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| | General Talks Feel free to talk about anything and everything... | | New Member | | Posts: 6 Thanks: 0
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Join Date: May 2007 Location: pnw | | | Just want general direction/advice -
16-05-2007, 01:45 AM
I don't want to get into the hoopla of la la land that happens on the internet with people interfering with those that really want help.
I am a 41 year old female who had a grandmother that died with Alzheimers Disease.
I am finding myself with tendencies she had that I noticed when I was a little girl. Can't find things, can't locate things, and why would I have put that there kinda things......
Is Alz genetic? I drink and smoke, but my grandmother never did, and I keep my drinking on a limit. The times I can't find things is when I haven't had anything to drink.
Someone please respond. I questioned my sanity today, for the 2nd time.
Karrie | | Senior Member | | Posts: 937 Thanks: 37
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Join Date: Oct 2005 Location: bhaktapur | | | Re: Just want general direction/advice -
16-05-2007, 03:04 AM
hey karrie20x, we feel so sorry for your grandmother...
and hey dont get upset... noone can tell anything for sure without having proper checkup and investigations... so what i suggest you is ... be bold and consult your physician.. have a detail checkup... i am sure you will have a much clearer picture of your health that way..... Dr. Suvash Shrestha, Intern
Kathmandu Medical College | | Senior Member | | Posts: 937 Thanks: 37
Thanked 346 Times in 331 Posts
Join Date: Oct 2005 Location: bhaktapur | | | Re: Just want general direction/advice -
16-05-2007, 03:21 AM
hey karrie, may be this will provide you some help..... Quote:
Alzheimer's disease (AD), also known simply as Alzheimer's, is a neurodegenerative disease characterized by progressive cognitive deterioration together with declining activities of daily living and neuropsychiatric symptoms or behavioral changes. It is the most common type of dementia.
The most striking early symptom is loss of memory (amnesia), which usually manifests as minor forgetfulness that becomes steadily more pronounced with illness progression, with relative preservation of older memories. As the disorder progresses, cognitive (intellectual) impairment extends to the domains of language (aphasia), skilled movements (apraxia), recognition (agnosia), and those functions (such as decision-making and planning) closely related to the frontal and temporal lobes of the brain as they become disconnected from the limbic system, reflecting extension of the underlying pathological process. This pathological process consists principally of neuronal loss or atrophy, principally in the temporoparietal cortex, but also in the frontal cortex, together with an inflammatory response to the deposition of amyloid plaques and neurofibrillary tangles.
The ultimate cause of the disease is unknown. Genetic factors are known to be important, and dominant mutations in three different genes have been identified that account for a much smaller number of cases of familial, early-onset AD. For the more common form of late onset AD (LOAD), ApoE is the only repeatibly confirmed susceptibility genes for AD. In 2007, evidence suggested a possible association between SORL1 alleles and AD.[1] Stages and symptoms
Mild — At the early stage of the disease, patients have a tendency to become less energetic or spontaneous, though changes in their behavior often go unnoticed even by the patients' immediate family. This stage of the disease has also been termed Mild Cognitive Impairment (MCI) although this term remains somewhat controversial.[4]
Moderate — As the disease progresses to the middle stage, the patient might still be able to perform tasks independently, but may need assistance with more complicated activities.
Severe — As the disease progresses from the middle to late stage, the patient will undoubtedly not be able to perform even the simplest of tasks on their own and will need constant supervision. They may even lose the ability to walk or eat without assistance. They might forget to eat and starve.
Diagnosis
The diagnosis is made primarily on the basis of history, clinical observation, memory tests and intellectual functioning over a series of weeks or months, with various physical tests (blood tests and neuroimaging) being performed to rule out alternative diagnoses. No medical tests are available to diagnose Alzheimer's disease conclusively pre-mortem. Expert clinicians who specialize in memory disorders can now diagnose AD with an accuracy of 85–90%, but a definitive diagnosis of Alzheimer's disease must await microscopic examination of brain tissue, generally at autopsy. Functional neuroimaging studies such as PET and SPECT scans can provide a supporting role where dementia is clearly present, but the type of dementia is questioned. Recent studies suggest that SPECT neuroimaging approaches clinical exam in diagnostic accuracy and may outperform exam at differentiating types of dementia (Alzheimer's disease vs. vascular dementia).[5][6] However, Alzheimer's disease remains a primarily clinical diagnosis based on the presence of characteristic neurological features and the absence of alternative diagnoses, with possible neuroimaging assistance. Interviews with family members and/or caregivers are extremely important in the initial assessment, as the sufferer him/herself may tend to minimize his symptomatology or may undergo evaluation at a time when his/her symptoms are less apparent, as quotidian fluctuations ("good days and bad days") are a fairly common feature. Such interviews also provide important information on the affected individual's functional abilities, which are a key indicator of the significance of the symptoms and the stage of dementia.
