Blog Comments

I've just discovered your blog on this site. I only joined yesterday, when my husband was confirmed as having Alzheimers disease. I'm sure your reseaarch and blog will be really interesting and useful to me. Will come back and explore all your posts - just wanted to say thanks.

[url=http://longevity.about.com/od/researchandmedicine/p/crosslinking.htm]How Sugar Makes Us Age - Protein Cross-Linking and Aging[/url]
[quote]"Researchers believe that if the concentration of sugar in the blood is high, then more cross-linking occurs. Everyone could benefit from keeping their blood sugar from spiking. Foods with a high glycemic index, such as sugary sodas and juices, release sugar into the body quickly. These foods have been associated with cardiovascular disease, possibly because of protein cross-linking."[/quote]
The way to stop you blood glucose levels spiking or getting high and staying too high for too long is to abstain from eating/drinking high sugar/fructose food items.

don't forget to watch part 2 of Cynthia Kenyon's talk.
[url=http://www.youtube.com/watch?v=HxfLm30FHwA][IMG]http://i1.ytimg.com/vi/HxfLm30FHwA/default.jpg[/IMG]
Cynthia Kenyon(UCSF) Part 2: :The Regulation of Aging by Signals from the Reproductive System[/url]

For those that like to understand the mechanism underlying human ageing this talk is interesting.
[url=http://www.youtube.com/watch?v=V48M5j-6zdE][IMG]http://i3.ytimg.com/vi/V48M5j-6zdE/default.jpg[/IMG]Cynthia Kenyon: Experiments that hint of longer lives[/url]

It's worth following on from that to understand what Professor Kenyon does herself to slow the ageing process
here is a easy to understand Daily Mail article.
[url=http://www.dailymail.co.uk/health/article-1323758/Can-cutting-Carbohydrates-diet-make-live-longer.html#ixzz1eFAHBR53]Can cutting carbohydrates from your diet make you live longer?[/url]
[quote]Carbohydrates, and especially refined ones like sugar, make you produce lots of extra insulin. I’ve been keeping my intake really low ever since I discovered this.
‘I’ve cut out all starch such as potatoes, noodles, rice, bread and pasta. Instead I have salads, but no sweet dressing, lots of olive oil and nuts, tons of green vegetables along with cheese, chicken and eggs.
‘I’ll have a hamburger without a bun and fish without batter or chips. I eat some fruit every day, but not too much and almost no processed food. I stay away from sweets, except 80 per cent chocolate.’[/quote]
If you feel you need to watch the initial video again it may help to watch this more detailed previous version of a similar talk
[url=http://www.youtube.com/watch?v=DT4PWu43e9U][IMG]http://i1.ytimg.com/vi/DT4PWu43e9U/default.jpg[/IMG]Cynthia Kenyon (UCSF) Part 1: Genes that Control Aging[/url]

[url=http://www.ncbi.nlm.nih.gov/pubmed/22064069]Blood Folate is Associated with Asymptomatic or Partially Symptomatic Alzheimer's Disease in the Nun Study.[/url][quote]Abstract
Asymptomatic and partially symptomatic Alzheimer's disease (APSYMAD) are a series of cognitive states wherein subjects have substantial Alzheimer's disease (AD) pathology (classification B or C by the Consortium to Establish a Registry for AD criteria), but have normal or only partially impaired cognitive function; all of these subjects are non-demented.
These cognitive states may arise from the prevention or delay of clinical symptom expression by exposure to certain nutritional factors.
This study examined blood levels of folate and antioxidants (i.e., carotenoids) in relation to APSYMAD, nested in the Nun study, a longitudinal study of aging and AD.
Sixty elderly female subjects, who had AD on the basis of neuropathology exams, were included.
Following adjustment for APOE4 status, education level, and age at blood draw, subjects with the highest blood folate levels had a higher likelihood of being in the APSYMAD group as compared to the demented (AD) group (odds ratio = 1.09, 95% CI = 1.00-1.18. p < 0.06).
This association was not significantly influenced by additional adjustment for blood concentrations of carotenoids.
Restriction of the population to subjects with near normal cognition on the cognitive state score (score = 1-3) indicated an elevated association with blood folate (odds ratio = 1.12, 95% CI = 1.01-1.25, p < 0.04).
Blood carotenoids were not associated with APSYMAD.
Thus, folate status may influence the expression of clinical symptoms of AD disease and aid in the delay or prevention of dementia.[/quote]

These nums would not have been identified as Pre Alzheimer's had they not been part of a trial. They were all normal or only partially impaired cognitive function; all of these subjects are non-demented. If ensuring you take an effective form of folate allows you to remain "normal" and not demented (albeit with indicators of Alzheimer') then this is the point at which cheap effective , side effect free interventions are most likely to delay the progress of the condition.

