seniors

Alzheimer's Disease

Alzheimer's disease currently affects one in 10 people over age 65 and nearly half of those over age 85.

More than 19 million Americans say they have a family member with the disease, and 37 million say they know somebody affected with Alzheimer's.

In the United States, the average lifetime cost per Alzheimer patient is US$174,000. (These figures are from the U.S. Alzheimer's Association).

Resources:

For information about Alzheimer's, see the Alzheimer's Disease Education and Referral (ADEAR) Center's website (www.alzheimers.org). ADEAR is run by the National Institute on Aging (one of the US Government's National Institutes of Health).

Other useful resources include:

The Alzheimer Research Forum: "A scientific knowledge base on Alzheimer disease, with research news, expert commentaries, and databases for peer-reviewed articles, drugs, research reagents, grants, jobs, conferences, and more."
www.alzforum.org

Cognitive Neurology and Alzheimer's Disease Center at Northwestern University
http://www.brain.northwestern.edu/mdad/index.html

Medline Plus
http://www.nlm.nih.gov/medlineplus/alzheimersdisease.html

Links to national organizations that offer support:

http://www.alz.org/ Site of the U.S. Alzheimer’s Association.

http://www.alzheimers.org.uk/ Site of the U.K. Alzheimer's Society

http://www.alzheimer.ca/ Site of the Canadian Alzheimer's Association

http://www.alzheimers.org.au/ Site of the Australian Alzheimer's Association

www.alzheimers.org.nz Site of Alzheimer's New Zealand

Some articles of interest:

a good introduction from the Harvard Mahoney Neuroscience Newsletter:

http://www.med.harvard.edu/publications/On_The_Brain/Volume2/Special/SPAlz.html

Montessori for Alzheimer's patients

Movement with Meaning

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Parkinson's Disease Dementia

alence of Parkinson's Disease

After Alzheimer's disease, the second most common neurodegenerative disorder is Parkinson’s disease. In the U.S., at least 500,000 are believed to have Parkinson’s, and about 50,000 new cases are diagnosed every year1 (I have seen other estimates of 1 million and 1.5 million — and researchers saying the numbers are consistently over-estimated while others that they are consistently under-estimated!). In the U.K., the numbers are 120,000 and 10,0002.

Part of the problem in estimating national and global prevalence is that Parkinson's is very much affected by environmental factors. The Amish, Nebraska, the area around the ferromanganese plants in Breccia (Italy), and the Parsi of Mumbai (India), have the highest rates of Parkinson's in the world. Pesticide use, and some occupations and foods, are all thought to increase the risk of Parkinson's. So is head trauma.

There may also be ethnic differences. A recent analysis of Medicare data3 from more than 450,000 patients with PD in the United States has found substantial variation between whites, African Americans, and Asians, with whites showing dramatically greater rates (158.21 per 100,000 in white men compared to 75.57 and 84.95 for African Americans and Asians, respectively). These differences, however, may well reflect factors other than ethnicity, given the significant role that environmental factors play in Parkinson's. Most patients were found to live in the Midwest and Mid-Atlantic regions (areas with very high proportions of whites).

Of course Parkinson’s, like Alzheimer’s, is a disorder of age (although in both cases, a minority suffer early onset). Figures from a 1997 European study4 that estimated the overall, age-adjusted prevalence in Europe at 1.6% gave this age breakdown:
65-69: 0.6%
70-74: 1.0%
75-79: 2.7%
80-84: 3.6%
85-89: 3.5%
As you can see, there is a sharp rise in the later half of the 70s, rising to a peak in the 80s (studies suggest it declines in the 90s).

Risk of developing dementia

Parkinson’s is of course primarily a movement disorder, not a cognitive one. However, it can lead to dementia. As with the numbers of Parkinson's sufferers, the risk of that is so variously estimated that estimates range from 20-80%!

Part of the problem is disentangling mortality — as with Alzheimer’s, many die before the symptoms of dementia have had time to develop. It is helpful to deconstruct that top statistic.