Initial suspicion of dementia may be strengthened by performing the mini mental state examination, after excluding clinical depression. Psychological testing generally focuses on memory, attention, abstract thinking, the ability to name objects, visuospatial abilities, and other cognitive functions. Results of psychological tests may not readily distinguish Alzheimer's disease from other types of dementia, but can be helpful in establishing the presence of and severity of dementia. They can also be useful in distinguishing true dementia from temporary (and more treatable) cognitive impairment due to depression or psychosis, which has sometimes been termed "pseudodementia". In addition, a 2004 study by Cervilla and colleagues showed that tests of cognitive ability provide useful predictive information up to a decade before the onset of dementia.[7] However, when diagnosing individuals with a higher level of cognitive ability, in this study those with IQs of 120 or more,[8] patients should not be diagnosed from the standard norm but from an adjusted high-I.Q norm that measured changes against the individual's higher ability level. genetic linkage
Alzheimer's disease is definitely linked to the 1st, 14th,[49] and 21st chromosomes, but other linkages are controversial and not yet confirmed. While some genes predisposing to AD have been identified , such as ApoE4 on chromosome 19, sporadic AD also involves other risk and protective genes still awaiting confirmation. Risk reducers
Intellectual stimulation (e.g., playing chess or doing crosswords)[53]
Regular physical exercise[54]
Regular social interaction [9]
A Mediterranean diet with fruits and vegetables and low in saturated fat,[55] supplemented in particular with:
B vitamins[56]
Omega-3 fatty acids, especially Docosahexaenoic acid[57][58]
Fruit and vegetable juice[59][60]
High doses of the antioxidant Vitamin E (in combination with vitamin C) seem to reduce Alzheimer's risk in cross sectional studies but not in a randomized trial and so are not currently a recommended preventive measure because of observed increases in overall mortality[61][62]
Cholesterol-lowering drugs (statins) reduce Alzheimer's risk in observational studies but so far not in randomized controlled trials[63]
Female Hormone replacement therapy is no longer thought to prevent dementia based on data from the Women's Health Initiative
Long-term usage of non-steroidal anti-inflammatory drugs (NSAIDs), used to reduce joint inflammation and pain, are associated with a reduced likelihood of developing AD, according to some observational studies.[64][65] The risks appear to outweigh the drugs' benefit as a method of primary prevention.[66]
One recent research study has found that cannabinoids, the psychoactive compounds in marijuana, "succeed in preventing the neurodegenerative process occurring in the disease."[67] Treatment
There is currently no cure for Alzheimer's disease. Currently available medications offer relatively small symptomatic benefit for some patients but do not slow disease progression. It helps a little for the memory. The American Association for Geriatric Psychiatry published a consensus statement on Alzheimer's treatment in 2006.[66] Acetylcholinesterase inhibitors
Acetylcholinesterase (AChE) inhibition was thought to be important because there is a reduction in activity of the cholinergic neurons. AChE-inhibitors reduce the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain (combatting the loss of ACh caused by the death of the cholinergin neurons). Acetylcholinesterase-inhibitors seemed to modestly moderate symptoms but do not alter the course of the underlying dementing process.[72][73][74]
Examples include:
tacrine - no longer clinically used
donepezil - (marketed as Aricept)
galantamine - (marketed as Razadyne in the U.S.A. Marketed as Reminyl or Nivalin in the rest of the world)
rivastigmine - (marketed as Exelon)
There is significant doubt as to the effectiveness of cholinesterase inhibitors. A number of recent articles have criticized the design of studies reporting benefit from these drugs, concluding that they have doubtful clinical utility, are costly, and confer many side effects.[75][76] The pharmaceutical companies, but also some independent clinicians, dispute the conclusions of these articles. A transdermal patch is under development that may ease administration of rivastigmine.[77] Ginkgo biloba
