.
Symptoms:
Trouble remembering close friends and family.
Getting dressed is near impossible.
Beginning of Hallucinations.
Delusions occur.
Paranoia sets in.
Stage 6: Severe Memory Loss (Severe Symptoms)
incapable of responding to the world around them. Communicating becomes challenging. Expressing emotions could be challenging.
Symptoms:
Increased Anxiety, Hallucinations, Delusions, and Paranoia.
Frustration with loved ones.
Stage 7: Complete Neuron Death (End of Life stages)
the body begins to shut down because of the death of brain cells. unable to sit or walk without help. Will need help with swallowing food.
Symptoms:
Increased risk of life-threatening infections, such as pneumonia.
Death.
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Steve Woody
For those interested, I made a full transcript of this video. Hope this helps someone else out, especially those writing papers! I double checked everything, but please let me know if I missed anything.
"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 can be caused by a variety of diseases. Alzheimer's disease, now referred to as Alzheimer disease is the most common cause of dementia. Alzheimer 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, leads to the symptoms characteristic of dementia. although the cause of Alzheimer disease isn't completely understood, two major players that are often cited in its progression are plaques in tangles.
All right, so here we've got this cell membrane of a neuron 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 end’s outside the cell. It's thought that this guy helps the neuron grow and repair itself after an injury. since APP’s a protein just like other proteins, it gets used and overtime it gets broken down and recycled. Normally, it gets chopped up by an enzyme called Alpha secretase and its buddy, Gamma secretase. This chopped up peptide is soluble and goes away and everything is all good. if another enzyme, beta secretase, teams up with gamma secretase instead then we've got a problem. 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 are 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 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 cause inflammation which might damage surrounding neurons.
Amyloid plaque can also deposit around blood vessels in the brain called amyloid angiopathy, 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 disease are tangles, 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 cytoskeleton 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 makes sure that these tracks don't break apart, kind of like railway ties. Although again it's not completely understood, it's thought that the beta amyloid plaque buildup outside the neuron initiates pathways inside the neuron that lead to activation of kinase an enzyme that transfers phosphate groups to the Tau protein. The Tau protein then changes shape, stops supporting the microtubules, and clumps up with other Tau proteins and gets tangled and leads to the other characteristic finding of Alzheimer disease, neurofibrillary tangles.
Neurons with tangles in non-functioning microtubules can't signal as well and sometimes end up undergoing apoptosis, or programmed cell death. Here's an image of Histology showing these neurofibrillary tangles formed inside the neuron. As neurons die, large scale changes start to take place in the brain. For one, the brain atrophies, or shrinks, and the Gyri get narrower (which are the characteristic ridges of the brain). As those get narrower the Sulci, which are the groups between the Gyri, get wider. With atrophy the ventricles, or fluid filled cavities in the brain, get larger as well.
So, that's the pathophysiology part, but why does this happen in some people and not others? well Alzheimer disease can be split into two groups sporadic and familial. Sporadic is used to describe the late onset type where the exact cause isn't very well defined and is probably a combination of genetic and environmental risk factors. And sporadic accounts for the vast majority of cases. With sporadic Alzheimer's, the risk increases significantly with age affecting around 1% of people between ages 60-65 and 50% of people over the age of 85. In fact, a gene that's been identified as possibly contributing to an increased risk of Alzheimer disease is the e4 allele of apolipoprotein E gene or APOE e4. Researchers have shown that the risk of developing Alzheimer disease increases for patients that inherit one e4 allele and increases even more for patients who inherited two e4 alleles, one from each parent. Apolipoprotein E helps breakdown beta amyloid, but the E4 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% of cases and could be caused by several gene mutations. First, mutations in the PSEN-1 or PSEN-2 genes on chromosome 14 or chromosome 1, respectively, had been linked to early-onset Alzheimer's. These genes encode for presenilin 1 and presenilin 2, both protein subunits of gamma secretase. Mutations in these PSEN-1 or PSEN-2 genes can change the location where gamma secretase chops APP, producing different length beta amyloid molecules, which seem to be better at clumping up and forming plaques.
Another known 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 APP gene and presumably increased expression of APP, potentially increasing the amount of amyloid plaque buildup. For this reason, familial Alzheimer disease often progresses by age 40 in patients with Down Syndrome.
Symptoms of Alzheimer disease worsen as plaques and tangles buildup 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 progress to a 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 1st 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 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 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."
OneClique
I think i have alzheimer cuz i dont remember asking