The 2003 Norwegian study5 that appears to be the source of this 80% calculated an 8-year prevalence estimate of 78.2% from an 8 year study involving 224 Parkinson’s patients. At the beginning of the study, 51 of these 224 had dementia. After 4 years, 36 of the non-demented had died, and 7 refused to continue their participation; of the 51 demented, 42 had died (according to my calculations – this figure, and several others, were not given). Of the 139 patients remaining in the study at year 4, 43 of the previously non-demented had developed dementia, meaning (according to my calculations) that 52 in total now had dementia, and 87 had not. After another 4 years, there were only 87 patients remaining in the study, 19 of those 87 non-demented having died, a further 3 refusing to continue, and (my calculation) 30 of the 52 demented having died. At this time, year 8, 28 of the previously non-demented had now developed dementia, leaving (my calculation) 37 non-demented survivors.

In other words, over a period of 8 years, after having had Parkinson’s for over 9 years, on average, when the study began, just over half (54.5%; 122/224) developed dementia. About the same number (56.7%; 127) had died. At that point, after having had Parkinson’s for an average of 17 years (they were now on average 73 years old), 50 (22%) were still alive but with dementia, and 37 (16.5%) were still alive and non-demented (the percentage is only slightly increased by subtracting those who refused to continue participating).

Importantly, those 37 had no more cognitive decline than was evident in age-matched controls.

Note also that the average life expectancy after being diagnosed with Parkinson's is about 9 years -- hence, those who participated were already at this point at the beginning of the study. We don't know how many people developed dementia and died between diagnosis and the study beginning, but we do know that 23% (51/224) had dementia at the beginning of the study, after having had Parkinson's for an average of 11 years (their average was higher than the group average) -- which is already longer than the average survival rate.

In other words, we need a study that follows PD sufferers from diagnosis until death to truly give an accurate estimate of the likelihood of developing dementia before death. We can however give an estimate of how many people survive PD for 17 years (nearly twice the average survival time) without developing dementia: 16.5% -- which is approaching half (42.5%) the number of people who survive that long.

We can also estimate how many PD sufferers who have had PD for an average of 9 years will not have dementia: 77% (173/224 — the number of non-demented at the beginning of the study). And how many will not have dementia after 13 years: 63% (87/139 — the number of non-demented at year 4 of the study).

The big question is of course, are there any signs that indicate which individuals will develop dementia. The researchers found6 that age, hallucinations, and more severe motor problems were all risk factors for developing dementia.

For more on Parkinson's:

Check out this youtube video: http://www.youtube.com/watch?v=ZPnpmVWU0Hk

See these websites:

http://www.ninds.nih.gov/disorders/parkinsons_disease/parkinsons_disease.htm

http://www.nhs.uk/Conditions/Parkinsons-disease/Pages/Introduction.aspx

http://viartis.net/parkinsons.disease/

Check out these books:
http://www.amazon.com/Dementia-Lewy-Bodies-Parkinsons-Disease/dp/1841843954

References: 

  1. From the National Institute of Neurological Disorders and Stroke website: http://www.ninds.nih.gov/disorders/parkinsons_disease/parkinsons_disease_backgrounder.htm
  2. From the National Health Service website: http://www.nhs.uk/Conditions/Parkinsons-disease/Pages/Introduction.aspx
  3. De Rijk, M.C. et al. 1997. Prevalence of parkinsonism and Parkinson's disease in Europe: the EUROPARKINSON Collaborative Study. European Community Concerted Action on the Epidemiology of Parkinson's disease. Journal of Neurology, Neurosurgery & Psychiatry, 62(1), 10-5.
  4. De Rijk, M.C. et al. 1997. Prevalence of parkinsonism and Parkinson's disease in Europe: the EUROPARKINSON Collaborative Study. European Community Concerted Action on the Epidemiology of Parkinson's disease. Journal of Neurology, Neurosurgery & Psychiatry, 62(1), 10-5.
  5. Aarsland, D. et al. 2003. Prevalence and characteristics of dementia in Parkinson disease: an 8-year prospective study. Archives of Neurology, 60(3), 387-92. http://tinyurl.com/yagw2a9
  6. Aarsland, D. et al. 2004. The Rate of Cognitive Decline in Parkinson Disease. Archives of Neurology, 61, 1906-1911.

