Alzheimer's disease and brain injury

[sontag]

Some people develop Alzheimer's disease after a blow to
the head. Has physical damage been done to nerve cell apparatus
e.g the endoplasmic reticulum,Golgi apparatus,by the pressure
of a blow to the head?

 

[DocToxyn]

Is it possible that you have Alzheimer's disease (AD) mixed up with Parkinson's disease (PD)? The neuropathology of AD is typically associated with neuronal/synaptic loss primarily in the hippocampus and neocortex, and sometimes at later stages in the locus ceruleus and dorsal raphe. This neuronal damage is accompanied by the accepted hallmarks of the disease: formation of amyloid plaques, hyperphosphorylated tau protein and neurofibrillary tangles. While there has been reported a loss of biogenic amine concentrations, including dopamine, this may be secondary to the pathology and not involved in precipitating the disease. AD is sometimes called Alzheimers dementia due to the effects of the disease on memory.

PD on the other hand is classically associated with a loss of dopaminergic neurons which originate in the substantia nigra and project to the caudate nucleus. Loss of dopamine receptors/transporters is a diagnostic indicator of this disease, which manifests itself primarily as a movement disorder, although in late stages it can also have a component of dementia.

While an event such as head trauma, will not likely lead to these diseases in the short-term, it could possibly enhance or initiate processes that are involved with the progression of these diseases. This is purely hypothetical since the causes of both of these diseases are not well understood and are currently the topic of a considerable amount of scientific research.

The only documented case of brain injury leading to a parkinson's-like syndrome, that I'm aware of, occurred when several teenagers injected an illicit drug which contained a compound called MPTP. They went on to develop symptoms remarkably similar to PD in a very short time and it has since been determined that the drug selectively destroys dopaminergic neuorns of the substantia nigra. This drug is now used as a model to study PD in animals.

Note: I put this together before you edited your question, but I think it still answers your post.

 

[sontag]

Could the soundwaves/pressure from a blow to the head
cause organelles to be damaged?

 

[Monique]

Don't you mean stroke?

As DocToxyn says I don't see how AD or PD are induced by traumatic injury.

 

[DocToxyn]

Could the soundwaves/pressure from a blow to the head
cause organelles to be damaged?

You could most certainly attain damage to cells in general from any traumatic head injury, however, your concerns would be better focused on the acute effects of the injury such as inflammation, loss of blood supply to specific regions, etc. In the long-term, how these injuries may then impact aged-related neurodegeneration is still not well understood. This review should give some interesting aspects of this topic. The problem lies mainly in that we don't know all the factors that can lead to a person developing these diseases. Thus we can only make associations and best guesses about certain relationships, i.e. head trauma leads to AD, that may or may not turn out to be truly causal.

 

[zoobyshoe]

The notion that a blow to the head can cause alzheimers may result from someone casually misrefering to trauma-induced memory loss or agnosia as "alzheimers", particularly if it's chronic.

Complex-partial seizures, which are non-convulsive, often produce symptoms that look much like alzheimer's. The book Seized by Eve LaPlante tells the story of "Charlie", (among others) who had his first complex-partial seizure in early old age. It was precipitated by the physical activity of chopping wood on his Vermont farm. He wandered the woods for hours, unable to recognise where he was. His daughter became worried and went out to find him. When she did he looked at her and asked "Who are you?" Thinking he'd had a stroke she got him to the doctor where an EEG revealed clear temporal lobe seizure activity.

A blow to the head can, of course, lead to complex-partial seizures which might, then, go on to be misinterpreted as alzheimer's.

 

[DocToxyn]

A blow to the head can, of course, lead to complex-partial seizures which might, then, go on to be misinterpreted as alzheimer's.

I can appreciate how the complex-partial seizure symptoms would be potentially misdiagnosed at least under examination of the external symptoms in a clinical setting. However, are the pathological lesions such as the plaques and tangles also found in this condition upon autopsy? I would imagine that the epidemiological studies which make the potential association between head trauma and AD would have controlled for this.

