I don't think it's silly at all. So many have found comfort here finding out the similarities in their spouse with other AD spouses. It is just one more thing more people may find in common. What it would lead to, I don't know. But certainly the spouses of AD have found more similarities than the medical community on this site.
That may be so from the alz assoc about aluminum but if I have heard a common denominator on autopsy was aluminum buildup in AD patients brains ./ maybe sunshyne can inform us better with her scientific edge or anything to back up either way-. if the aluminum buildup is present how do we justify this is we arent consuming it from daily useages over time? just questioning because like alot of things that are bad for us, our govt dont always say it upfront -eliminating aluminum from our lives would play havoc on our infructure i think? i have tried to go to plastic when possible not aluminum if i have a choice. not much better plastics have nasty stuff too-no win situation..:) divvi
if interested in the aluminum/AD relationship there are TONS of articles if you google aluminum and AD together. plus Fda.gov/search-aluminum toxicity has interesting pages to read as well. aluminum is everywhere. some articles are recent some are from previous yrs but all question the AD/aluminum factor. what i dont think is true is its a MYTH. theres still too much controversary. did you know our drinking water also has aluminum...lots of debate on that as well. surely is alot to ponder either way you think about it. divvi
Yes to Blue eyes for my husband; No to red splotch
My husb started taking Lipitor and if I go way back, I bet that's when his trouble started. It was for high cholesterol. I also remember him having a colonoscopy back when they really put you out with anethesia...after that, it took him a while to come out of it too. And, he drank ALOT of milk as a child. His former PCP thought it had to do with pasterization of milk years ago...
My wife has a faint red spot (never noticed it before) and blue eyes.
Regarding Lipitor, DW's AD doctor put her on Lipitor since it has some beneficial effect. It did cause a rise in liver enzymes, but he was not concerned.
We checked her for heavy metals, but found none. Don't know about the Aluminum idea except that no strong evidence has been found. No exposure to fumes, etc.; non-smoker; type II diabetic and NOT overweight; no surgery or anesthesia in almost 50 years; no significant infections other than severe ear infection as child so she missed one year of school.
I think there are probably multiple causes for AD - genetics, exposures to toxins, infections, etc. with each playing a role in the individual patient.
marsh, not only are there multiple causes, these are multiple diseases. In most cases dementia is a symptom. It is only considered Alzheimer's if they can't find another disease that causes dementia.
The red spot is very interesting. Now I'd like to know if those LOs with the red spot are Alzheimer's patients or if they are diagnosed with one of the other diseases that cause dementia. My husband does NOT have a red spot, and he also has a NON-Alzheimer's diagnosis.
This is the kind of thing that I wish someone with a scientific bend would do a huge spreadsheet on.
my DH was first dx with vascular dementia AND/OR alzheimers -and his red blotch is significant. i think the red blotch has spread over the yrs. it was not this big-i agree starling, on the spreadsheet, also,i would very much like to know WHERE in our country are the HIGHEST RATIOS of AD prominent?? like in what states, and what section of that state. i say this because there may be a telltale significant factor in common if there are more cases in one specific area. you'd think this would have been done ??? divvi with the difficulty of getting a dr to even diagnose the AD or dementia this may be problematic and not represent a true picture to a possible much bigger picture overall.
My husband had aseptic meningitis (which I think is a misnomer if I ever heard of one) several years before he started having dementia-like symptoms. When he was finally diagnosed in '94 he had been having symptoms since '91. Since he has had his"red spot" as long as I have known him, his couldn't be related to med. His eyes are brown. Regarding the seizures mentioned earlier-he had one 3 years ago but none since and is not on any medication.
I'll check on a red spot, she does have blue eyes, and she was always annoyed with her skin being red in the cheeks area. Weird...
My WAG always had to do with headaches...has anyone had the AD spouse with a history of annoying headaches? Not even necessarily migraines, but just headaches beyond what the population in general gets (in number or severity).
No red blotch. He says y'all are nuts, but he was willing to undergo the examination in the interests of science.
Mawzy, the only clear genetic link associated with a form of AD that gets passed to offspring is the one that causes the familial form of early-onset. Familial EOAD is extremely rare and the EOAD always develops in younger individuals. Some genes, such as the APOE4, are RISK factors, i.e., one may be more likely to develop AD if one has this gene, BUT just because you have that gene does not mean that you actually will develop AD.