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Vascular & Mixed Dementia

alence

Vascular dementia, as its name suggests, is caused by poor blood flow, produced by a single, localized stroke, or series of strokes.

It is the second most common dementia, accounting for perhaps 17% of dementias. It also co-occurs with Alzheimer's in 25-45% of cases. Although there are other types of dementia that also co-occur with Alzheimer's, mixed dementia generally refers to the co-occurrence of Alzheimer's and vascular dementia.

Risk factors

In general, unsurprisingly, vascular dementia has the same risk factors as cerebrovascular disease.

A study1 of 173 people from the Scottish Mental Survey of 1932 who have developed dementia has found that, compared to matched controls, those with vascular dementia were 40% more likely to have low IQ scores when they were children than the people who did not develop dementia. Because this was not true for those with Alzheimer's disease, it suggests that low childhood IQ may act as a risk factor for vascular dementia through vascular risks rather than the "cognitive reserve" theory.

Prevention

The exciting thing about vascular dementia is that it is far more preventable than other forms of dementia. As with risk, as a general rule, the same things that help you protect you from heart attacks and stroke will help protect you from vascular dementia. This means diet, and it means exercise.

A four-year study2 involving 749 older adults has found that the top one-third of participants who exerted the most energy in moderate activities such as walking were significantly less likely to develop vascular dementia than those people in the bottom one-third of the group.

Treatment

Apart from normal medical treatment for cerebrovascular problems, there are a couple of interesting Chinese studies that have looked specifically at vascular dementia.

The herb gastrodine has been used in China for centuries to treat disorders such as dizziness, headache and even ischemic stroke. A 12-week, randomized, double-blind trial3 involving 120 stroke patients who were diagnosed with mild to moderate vascular dementia has found that  gastrodine and Duxil® (a drug used to treat stroke patients in China) produced similar overall levels of cognitive improvement -- although more patients showed 'much improvement' with gastrodine (23% vs 14%).

A Chinese pilot study4 involving 25 patients with mild to moderate vascular dementia found that ginseng compound significantly improved their average memory function after 12 weeks, but more research (larger samples, placebo-controls) is needed before this finding can be confirmed. Five years on I have still not seen such a study.

References: 

  1. McGurn, B., Deary, I.J. & Starr, J.M. 2008. Childhood cognitive ability and risk of late-onset Alzheimer and vascular dementia. Neurology, first published on June 25, 2008 as doi: doi:10.1212/01.wnl.0000319692.20283.10
  2. Ravaglia, G. et al. 2007. Physical activity and dementia risk in the elderly. Findings from a prospective Italian study. Neurology, published online ahead of print December 19.
  3. Tian, J.Z. et al. 2003. A double-blind, randomized controlled clinical trial of compound of Gastrodine in treatment of mild and moderate vascular dementia in Beijing, China. Presented at the American Heart Association's Second Asia Pacific Scientific Forum in Honolulu on June 10.
  4. Tian, J.Z. et al. 2003. Presented at the American Stroke Association's 28th International Stroke Conference on February 14 in Phoenix. Press release

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Dementia with Lewy Bodies

LBD: What is it?

Lewy Body Dementia is so called because the brains of affected people develop abnormal spherical masses of protein, called Lewy bodies, inside nerve cells. Lewy bodies are associated with Parkinson’s disease as well as dementia. Thus Lewy body dementia can refer to both Parkinson’s disease dementia and “dementia with Lewy bodies”. Lewy bodies are also often found in the brains of those with Alzheimer’s disease.

Unlike Alzheimer’s, however, dementia with Lewy bodies characteristically (but not invariably) begins with visual hallucinations.

Prevalence of LBD

Estimates of its prevalence are complicated by the lack of clearly defined clinical criteria, and vary widely. A 2005 review1 concluded that the range probably falls between 0 to 5% in the general population, and from 0 to 30.5% of all dementia cases (the very broad range reflects the confusion between Parkinson’s disease dementia (PDD), dementia with Lewy bodies, and Alzheimer’s where Lewy bodies are present).