Here is a recent paper showing the way magnesium may be a good idea to for reducing the damaging consequences Ca(2+) induced neuroinflammation in degenerative neurological disorders such as Alzheimer disease and Parkinson disease.

[url=http://www.ncbi.nlm.nih.gov/pubmed/21040713]Mg2+ ions reduce microglial and THP-1 cell neurotoxicity by inhibiting Ca2+ entry through purinergic channels.[/url]

and another
[url=http://www.ncbi.nlm.nih.gov/pubmed/21951617]Altered ionized magnesium levels in mild-to-moderate Alzheimer's disease.[/url] showing low levels of magnesium in AD patients and Mg-ion levels were significantly and directly related to cognitive function.

Here is another press article by the lead author of the above research.
[url=http://seattletimes.nwsource.com/html/health/2015981629_alz24.html?prmid=obnetwork]Alzheimer's prevention as elusive as disease itself
Will a healthy lifestyle help prevent Alzheimer's disease, or at least delay its onset?[/url]
This is quite interesting as he puts some numbers on the risk factors.
[quote]Lack of exercise 21% of Alzheimer's in America, and high blood pressure 8 %, the study theorizes, while low educational attainment and midlife obesity might each cause 7%. Diabetes 3%.[/quote] I think that diabetes number is much lower than is true because diabetes is actually shortening folks lives. Dying sooner may be a way of reducing Alzheimer's incidence but not a route that I want to choose.

[url=http://www.medpagetoday.com/upload/2011/9/20/Neurology-2011-Ohara-1126-34.pdf]Glucose tolerance status and risk of dementia in the community :The Hisayama Study[/url] This paper puts some numbers on the increased risk of dementia from having a high blood glucose level.

[url=http://www.sciencedaily.com/releases/2011/09/110919163947.htm]Science Daily plain English report of study findings[/url] "people with diabetes were twice as likely to develop dementia as people with normal blood sugar levels."

[URL=http://www.eurekalert.org/pub_releases/2011-08/aaon-hbp072611.php]High blood pressure, diabetes, smoking and obesity in middle age may shrink brain, damage thinking[/URL]
[QUOTE]T. PAUL, Minn. – A new study suggests smoking, high blood pressure, diabetes and being overweight in middle age may cause brain shrinkage and lead to cognitive problems up to a decade later. The study is published in the August 2, 2011, print issue of Neurology®, the medical journal of the American Academy of Neurology.

"These factors appeared to cause the brain to lose volume, to develop lesions secondary to presumed vascular injury, and also appeared to affect its ability to plan and make decisions as quickly as 10 years later. A different pattern of association was observed for each of the factors," said study author Charles DeCarli, MD, with the University of California at Davis in Sacramento and a Fellow of the American Academy of Neurology. "Our findings provide evidence that identifying these risk factors early in people of middle age could be useful in screening people for at-risk dementia and encouraging people to make changes to their lifestyle before it's too late."

The study involved 1,352 people without dementia from the Framingham Offspring Study with an average age of 54.

Participants had body mass and waist circumference measures taken and were given blood pressure, cholesterol and diabetes tests. They also underwent brain MRI scans over the span of a decade, the first starting about seven years after the initial risk factor exam. Participants with stroke and dementia at baseline were excluded, and between the first and last MRI exams, 19 people had a stroke and two developed dementia.

The study found that people with high blood pressure developed white matter hyperintensities, or small areas of vascular brain damage, at a faster rate than those with normal blood pressure readings and had a more rapid worsening of scores on tests of executive function, or planning and decision making, corresponding to five and eight years of chronological aging respectively.

People with diabetes in middle age lost brain volume in the hippocampus (measured indirectly using a surrogate marker) at a faster rate than those without diabetes. Smokers lost brain volume overall and in the hippocampus at a faster rate than nonsmokers and were also more likely to have a rapid increase in white matter hyperintensities.