I think AD sometimes appears to run in families just because members of those families tend to live to ripe old ages, and the older you are, the more likely you'll develop AD.
Mary in Montana, Borrelia burgdorferi, the organism that causes Lyme disease, is one of the pathogens that has been correlated with AD in some patients. So although your husband may not be exhibiting signs of Lyme disease itself, you could be right that the tick started it all.
kelly5000, a couple of studies I found tentatively linked Herpes simplex encephalitis with the development of AD in a couple of studies, but I've seen more studies on its correlation with Parkinson's.
I believe the myth regarding aluminum is that the use of aluminum pans etc can cause AD by exposing people to toxic levels of aluminum, NOT whether aluminum has been linked with AD. Most forms of aluminum are not soluble at physiologic pH and so most ingested aluminum remains unabsorbed by the body, and aluminum deposits are not typically found in body tissues. Nevertheless, localized aluminum deposits HAVE been associated with a number of neurodegenerative disorders, and have been identified in specific pathologic lesions by which these diseases are characterized, especially neurofibrillary tangles. In in vitro studies, aluminum has been shown to be capable of causing the conformational changes of amyloid beta protein that are seen in AD. So current studies are attempting to elucidate the mechanism(s) that might be involved in aluminum transport to / into the brain, and whether / how aluminum actually causes the protein conformational change or simply gets attached to the abeta protein.
Horrible, horrible headaches. On meds for them from the family doctor. Headaches are one of the things that we are asked about on the multi-page medical history and changes I fill out on every visit to the neurologist. They predate his diagnosis last year. They probably predate his EVENT as well.
I went checking my whole family for red blotches LOL None have AD except Lynn, and he doesn't have the red spot. But my mom does!! But she is sharp as a tack. Just out of curiosity, have any of you ever brought your loved one to a dermatologist? or mentioned it to your doctors?
There are only three significant things that have ever happened to Lynn.
1)He fell off a roof he was working on when he was in his 30's and has had double vision ever since.
2) He had a bad car accident in 1994 (or there about). A moose ran out and rolled over the top of the car and hood. He of course had massive tests and nothing has ever shown up. He was really messed up, and had trouble for a few days "clearing his head" but the doctors said he was fine and the tests showed no brain damage was done. But I often wonder about it. He did start having minor memory issues after the accident but his doctor said I probably only noticed it because I was tuned in to it. That could be true. How much of it was from the accident, or simply age ...or early AD I will never know.
3) he had a bad blood infection, due to a silent UTI. His PSA was really high, and he was put on IV meds for 2 weeks and then cypro for an additional 3 months. He was delusional with the high fever, and again... I noticed after this his memory got worse.
His heart is in excellent shape. BP and cholesterol are both good as well. Trisinger, Yes.. Lynn has suffered with headaches since he was a child.
i dont think anyone has consulted a dr about this red blotch stuff yet, we just are noticing others with AD have this same phenomenon as well in the last 2days. i doubt my dermatologist or neuro would even KNOW what it is. i have found lots of educated 'guessing' lately when asking about things assoc to AD-. it must have some sort of common ground somewhere for so many to have the 'blotch'..i can hear it being called, 'dermatitis' or such from shampoos, heat rash, etc. you know the normal things. that very well could be except maybe half or so of members here are posting otherwise. its very wierd indeed. maybe joans scientific researcher can look in to it..divvi
right, I know it has only been the last 2 days of posting, but Mary who brought it up already knew about it. So I was wondering if any of those who did know had ever had it looked at. I am not dismissing it, or mocking it, I just think it is an odd coincidence and nothing more. Perhaps it has more to do with age? Like I said earlier I googled red splotch spot etc on scalp, base of neck and got tons of hits, so I don’t think it is just some AD patients. I think it would have made medical literature by now if a significant number of people had a red splotch, if not while treating the patient perhaps during autopsies. Lynn does have AD, no spot. My mom does not have AD, but does have a spot. Odd
i also googled, and found something that said psoriasis an autoimmune skin disease could be assoc with AD?. so i think maybe the blotch is psoriasis of the scalp? from there is an interesting article in Journal of Neuroinflammation (jneuroinflammation.com) about ENBREL which is a med for psoriasis, and when injected directly into the brain of AD patients the results were dramatic in just minutes..dated jan 9,2008. sunshyne, you read this too in sciencedaily.com?? google enbrel and alzheimers...i hope its true. enbrel hasnt been approved for this but who knows after reading this. divvi
divvi, in my opinion, the guy who is pushing the enbrel treatment is a quack of the worst sort, preying on AD patients and their desperate caregivers. He has already been disciplined for pushing enbrel for another treatment without any evidence that it actually works. His latest venture requires an injection into the spinal column at the base of the skull once a week. Last I heard, he was charging in the neighborhood of $42,000 per year, but that may have gone up -- recently, he started charging something like $600 just for a phone consultation to answer questions. Plus enbrel has some nasty side-effects even when it is used the way FDA has approved. And there haven't ever been any clinical trials for using it to treat AD.