One of the natural extracts that has been examined in Alzheimer's is Ginkgo (Ginkgo biloba), also known as the Maidenhair Tree. The extract of the Ginkgo leaves contains flavonoid glycosides and terpenoids, and both seeds and leaves have been used pharmaceutically in China and the West. Examining over 50 studies conducted on Ginkgo for the treatment of "cognitive impairment and dementia," a Cochrane Review concludes that "there is promising evidence of improvement in cognition and function associated with Ginkgo." According to this review the two randomized controlled studies that focused on Alzheimer's patients both showed significant improvement in these areas. The review calls for a large study which can "provide robust estimates of the size and mechanism of any treatment effects."[78] The AAGP review[66] did not recommend Ginkgo neither did it warn against its use. A large, randomized clinical study in the US called the GEM study is underway (fully enrolled) and examining the effect of Ginkgo to prevent dementia.[79] NMDA antagonists
Recent evidence of the involvement of glutamatergic neuronal excitotoxicity causes Alzheimer's disease led to the development and introduction of memantine. Memantine is a novel NMDA receptor antagonist, and has been shown to be moderately clinically efficacious.[80] Memantine is marketed as Akatinol, Axura, Ebixa and Namenda. Psychosocial interventions
Cognitive and behavioral interventions and rehabilitation strategies may be used as an adjunct to pharmacologic treatment, especially in the early to moderately advanced stages of disease. Treatment modalities include counseling, psychotherapy (if cognitive functioning is adequate), reminiscent therapy, reality orientation therapy, and behavioral reinforcements as well as cognitive rehabilitation training.[81][82] Treatments in clinical development
A large number of potential treatments for Alzheimer's disease are currently under investigation, including four compounds being studied in phase 3 clinical trials. Xaliproden had been shown to reduce neurodegeneration in animal studies.[83] Tramiprosate (3APS or Alzhemed) is a GAG-mimetic molecule that is believed to act by binding to soluble amyloid beta to prevent the accumulation of the toxic plaques. R-flurbiprofen (MPC-7869) is a gamma secretase modulator sometimes called a selective amyloid beta 42 lowering agent. It is believed to reduce the production of the toxic amyloid beta in favor of shorter forms of the peptide.[84][85] Leuprolide has also been studied for Alzheimer’s. It is hypothesized to work by reducing leutenizing hormone levels which may be causing damage in the brain as one ages.[86]
Vaccines or immunotherapy for Alzheimer's, unlike typical vaccines, would be used to treat diagnosed patients rather than for disease prevention. Ongoing efforts are based on the idea that, by training the immune system to recognize and attack beta-amyloid, the immune system might reverse deposition of amyloid and thus stop the disease. Initial results using this approach in animals were promising, and clinical trials of the drug candidate AN-1792 showed results in 20% of patients. However, in 2002 it was reported that 6% of multi-dosed participants (18 of 300) developed symptoms resembling meningoencephalitis, and the trials were stopped. Participants in the halted trials continued to be followed, and 20% "developed high levels of antibodies to beta-amyloid" and some showed slower progression of the disease, maintaining memory-test levels while placebo-patients worsened. Microcerebral haemorrhages with passive immunisation and meningoencephalitis with active immunisation still remains to be potent threats to this strategy.[87] Work is continuing on less toxic Aβ vaccines, such as a DNA-based therapy that recently showed promise in mice.[88] Researchers from University of South Florida announced a patch version of the drug was shown to be safe and effective when tested on mice.[89]
Proposed alternative treatments for Alzheimer's include a range of herbal compounds and dietary supplements. In the AAGP review from 2006,[66] Vitamin E in doses below 400 IU was mentioned as having conflicting evidence in efficacy to prevent AD. Higher doses were discouraged as these may be linked with higher mortality related to cardiac events.