People who were obese at middle age were more likely to be in the top 25 percent of those with the faster rate of decline in scores on tests of executive function, DeCarli said. People with a high waist-to-hip ratio were more likely to be in the top 25 percent of those with faster decrease in their brain volume.[/QUOTE]

I think this follows on nicely from the previous blog which may give people the idea that there is nothing that can be done (if there is no single cause underlying Alzheimer's) to prevent it. This study is showing that if we identify and control in midlife those risk factors that are remediable, then we can prevent loss of cognitive function / memory in later life.

There really shouldn't be any difficulty in getting people to check there blood pressure and take sensible measures to reduce blood pressure BEFORE it leads to damage in the brain. We should be telling people that they may be able to delay worsening of decision making/planing/executive function by between 5 ~ 8 years simply by reducing high blood pressure. The sooner they start the longer the delay.

Those with a high waist to hip ratio (obesity) are in the top quarter of those most likely to display loss of executive function and rapid rate of cognitive decline. This is something we can alter by reducing the amount of refined carbohydrate and sugar/HFCS we eat. These processed foods also lead to diabetes and this report is telling us that developing diabetes in middle age also is associated with loss of brain volume, in the memory-forming hippocampus region, at a much faster rate than non-diabetics.

Similarly smoking is a risk factor we can eliminate. Smokers lost brain volume overall and in the hippocampus at a faster rate than non-smokers.

I think we need to be more proactive in encouraging others to identify risk factors early, before or while people are middle-aged and encourage them to make changes to their lifestyle then, before it's too late.

This is the study the press release above came from
[url=http://www.ncbi.nlm.nih.gov/pubmed/21810696]Midlife vascular risk factor exposure accelerates structural brain aging and cognitive decline.[/url]

[url=http://inhumanexperiment.blogspot.com/2009/04/l-carnitine-acetyl-l-carnitine-and_13.html] Acetyl-L-Carnitine and Cognitive Function in Humans[/url]
This is a detailed evidence based blog that details the way Carnitine supplements may help those with age-related mental decline. It was posted a couple of years ago.

Here is a newer piece of research showing how [url=http://www.ncbi.nlm.nih.gov/pubmed/21443422]Acetyl-L-carnitine reduces depression and improves quality of life in patients with minimal hepatic encephalopathy.[/url] here we see ALC treatment is associated with significant improvement in energy levels, general functioning and well-being. The improvement of quality of life is associated with reduction of anxiety and depression.

[url=http://www.ncbi.nlm.nih.gov/pubmed/21978079]Acetyl-l-Carnitine Attenuates Homocysteine-Induced Alzheimer-Like Histopathological and Behavioral Abnormalities.[/url]
[quote]Abstract Hyperhomocystinemia could induce tau protein hyperphosphorylation, β-amyloid (Aβ) accumulation, and memory deficits as seen in Alzheimer disease (AD), the most common cause of senile dementia with no effective cure currently.
To search for possible treatment for AD, we produced a hyperhomocysteinemia model by vena caudalis injection of homocystine (Hcy) for 2 weeks and studied the effects of acetyl-l-carnitine (ALC) in rats.
We found that simultaneous supplement of ALC could improve the Hcy-induced memory deficits remarkably, with attenuation of tau hyperphosphorylation and Aβ accumulation.
Supplement of ALC almost abolished the Hcy-induced tau hyperphosphorylation at multiple AD-related sites.
Supplementation of ALC also suppressed the phosphorylation of β-amyloid precursor proteins (APP), which may underlie the reduction of Aβ.
Our data suggest that ALC could be a promising candidate for arresting Hcy-induced AD-like pathological and behavioral impairments.[/quote]
I'm sure most people here understand the dangers of high homocystine levels and are aware of the role of B vitamins, folate, B6 and B12 that reduce those levels. Here we see how using ALC carnitine stopped tau hyperphosphorylation and the build up of amyloid beta and in doing so improved memory.

We also know that the Alzheimer's drug Aricept works by maintaining acetylcholine.for longer in the brain.

[url=http://www.ncbi.nlm.nih.gov/pubmed/2215852]Acetyl-L-carnitine as a precursor of acetylcholine.[/url] explains why it's probably a good reason to use acetyl-L-carnitine as a support for the treatment of age-related cholinergic deficits.