This is a general review, "Bacterial and Viral Infections in Neurodegenerative and Neurobehavioral Diseases": http://www.medscape.com/viewarticle/574944_print
This article mentions the association, and references another article, but the latter is apparently not readily available for free: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1143670
There are dozens of articles on the link between viruses such as herpes simplex virus 1 (HSV-1) and Alzheimer's. For example, see: Neurochem Int. 2008 May;52(6):920-34. Interactions between the products of the Herpes simplex genome and Alzheimer's disease susceptibility genes: relevance to pathological-signalling cascades. Carter CJ. The products of the Herpes simplex (HSV-1) genome interact with many Alzheimer's disease susceptibility genes or proteins. These in turn affect those of the virus. For example, HSV-1 binds to heparan sulphate proteoglycans (HSPG2), or alpha-2-macroglobulin (A2M), and enters cells via nectin receptors, which are cleaved by gamma-secretase (APH1B, PSEN1, PSEN2, PEN2, NCSTN). The virus also binds to blood-borne lipoproteins and apolipoprotein E (APOE) is able to modify its infectivity. Viral uptake is cholesterol- and lipid raft-dependent (DHCR24, HMGCR, FDPS, RAFTLIN, SREBF1). The virus is transported to the nucleus via the dynein and kinesin (KNS2) motors associated with the microtubule network (MAPT). Amyloid precursor protein (APP) plays a role in this transport. Nuclear export is mediated via disruption of the nuclear lamina and binding to LMNA. Herpes simplex activates kinases (CDC2 and casein kinase 2) whose substrates include APOE, APP, MAPT, PSEN2, and SREBF1. A viral protein is also able to delete mitochondrial DNA, a situation prevalent in Alzheimer's disease. The virus binds to the host transcription factors transcription factor CP2 (TFCP2) and POU2F1 that control many other genes associated with Alzheimer's disease. Viral latency is controlled by IL6 and IL1B and at different stages of its life cycle the virus can either promote or attenuate apoptosis via Fas and tumor necrosis factor pathways (FAS, TNF, DAPK1, PARP1). Viral evasion strategies include inhibition of the antigen processor TAP2, the production of an Fc immunoglobulin receptor mimic (FCER1G) and inhibition of the viral-activated kinase EIF2AK2. These and other host/viral interactions, targeted to certain Alzheimer's disease susceptibility genes, support the idea that some form of synergy between the pathogen and genetic factors may play a role in the pathology of late-onset Alzheimer's disease.
HSV is the most common cause of severe sporadic encephalitis in the Western world, with ~90% of cases caused by HSV-1. So any of the many articles on HSV-1 infections linked to AD may be relevant. (Note, however, that HSV causes only ~5-10% of acute viral encephalitis in the US ... I didn't find what causes the majority. I know there are dozens -- HIV can cause encephalitis and dementia, and arboviruses, flaviviruses, and Epstein-Barr virus can cause encephalitis.)
The following are articles that actually discussed the link between encephalitis and AD.