 

[zoobyshoe]

However, are the pathological lesions such as the plaques and tangles also found in this condition upon autopsy?

Lesions of one kind or another, usually present. The plaques and tangles of Alzheimer's, though, wouldn't be caused by a seizure disorder.

 

[sontag]

The fact that young people with head injury can get microtubule damage
suggests that inflammation could be a contributing factor to Alzheimer's, because old
people in their 80s have a weaker immune response than young people
(there is an inflammatory immune response to free radicals that result from beta amyloid
processing) but have had more time to accumulate microtubule damage that could result from
inflammation.

 

[Monique]

The fact that young people with head injury can get microtubule damage
suggests that inflammation could be a contributing factor to Alzheimer's, because old
people in their 80s have a weaker immune response than young people
(there is an inflammatory immune response to free radicals that result from beta amyloid
processing) but have had more time to accumulate microtubule damage that could result from
inflammation.

I don't follow your logic here

1) where do you get the information that microtubule damage results from head injury
2) how do you link young people with head injury to Alzheimer's disease

 

[sontag]

I got the information from Doctoxyn's post (where tau protein is mentioned):

http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=15542981

It actually says "younger" people and not "young" people.

 

[hitssquad]

how do you link young people with head injury to Alzheimer's disease

Both are associated with inflammation.

 

[sontag]

What exactly is the "blood-brain" barrier and does it play any role in Alzheimer's or
Parkinson's disease? I read that blood vessel cells have no gaps between them in the
brain - is this the blood-brain barrier? Also when these blood vessel cells are forced apart by high blood pressure charged particles and large molecules can reach neurons.
Is there any evidence that Alzheimer's can be caused/ made worse by
an inflow of charged particles or large molecules?
Are neurons in the brain easier to damage than other cell types
in the body and if so,why?

 

[DocToxyn]

The blood brain barrier is the sum total of a number of different cell types, characteristics and processes which achieves a "separation" between the brain and the rest of the body. Cells involved include endothelial cells of the blood vessels, astrocytes and pericytes. Some of the structures/connections involved with these cells are tight endothelial junctions, the basal lamina (a type of basement membrane) and pervascular endfeet of the astrocytes. Overall the BBB serves to control the passage of large (proteins) and small (glucose, amino acids) molecules into the brain. A number of inactive (tight junctions) and active (membrane pumps) funtion to provide this selection of what gets in and what does not. Certain regions of the brain, the circumventricular organs (not really organs, more like regions), have leaky BBB function to allow these regions to sense what is going on in the blood stream. The area postrema is a good example of this, it is involved in vomiting and presumably can detect blood borne mediators of the emetic process. Take a look at http://users.ahsc.arizona.edu/davis/bbbtransport.htm for a great illustration of the BBB.

As far as its role in AD, I think I might disappoint you again. It seems that we are always saying "maybe" and here is another example. It is logical that if you compromise the BBB and elicit inflammation and that inflammation leads to initiation or progression of neurodegeneration then it could influence the AD process. Again I steer you to do a search on PubMed and look for BBB and AD and you will find a lot of info. Most of our lack of solid information about AD as a disease process comes from the fact that we are still trying to understand the disease as a whole and don't know what other factors play a role in its development.

For the vulnerability of neurons as compared to other cells, it could be argued that they are more sensitive, but it may just be a matter of perpective. For one, the brain requires significant amounts of oxygen and nutrients, thus depriving it of these by resticting blood flow may have a greater impact per unit time of deprivation, than say in the liver. Also, as we have talked about in other threads, the regenerative properties of the brain are very poor, thus making injury a typically permanent condition. Taking it down to the cellular level, if you had a dish full of neurons and a dish full of liver cells, there are certain things that you could do to damage one that may not affect the other. It all has to do with the specific complement of proteins and other charactersitics of the cell that it has in order to do its job. Overall, I would say that the brain is generally more sensitive that most organs, but I'm kinda biased since I'm a brain guy.