[url=http://www.medpagetoday.com/upload/2011/9/20/Neurology-2011-Ohara-1126-34.pdf]Glucose tolerance status and risk of dementia in the community The Hisayama Study[/url] full text of paper here

[url=http://www.medpagetoday.com/Endocrinology/Diabetes/28618][SIZE="3"]Diabetes Linked to Alzheimer's Risk[/SIZE][/url]
[quote]Dementia risk may rise when glucose gets out of control, particularly after meals, according to a longitudinal Japanese study.

Diabetes patients were 74% more likely to develop dementia of any type over 15 years of follow-up after adjustment for other confounding factors (P=0.004), Yutaka Kiyohara, MD, PhD, of Kyushu University in Fukuoka, Japan, and colleagues found.

And Alzheimer's disease developed 2.05-fold more often with diabetes than with normal glucose tolerance after similar adjustment (P=0.01), the group reported in the Sept. 20 issue of Neurology.

Perhaps more interesting, though, was the strong risk prediction of postload glucose levels during the oral glucose tolerance test, mimicking how meals are metabolized, commented Richard Bergenstal, MD, of the International Diabetes Center at Park Nicollet in Minneapolis.

Higher two-hour postload glucose levels correlated with greater risk of developing dementia (P<0.001 for trend for all-cause dementia and Alzheimer's disease, P=0.02 for trend for vascular dementia)

After adjustment for age, sex, hypertension, electrocardiogram abnormalities, body mass index, waist-to-hip ratio, total cholesterol, prior stroke, education, smoking, alcohol intake, and physical activity in the multivariate analysis:

Two-hour postload glucose levels of 7.8 to 11.0 mmol/L predicted 50% elevated risk of all-cause dementia and 87% elevated likelihood of Alzheimer's disease (both P=0.02).
Two-hour postload glucose levels above 11.0 mmol/L predicted 2.47-fold higher risk of all-cause dementia and 3.42-fold elevated Alzheimer's risk (both P<0.001) and 2.66-fold elevated vascular dementia risk (P=0.01).
Those findings suggested "that postprandial glucose regulation is critical to prevent future dementia," Kiyohara's group argued.

Bergenstal, a past president of the American Diabetes Association, cautioned that it's not yet clear whether better control of mealtime insulin levels could impact risk for patients who have already developed diabetes.

Awareness of the link may be the bigger message, he suggested in an interview with Medpage Today.

"We need to understand it a lot better before we build this into our clinical practice," he said. "We don't know yet from these studies how to intervene."

Some prior epidemiologic studies have also implicated diabetes in dementia risk, though not consistently so, they noted.

"Our findings emphasize the need to consider diabetes as a potential risk factor for all-cause dementia, Alzheimer's disease, and probably vascular dementia," Kiyohara and colleagues agreed in the paper.

In the study, diabetes detected on an oral glucose tolerance test was associated with 2.07-fold higher age- and sex-adjusted risk of vascular dementia during follow-up compared with those with normal glucose tolerance (P=0.04). But the vascular dementia link lost statistical significance with further multivariable adjustment, though it still trended (HR 1.82, P=0.09).

This might have been due to small numbers of vascular dementia cases, or because diabetes impacts vascular dementia by mediating hypertension and other cardiovascular risk factors that were controlled for in the multivariate analysis, the researchers explained.

Hyperglycemia itself may have an impact on the brain through atherosclerosis, oxidative stress and accumulation of advanced protein glycation, and changes in insulin metabolism yielding distorted amyloid metabolism, they noted.

Their prospective Hisayama Study included 1,017 community-dwelling older adults without baseline dementia in Japan who had an oral glucose tolerance test at age 60 or older and were followed for dementia status for 15 years.

Unlike oral glucose tolerance test results, fasting plasma glucose levels at baseline didn't correlate with dementia overall or by dementia subtype.

Impaired glucose tolerance did show some trends and borderline significance in predicting dementia of any type and Alzheimer's.

Adding those prediabetes cases together with overt diabetes also significantly predicted both in the multivariate-adjusted model.

Diabetes and prediabetes together appeared to account for 14.6% of all-cause dementia, 20.1% of Alzheimer's disease, and 17.0% of vascular dementia risk in the population studied.