This article supports the hypothesis that latent HSV in the central nervous system can be reactivated and serve as a mechanism for triggering diseases such as Alzheimer's, using a mouse model. It is available at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17005636 J Virol. 2006 Dec;80(24):12387-92. Efficient reactivation of latent herpes simplex virus from mouse central nervous system tissues. Chen SH, Yao HW, Huang WY, Hsu KS, Lei HY, Shiau AL, Chen SH. For decades, numerous ex vivo studies have documented that latent herpes simplex virus (HSV) reactivates efficiently from ganglia, but rarely from the central nervous systems (CNS), of mice when assayed by mincing tissues before explant culture, despite the presence of viral genomes in both sites. Here we show that 88% of mouse brain stems reactivated latent virus when they were dissociated into cell suspensions before ex vivo explant culture. The efficient reactivation of HSV from the mouse CNS was demonstrated with more than one viral strain, viral serotype, and mouse strain, further indicating that the CNS can be an authentic latency site for HSV with the potential to cause recurrent disease.
Continuing (since this site can't stand loooooooooooong posts):
Cell Mol Biol (Noisy-le-grand). 2003 Dec;49(8):1233-40. Coexistence of Alzheimer disease neuropathology with herpes simplex encephalitis. Denaro FJ, Staub P, Colmer J, Freed DM. Several unusual features were observed during routine histopathological confirmation of a clinical diagnosis of Alzheimer's disease (AD) in an 85-year-old, right-handed, married male. The patient presented with a 12-year history of slowly progressive cognitive impairment, which increased in severity just prior to death. Detailed postmortem examination of the frontal lobes revealed a significant number of neuritic plaques and neurofibrillary tangles. Multifocal spongiform encephalopathic changes, mononuclear perivascular infiltrates, subcortical demyelination and gliosis were also found. Of particular interest were well-defined neuronal and astrocytic intranuclear inclusion bodies (Cowdry type I and I), suggestive of viral disease. Electron microscopy, immunohistochemical and immunohistofluorescent studies confirmed a Herpes simplex type I encephalitis (HSV-I). These histological results and the clinical history of progression suggest that reactivation of a latent viral infection may have contributed to the rapid progression of dementia prior to death. The present analysis underscores the fact that multiple etiologic factors may act simultaneously to produce dementia. While one such process may be identified or diagnosed (in the present case AD), it is necessary to be open to the possibility that another mechanism may come into play during the time course of that illness. A differential diagnosis may be difficult when the symptoms of the two disease processes are very similar. Such may be the case if there is reactivation of a previously undiagnosed herpes virus infection. With the development of PCR and in situ hybridization diagnosis will be simplified and more definitive.
J Med Virol. 2005 Feb;75(2):300-6. Productive herpes simplex virus in brain of elderly normal subjects and Alzheimer's disease patients. Wozniak MA, Shipley SJ, Combrinck M, Wilcock GK, Itzhaki RF. It was previously shown that herpes simplex virus type 1 (HSV1) DNA resides latently in a high proportion of aged brains and that in carriers of the type 4 allele of the apolipoprotein E gene (APOE-epsilon4), it confers a strong risk of Alzheimer's disease. It was suggested that initial entry of brain by HSV1 and any subsequent reactivation(s) would cause a type of limited encephalitis, the resulting damage being more harmful in APOE-epsilon4 carriers. Reactivation(s) would induce synthesis of intrathecal antibodies; these are long-lived after herpes simplex encephalitis so they were sought in cerebrospinal fluid (CSF) of Alzheimer's disease patients and age-matched normal subjects. Intrathecal antibodies to human herpesvirus 6 (HHV6) were also sought as DNA of this virus has been detected previously in a high proportion of Alzheimer's disease brains. Antibody indices for HSV and HHV6 were measured using indirect ELISA for IgG antibody, and single radial immunodiffusion was used for albumin, in serum and CSF. A raised antibody index (>1.5) indicative of virus-specific intrathecal HSV1 IgG synthesis was found in 14/27 (52%) Alzheimer's disease patients and 9/13 (69%) age-matched normals (difference non-significant). A raised antibody index to HHV6 was detected in 22% of the Alzheimer's disease patients and in no normals, so presumably this virus either did not reactivate in brain or it elicited only short-lived intrathecal antibodies. The HSV1 results confirm the original PCR findings that show the presence of HSV1 DNA sequences in many elderly brains, and indicate also that the whole functional HSV1 genome is present, and that the virus has replicated.