Laboratory studies with cells and animals continually fuel the pipeline of potential treatments. Some currently approved drugs such as statins and thiazolidinediones[90] have also been under investigation for the treatment and prevention of Alzheimer’s. Recent clinical trials for Phase 2 and Phase 3 in this category have taken 12 to 18 months under study drug, plus additional months for patient enrollment and analysis. Compounds that are just entering into human trials or are in pre-clinical trials would be at least 4 years from being available to the public and would be available only if they can demonstrate safety and efficacy in human trials. Occupational and lifestyle therapies
Modifications to the living environment and lifestyle of the Alzheimer's patient can improve functional performance and ease caretaker burden. Assessment by an occupational therapist is often indicated. Adherence to simplified routines and labeling of household items to cue the patient can aid with activities of daily living, while placing safety locks on cabinets, doors, and gates and securing hazardous chemicals and guns can prevent accidents and wandering. Changes in routine or environment can trigger or exacerbate agitation, whereas well-lit rooms, adequate rest, and avoidance of excess stimulation all help prevent such episodes.[91] Appropriate social and visual stimulation, however, can improve function by increasing awareness and orientation. For instance, boldly colored tableware aids those with severe AD, helping people overcome a diminished sensitivity to visual contrast to increase food and beverage intake.[92] Social issues
Alzheimer's is a major public health challenge since the median age of the industrialized world's population is increasing gradually.[93] Indeed, much of the concern about the solvency of governmental social safety nets is founded on estimates of the costs of caring for baby boomers, assuming that they develop Alzheimer's in the same proportions as earlier generations. For this reason, money spent informing the public of available effective prevention methods may yield disproportionate benefits.
The role of family caregivers has also become more prominent, as care in the familiar surroundings of home may delay onset of some symptoms and delay or eliminate the need for more professional and costly levels of care. However, home-based care may entail tremendous economic, emotional, and even psychological costs as well (see elderly care). Family caregivers often give up time from work and forego pay to spend 47 hours per week on average with an affected loved one who frequently cannot be left alone. From a survey of patients with long term care insurance, direct and indirect costs of caring for an Alzheimer's patient average $77,500 per year.[94] Statistics on Alzheimer's disease
In the United States of America, AD was the 7th leading cause of death in 2004, with 65,829 number of deaths (and rising).[95]
At over $100 billion per year, AD is the third most costly disease in the U.S., after heart disease and cancer.[96]
There are an estimated 24 million people with dementia worldwide.[97] By 2040, it is projected that this figure will have increased to 81 million.
More than 5 million Americans are estimated to have Alzheimer’s disease.[98] It is projected that 14.3 million Americans will have the disease by mid-century: a 350 percent increase from 2000.[99]
The federal government estimates spending approximately $647 million for Alzheimer’s disease research in fiscal year 2005.[98]
| source: Alzheimer's disease Dr. Suvash Shrestha, Intern
Kathmandu Medical College | | New Member | | Posts: 6 Thanks: 0
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Join Date: May 2007 Location: pnw | | | Re: Just want general direction/advice -
16-05-2007, 04:00 AM
Thank you so very much for your information. I can't help but wonder if I'm not going through a genetic problem. The history is just there. I printed out what you had to say and will talk to my doctor about it.
I hope before I get much older that they come up with more answeres about AZ. It scares me to think about it at my age - we all grew up as little kids and invinsible. I have fybro to top it off. That is dealable and under wraps. I function. I just can't handle the thought of losing my mind.
My email is karebear_dunno@yahoo.com if you want to further contact me.
Glad I found you and thank you for your help and info.
Karrie |  | Senior Member | | Posts: 167 Thanks: 0
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Join Date: Dec 2005 Location: kathmandu, sinamangal | | | Re: Just want general direction/advice -
16-05-2007, 08:53 AM
well karrie, what i suggest you is, u go and talk to a doctor. tell him/her your problem and problem u're facing of something like losing ur mind... may be he'll guide u through the best remedies.......
believe me, just complaining ain't gonna help, be positive and head for consultation........ doors will open...
believe on yourself , be bold.. 7th batch, kmc  " never give up trying " | | Senior Member | | Posts: 937 Thanks: 37
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Join Date: Oct 2005 Location: bhaktapur | | | Re: Just want general direction/advice -
16-05-2007, 10:12 PM
hey karrie, nice to hear from you and karrie, i would consider it my great pleasure if i could be of any help to you.... and, we all pray for you - i know everything will go well with you.... so, stop worrying.. and keep smiling.... life is too precious to waste worrying..... enjoy every moment to the maximum! and hey we are all here for you! Dr. Suvash Shrestha, Intern
Kathmandu Medical College | | New Member | | Posts: 6 Thanks: 0
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Join Date: May 2007 Location: pnw | | | Re: Just want general direction/advice -
17-05-2007, 12:57 AM
Thank you and I received your email and responded! :-) | | Thread Tools | Search this Thread | | | | | Display Modes | Linear Mode |
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