The researchers cautioned that generalizability to other ethnic populations needs confirmation in further studies.

Other limitations included a single baseline measurement of diabetes status and inability to account for changes participants made in their risk factors during follow-up.[/quote]
It's worth listening to the audio clip at the above link as well.

[url=http://myoptimalhealthresource.blogspot.com/2011/09/vitamin-d-alters-brain-proteins-to.html]Vitamin D Prevents Amyloid Plaque Buildup in the Brain[/url]
Blog post on the same topic.
[quote] the optimal blood level of the prohormone is between 50 ng/ml and 80 ng/ml to dramatically lower the risk from many cancer lines. Most health conscious adults will need to supplement with an oil-based vitamin D supplement to achieve this goal and attain protection from this deadly form of dementia.[/quote] To get to those levels in the UK generally requires as much sun exposure as is available PLUS at least 5000iu/daily,. It may be a good idea to use 10,000iu daily for 12 weeks at least to catch up. This time of year your vitamin d level is already dropping from it's Summer peak.
You may be lucky if you can get outside and get some full body sun exposure midday this weekend coming but the sun has now lost a lot of it's power and midday sun exposure now may only hold status where it is rather than adding extra vitamin d. Of course you could move to the Canaries for the Winter or perhaps you've some relatives in Australia/New Zealand who would be pleased to see you for a few weeks.

Most elderly people have vitamin D levels around 10~20nmol/l = 4~ 8ng/ml so need a huge amount of vitamin D to get up to the levels at which they have a stored reserve of D3 to improve immune function..

Thank you Ted for your detailed and insightful research. I am going to pass this info on to the Manager of my relative's nursing home. He will, I know, find this extremely interesting.

I'm not a doctor, I just enjoy reading science papers to understand how best to improve my health.
We have to understand that melatonin secretion declines as we age and in the case of those with AD the decrease in melatonin secretion is greater.
[url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3001215/?tool=pubmed]Clinical Aspects of Melatonin Intervention in Alzheimer’s Disease Progression[/url][quote]Melatonin secretion decreases in Alzheimer´s disease (AD) and this decrease has been postulated as responsible for the circadian disorganization, decrease in sleep efficiency and impaired cognitive function seen in those patients. Half of severely ill AD patients develop chronobiological day-night rhythm disturbances like an agitated behavior during the evening hours (so-called “sundowning”). Melatonin replacement has been shown effective to treat sundowning and other sleep wake disorders in AD patients. The antioxidant, mitochondrial and antiamyloidogenic effects of melatonin indicate its potentiality to interfere with the onset of the disease. This is of particularly importance in mild cognitive impairment (MCI), an etiologically heterogeneous syndrome that precedes dementia[/quote]
Replacing the missing melatonin is treating the cause of the problem, using prescription sleeping medications is simply treating the symptoms.
Melatonin has a multitude of other actions in the body it's anti inflammatory , anti biotic and anti oxidant so correcting melatonin deficiency is more important than just attempting to correct sleep problems.

I've discussed melatonin in more detail in [url=http://forum.alzheimers.org.uk/entry.php?2037-Circadian-Rhythm-Disturbances-in-Patients-with-Alzheimer-s-Disease]a previous blog.[/url] and you'll see that I link to a post from Dr Davis where he uses 10mg ~ 12mg with his heart disease patients (to lower blood pressure) The older you are the more you are likely to require.
Melatonin is also useful for fighting cancer in which case 20mg is used.[url=http://www.ncbi.nlm.nih.gov/pubmed/21889572]Melatonin: The smart killer[/url]

With Autistic kids 6mg is a typical dose (bear in mind kids are much smaller to the amount per kg is relatively high) Very few side effects noted. Mainly feeling drousy the next moring but that could be not taking the melatonin early enough before bedtime or not getting sufficient bright light (to switch off natural melatonin secretion) the following morning.

[url=http://www.drugs.com/drug-interactions/melatonin.html]This drug interaction checker[/url] will allow you to work out which of his medications may cause problems.
On the whole melatonin (being a natural substance human bodies naturally produce and commonly found in red wine and olive oil) is extremely safe.
More vivid dreams are regularly reported initially however sadly you get adapted to it and the more exciting dreaming diminish.