my dh has the red spot at the back of his neck. i don't know if he has had it since birth,because he used to wear his hair longer,but i have cut his hair for years and i noticed it, but i have never thought anything about it because my mother always said these were birthmarks,i have seen several people with these marks. dh does have beautiful blue eyes,has had alot of headaches,daily sometimes,for years. we live in an area with alot of ticks and he has always gotten tick bites,but testing says no to lyme disease. he had rheumatic fever as a child,he also got shut up in a hot car for some time,before he was found. he got shocked severely,working on our washing machine,years ago and he was temperarely blinded. he has always worked on the family farm,and worked with chemicals for weed control,insect control etc. he was also a professional fireman for 20 yrs. before he retired in 2001. my views on alunimuim are,i quit using it years ago for cooking,my pressure cooker is stainless clad over the alunimum. my mother always used a pressure cooker and of course alunimium pots and pans,and she always cautioned us about not scraping the pan when getting food out,she knew even then,that it scraped off in our food and it couldn't be good for us. on the teflon issue,i don't use it either,i haven't for years,since my kids were little. we used to have pet birds and i read that if your teflon got to a certain temperature the fumes would kill your bird. many people had this to happen and weren't aware of the toxic effects on their bird,until it was too late. well i put 2 and 2 together and thought,if it would kill a bird,what was it doing to us? i had always heard that miners used to use canaries to check if a mine was safe for humans,if the bird lived after being put in the mine,then it was okay to work,and of course if it died,they would wait and redo the test later. i never forgot this lesson. it seemed to me to be the same principal,if something is not safe for your pet to be exposed to in your home,then it wasn't safe for humans to be exposed to either. i have thought of so many things that were unsafe for my family. i have never had my home sprayed for bugs,just killed them the old fashioned way. i have always tried to be as chemical free as possible. i always worried about the chemicals my dh was exposed to on the farm and have often wondered if any of these things were contributing factors in his eoad. jav
I have also always wondered if the chemicals my husband was exposed to on the farm & then in the (GM) foundry he worked in contributed to his dementia.
About the red blotch. Just to verify - (1) it's at the base of the neck, in back? (2) is it a 'raised' rash or is it like a birthmark?
If it's at the base of the neck, in back, and if it's like a birthmark - I know a woman (who unfortunately seems to be a good candidate to someday develop Alz but at 65 has not, yet) - she and her adult daughter each have such a birthmark type red blotch.
I'm wondering if anyone can take a photo with a digital camera, and upload it somewhere - Picasa? Kodak? etc. - so that there's no doubt about description?
OOooh! That Enebrel guy. So ANGRY!! Arrrgh. My sister (who is a scientist, so I tend to trust her on medical stuff) sent me an article about that treatment. (She was just trying to be helpful.) So I went though all kinds of trauma and emotions and finally gave them a call. As you say, they wanted $700 just to talk to me on the phone for an hour! That's when I came to my senses and realized this man is just preying on people like us, making money off other people's misery. It would be poetic justice if HE got AD.
I was enthralled to find while watching the 'Forgetting' the other nite, that the hippocampus area of the brain was the first affected during AD, which controls shorterm memory, spatial navigation, and can cause disorientation. also learned that damage to the hippocampus CAN include oxigen starvation-if i am not too far off, (if someone knows) this area the hippocampus is in two halfs and in the lower back portion of the brain...ie- around the red blotch area? the program was showing diagrams how the beta amyloid plaques and tangles attack the neuron cells..maybe this could be related to the blotch in some way?? just thinking out loud, divvi
beenthere, I couldn't agree with you more. That would definitely be poetic justice.
As Dazed said, there's a very long thread on the Alz Assn website, by people who are pursuing this treatment for their ADLOs. They are extremely vocal, and very, very defensive. I read the thread for a while, but started getting too upset. For example, one of the most ardent proponents recently posted that her ADLO had improved a little after the initial injections, and has held somewhat steady for four months. She thinks this is wonderful. My husband improved a LOT after the initial namenda pills, and between namenda and huperzine A, has held fairly steady for three years ... and he sure isn't paying $42,000 for the privilege of undergoing weekly injections. But there is no way to get these poor caregivers to understand they're being had. It's almost like a cult.
I don't know about the red blotch and the hippocampus area, but I do know that the shrinkage of the hippocampus was the first real evidence that we had that we were dealing with EOAD. The neuro showed me the films and it was obvious that something awful was going on in my husband's brain.
beenthere, according to the Alzheimer Research Forum article:
http://www.alzforum.org/new/detail.asp?id=1738
(which is one of the best reviews on Tobinick's enbrel treatment I've seen), Tobinick is a dermatologist who had been active in laser hair removal prior to "developing an interest in the use of enbrel for central nervous system indications." His Institute of Laser Medicine, where he does the hair removal, and his Institute for Neurological Research, where he treats AD patients, are in the same building and even in the same suite. (It's a private medical office and has nothing to do with the University.)
The Medical Board of California lists Tobinick as being on probation. He has been charged with unprofessional conduct relating to advertising an unproven treatment for disc-related back pain, also using enbrel. Other researchers performed a double-blind placebo-controlled, dose-response trial, and reported that the enbrel injection was not effective for this indication.
Tobinick sometimes claims to be a professor at UCLA, and uses UCLA physical and email addresses, to bolster his credentials for the enbrel treatments. He is actually a "voluntary assistant clinical professor" in the UCLA Division of Dermatology. I think I read somewhere else that he rents a small office from the university. He does not have any affiliation with the UCLA Alzheimer Disease Center.
Does anyone have theories on trumatic stress as a possible cause for AD? I think I read some articles on the AD site a couple of years ago. My LO was senior management in a large company and went through some seriously high level stress back in the mid 90s through his employment. Now, he's never been able to handle emotions and has pretty much always denied that he had them. (His nickname was the Iceman!) For our whole marriage he's been unable to express his feelings and when this situation began at work, he simply had no coping skills. He thought he ws having heart problems and went to a cardiologist for full testing only to be told that his heart was very healthy. After things had finally settled out and he was proven to be a quasi hero for the company, I began noticing the earliest symptoms. Like many we just wrote them off to life. He wasn't diagnosed until 2004 and by then wasn't able to keep up at work any longer. No issues with head injuries but he did work for short periods at chamical plants, but was management and didn't actually handle things. Headaches were among the early symptoms as he was having trouble keeping up. Any thoughts?
Liz, there is clearly a strong link between stress and AD, although most of the papers I have seen are studying the impact of stress on the progression of the disease, rather than stress actually causing it. However, many researchers feel chronic stress could indeed trigger AD, and I believe there are some studies under way. The link between stress and AD is a very hot area of study these days.
I became very interested in this, since it is clear that my husband's symptoms are very sensitive to stress. I tried to get him enrolled in studies at UCSD, but Guerry says she's only looking at patients who have MCI right now, and my husband has full-blown AD.
I tried to do a bit of googling on the subject this afternoon, but one of the key sources for papers seems to be down today. A few links you may find of interest:
http://www.sciencedaily.com/releases/2007/08/070827095121.htm (...this is about Guerry Peavy's research here at UCSD.)