The information I provided in the previous blog postings about improving natural melatonin secretion as much as possible through improving bright light exposure in the morning early afternoon, subduing evening light (particularly white light) and having as dark a bedroom as possible is important. We want to restore natural circadian rhythm as much as possible, but because melatonin has so many important roles, like vitamin D3, it's medical negligence not to restore natural levels.
Trouble with natural substances like melatonin/vitamin D3.is they aren't patentable so no one can profit from them.
It doesn't take much to work out what a years supply of these costs.
Natrol, Melatonin TR, Time Release, 5 mg, 100 Tablets $6.12 (£3.95)
Country Life, Vitamin D3, 5,000 IU, 200 Softgels $7.92 (£5.12)
So no one has any motive to educating health professionals as to their true value.

Hello, I am new to this forum and this entry in your blog caught my eye. Funny enough I was reading about the effect of light therapy and melatonin intake on patients with dementia this morning. My partner has been diagnosed with vascular dementia and one of his symptoms is a very disturbed sleep at night, sometimes getting up every hour or two hours. This is making caring for him and going to work in the morning extremely difficult. He is currently taking 0.25 mg clonazepam and 3.75 mg zopiclone which helps a little but not always. I would like to discuss melatonin with my partner's mediacal team. Are there any known side-effects associated with it or are there known conditions or situations when it should not be prescribed?

[url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2987503/?tool=pubmed]Could lysine supplementation prevent Alzheimer’s dementia? A novel hypothesis[/url]
Full text available at the link above.
Interesting idea that is easy to implement and unlikely to do any harm.

[url=http://www.youtube.com/watch?v=FSeSTq-N4U4]The Food Revolution - AHS 2011 Diet Doctor's AHS presentation
[IMG]http://i3.ytimg.com/vi/FSeSTq-N4U4/default.jpg[/IMG] [/url]

I've posted this link to this presentation as I feel it's particularly important as Alzheimer's like Diabetes is a problem with glucose metabolism so reducing our reliance on refined carbohydrates (sugars and flours) should reduce the damage and slow progression/reduce incidence.

[quote]Do you want to improve your weight and health by eating real food? With no calorie counting, no diet products, no hunger? This lecture from Ancestral Health Symposium 2011 shows you how to do it the natural way.

The epidemics of obesity and diabetes are continuing to spread across the western world. Now we know why. Modern science has revealed our mistake.

The unnecessary fear of natural food has inadvertently caused us to eat more of the new food that can make us hungrier, make us eat more, make us fat.

Ever more people are realizing the mistake and seeing the solution. The food revolution is here. Please help spread the word once you know.


Read more at [url]www.dietdoctor.com[/url]

Don't forget Ancestral Health Symposium 2012:
[url]http://ancestryfoundation.org/[/url][/quote]

[url=http://journals.lww.com/co-criticalcare/Abstract/2011/08000/Postoperative_cognitive_disorders.11.aspx]Postoperative cognitive disorders[/url]
[quote]Abstract
Purpose of review: The elderly are the fastest growing segment of the population and undergo 25–30% of all surgical procedures. Postoperative cognitive problems are common in older patients following major surgery. The socioeconomic implications of these cognitive disorders are profound; cognitive decline is associated with a loss of independence, a reduction in the quality of life, and death. This review will focus on the two most common cognitive problems following surgery: postoperative delirium and postoperative cognitive dysfunction (POCD).

Recent findings: For years, preoperative geriatric consultation/screening was the only intervention proven to decrease postoperative delirium. There are, however, several recent publications indicating that preoperative and postoperative pharmacological and medical (hydration, oxygenation) management can reduce postoperative delirium. Spinal anesthesia with minimal propofol sedation has been shown to decrease the incidence of postoperative delirium in hip-fracture patients. Likewise, dexmedetomidine sedation in mechanically ventilated patients in the ICU is associated with less postoperative delirium and shorter ventilator times. Preoperative levels of education and brain function (cognitive reserve) may predict patients at risk for postoperative cognitive problems. Reduced white matter integrity is reported to place patients at a higher risk for both postoperative delirium and POCD.

Summary: The etiology of postoperative cognitive problems is unknown, but there is emerging evidence that decreased preoperative cognitive function contributes to the development of postoperative delirium and POCD. There is growing concern that inhalation anesthetics may be neurotoxic to the aging brain, but there are no human data evaluating this hypothesis to date. Randomized controlled trials evaluating interventions to improve long-term cognitive outcomes in elderly patients are urgently needed.[/quote]
Here is another abstract on the same subject.
Again it's true that as there's no data it's difficult to make a decision.
Certainly it's worth considering all alternative strategies to surgery and/or other options for anesthetics, although I'm too much of a whimp to consider surgery without anesthetic.

[url=http://www.ncbi.nlm.nih.gov/pubmed/21474666]Postoperative cognitive dysfunction is independent of type of surgery and anesthetic.[/url]
[quote]Abstract
BACKGROUND:
Postoperative cognitive dysfunction (POCD) has been documented after cardiac and noncardiac surgery. The type of surgery and anesthetic has been assumed to be associated with the incidence but there are few prospective data comparing the incidence after different procedures. In this study, we sought to determine the association of the type of surgical procedure and anesthesia on the incidence of POCD after procedures involving light sedation, general anesthesia for noncardiac surgery, and general anesthesia for cardiac surgery involving cardiopulmonary bypass.
METHODS:
Eight neuropsychological tests were administered at baseline and at 7 days and 3 months postoperatively to subjects from 3 procedure groups and a nonoperative control group. Reliable change index was used to calculate POCD. The study sample consisted of subjects involved in 3 separate trials investigating coronary angiography (CA) (percutaneous diagnostic procedure) under sedation, major noncardiac surgery (total hip joint replacement [THJR] surgery) under general anesthesia, and coronary artery bypass graft (CABG) surgery under general anesthesia.
RESULTS:
Data were collected from 644 patients in the patient groups and 34 subjects in the control group. Neuropsychological results were available for POCD at day 7 for THJR surgery (n=162) and CABG surgery (n=281). The incidence of POCD at day 7 was 17% for THJR surgery and 43% for CABG surgery (adjusted odds ratio=0.2, 95% confidence interval [CI]: 0.1, 0.4; P<0.01). At 3 months, the incidence of POCD for all groups combined (n=636) was 17% (21% for CA under sedation, 16% for THJR surgery, and 16% for CABG surgery). The mean (95% CI) for the difference in proportions of POCD among groups was 0.00 (-0.07, 0.07) (P=0.91) for CABG versus THJR; -0.05 (-0.12, 0.03) (P=0.21) for CABG versus CA; and -0.05 (-0.13, 0.03) (P=0.24) for THJR versus CA. There were no significant differences among groups (adjusted odds ratio=1.21, 95% CI: 0.94, 1.55; P=0.13).
CONCLUSIONS:
The incidence of POCD in old and elderly patients at day 7 was higher after CABG surgery than THJR surgery, but POCD at 3 months was independent of the nature or the type of procedure or anesthetic when comparing CA, THJR, and CABG surgery groups. Cardiovascular risk factors were not predictive of POCD after any procedure.
© 2011 International Anesthesia Research Society[/quote]

This is the trouble when doing major surgery on elderly patients. If you cannot reliably use typical risk factors to help you decide if the risk is worth taking as even they aren't predictive you just have to do the best you can. That really means deciding balancing what happens without the surgery?
If it's a choice between the certainty I'll never walk again or a less than 10% chance the procedure MAY increase cognitive dysfunction I think I may choose the action that prevents what would otherwise be inevitable and take my chance.
I don't think we should be looking to blame anyone here, but maybe health professionals should take more time to explain the possible adverse outcomes to weigh against the benefits.

[url=http://www.anesthesiaweb.org/dementia.php]Anesthesia causes Personality Changes and even Dementia © G.M. Woerlee[/url]
Here is another article, text available free online, that put's some numbers on those with cognitive impairment 3 months after major/minor surgery involving Anesthesia.
It also has a list of possible risk factors that may help you decide if you're in a higher risk group.

[url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831066/?tool=pubmed]The Alzheimer's Disease-Associated Amyloid β-Protein Is an Antimicrobial Peptide[/url] full text at link.
[quote]Our findings suggest Aβ is a hitherto unrecognized Antimicrobial Peptide that may normally function in the innate immune system. This finding stands in stark contrast to current models of Aβ-mediated pathology and has important implications for ongoing and future AD treatment strategies.[/quote]