Jae-Eun Kang, John R. Cirrito, Hongxin Dong, John G. Csernansky, and David M. Holtzman. 2007. Acute stress increases interstitial fluid amyloid-β via corticotropin-releasing factor and neuronal activity. Proc Natl Acad Sci U S A 104(25): 10673–10678. Describes a possible mechanism by which stress may affect AD disease pathogenesis. Full article available at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1965571
P1-035Chronic stress accelerates learning and memory impairments and increases amyloid deposition in APPV717I-CT100 transgenic mice, an Alzheimer’s disease model Alzheimer's and Dementia, Volume 2, Issue 3, Supplement 1, July 2006, Page S104 Yun Ha Jeong1email address, Cheol Hyoung Park1, Jongman Yoo1, Ki Young Shin1, Sung-Min Ahn1, Hye-Sun Kim1, Sang Hyung Lee2, Piers C. Emson3, Yoo-Hun Suh1 available through the Alzheimer's Association: http://www.alzheimersanddementia.com/article/S1552-5260(06)02793-2/abstract
Neurosci Lett. 2008 Feb 6;431(3):197-200. Free full-text article available through PubMed The effect of stress on the expression of the amyloid precursor protein in rat brain. Sayer R, Robertson D, Balfour DJ, Breen KC, Stewart CA. The abnormal processing of the amyloid precursor protein (APP) is a pivotal event in the development of the unique pathology that defines Alzheimer's disease (AD). Stress, and the associated increase in corticosteroids, appear to accelerate brain ageing and may increase vulnerability to Alzheimer's disease via altered APP processing. In this study, rats were repeatedly exposed to an unavoidable stressor, an open elevated platform. Previous studies in this laboratory have shown that a single exposure produces a marked increase in plasma corticosterone levels but animals develop tolerance to this effect between 10 and 20 daily sessions. Twenty-four hours after stress, there was an increase in the ratio of the deglycosylated form of APP in the particulate fraction of the brain, which subsequently habituated after 20 days. The levels of soluble APP (APPs) tended to be lower in the stress groups compared to controls except for a significant increase in the hippocampus after 20 days of platform exposure. Since APPs is reported to have neurotrophic properties, this increased release may represent a neuroprotective response to repeated stress. It is possible that the ability to mount this response decreases with age thus increasing the vulnerability to stress-induced AD-related pathology.
M . Pardon , C . Marsden. 2008. The long-term impact of stress on brain function: From adaptation to mental diseases . Neuroscience & Biobehavioral Reviews 32(6): 1071 - 1072. No abstract available, and the paper is not available for free. I've sent off an email to Marie Pardon, requesting a reprint or .pdf. I'll let you know if she responds. She's in England.
my dh had an adnormal pituitory gland. when he had an mri the dr said the gland was flattened. this was during the testing to try to get a dx. ,maybe 4 yrs ago. did any of your lo's have any thing like this while being tested. i wonder if there is any connection to ad? i keep looking for common factors in all the ad patients. my dh is declining so fast,it is just such a pity to watch and not be able to help him get better. jav
My dh also has blue eyes. And he worked as a meat cutter for almost 30 years, our doc did think mad cow disease for a few seconds then blew it off as hes never ingested raw meat. He has a red mark but its on the side of his neck,not back of head.
jav, my DH has a pituitary gland tumor on the prolactin part. He has had it for at least 8 years that we can tell. The last MRI 1 1/2 years ago was the first where it was actually visible. the doctors knew it was there because of the elevated prolactin level. So in his case, it is an actual growing tumor. He takes medicine to lower the prolactin level and the medicine actually keeps the tumor from growing. They are going to ask him to get another MRI later this year. Does you DH have AD or FTD or something else?
At the SD Zoo? Really??? Oh, yeah, neat is sure the word for it! Doing what? Are they actually at the Zoo itself, or the Wild Animal Park?
Been thinking about grants, actually, spending a little time toying with ideas for subjects, and looking into what agencies or private foundations might be interested in funding them.
The big problem is that I don't have the academic credentials for doing a paper study (survey, data mining, that sort of thing) in the areas I've come up with, so I'd need to find teaming partners who would agree to let me tag along. Which isn't impossible -- I'm good at grant writing, and preparing a grant takes a lot of time, and people who are doing research are hard-pressed to find that kind of time ... so I could probably get a piece of the action if I did the lion's share of the work preparing the applications. If I could narrow down to a handful of good ideas, I could find the teaming partners -- I've done a lot of that in the past.
So let me ask you: what sorts of studies on AD and/or caregiving would you like to see done? Not diagnostics or drugs, those would take enormous physical resources (laboratories and instrumentation) and competition is very fierce -- something involving surveys or interviews, literature reviews, working with AD patients in nursing homes or at the university AD research center, establishing web-based information sources on a particular subject, etc.
Examples of my vague thoughts so far:
Potential benefits of pet therapy (I was originally thinking about therapy for the patient, but now that trisinger's kids are acting up, maybe therapy for the caregiver spouse instead...)
Sex and intimacy issues inside and/or outside the marriage.
Unique financial concerns of EOAD spouses.
Benefits of marital counseling (or lack thereof...)
sunshyne, the effects of stress and isolation of the caregiver and its correlation to caregiver death along with AD victims -' AD will take two if you let it""plus ALL of the above.divvi