How does LBD differ from Alzheimer's & PDD?

A comparison of these three disorders found that cognitive impairment in those with Alzheimer's disease and those with Lewy body dementia was similar, and more severe than in those with Parkinson's disease dementia.

The 1997 study2 also found that a simple test, in which patients are asked to draw and copy a clock face, distinguished those with Alzheimer’s and those with Lewy body dementia — of all the groups, only those with Lewy body dementia had equally poor scores in the “copy” part of the test compared to the “draw” part.

For more information:

Mayo Clinic: http://www.mayoclinic.com/health/lewy-body-dementia/DS00795

Lewy Body Dementia Association: http://www.lewybodydementia.org/

References: 

  1. Zaccai, J., McCracken, C. & Brayne, C. 2005. A systematic review of prevalence and incidence studies of dementia with Lewy bodies. Age and Ageing, 34(6), 561-566.
  2. Gnanalingham, K.K. et al. 1997. Motor and cognitive function in Lewy body dementia: comparison with Alzheimer's and Parkinson's diseases. Journal of Neurology, Neurosurgery, and Psychiatry, 62, 243-252.

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Frontotemporal Dementia

What is it?

Frontotemporal dementia is a disorder of the frontal lobes and includes what was known as primary progressive aphasia. Although it occurs far less often than Alzheimer's disease, among dementia sufferers younger than 65 it is estimated to occur at about the same rate. In other words, frontotemporal dementia is, unlike the most common dementias, not a disorder of age. Most sufferers become symptomatic in their 50s and 60s.

Frontotemporal dementia generally begins with a focal symptom, such as aphasia, before (usually a number of years later) progressing to more generalized dementia.

There are several types of frontotemporal dementia. The most common (around 60% of FTD cases) is known as the behavioral variant (also, Pick's disease). This is characterized by impairment in social and emotional skills. The other 40% of FTD cases have language impairments -- about half of these suffer from semantic FTD, characterized by difficulties in remembering the meanings of words; the other half suffer from progressive nonfluent aphasia, characterized by difficulties in producing language (although they understand what they're trying to say).

In around 15% of FTD cases (most usually the behavioral variant), motor neurone disease also develops.

Prevalence

A large-scale epidemiological study1 in the Netherlands indicated frontotemporal dementia occurs at a rate of 1.1 per 100,000, with the prevalence highest among those ages 60 to 69, at 9.4 per 100,000. The prevalence among people ages 45 to 64 was estimated to be 6.7 per 100,000 (this was after autopsies caused the number of diagnosed cases to go up, with 17 of 50 patients undiagnosed in life). Unlike other forms of dementia, where most occurrences begin in older adults, symptoms began after age 65 in only 22% of patients. The median age of onset was 58, with a range from 33 to 80.

A family history of dementia was present in 43% of patients. Interestingly, whites accounted for 99% of all cases despite an ample nonwhite population.

A large U.K. study2 found prevalences of early-onset FTD and Alzheimer's were the same in the 45-64 population: 15 per 100,000. The mean age at onset of FTD was 52.8 years and there was a striking male preponderance (14:3).

This rate is notably higher than that found in the Dutch study, and it has been suggested that the reason is ethnicity -- the Dutch study, as mentioned, had a significant proportion of non-Caucasians, while the British (Cambridge) study explicitly mentioned that minorities were under-represented.

It has been estimated that frontotemporal dementia accounts for approximately 8% of patients with dementia, but this is now thought to be an underestimation.

Genes as a factor

There is a high level of genetic involvement in this type of dementia.

As mentioned, the Dutch study found a family history of dementia in 43% of FTD patients. Another large Dutch study3 found 38% of FTD patients had one or more first-degree relatives with dementia before age 80 compared to 15% of age-matched controls; 10% had two or more first-degree relatives with dementia compared with 0.9% of the controls. FTD patients were also three times more likely to have 2 "Alzheimer's genes" (2 e4 alleles of the ApoE gene) than the controls: 7% vs 2.3%.

This study also supports findings with other dementias that earlier-onset is more likely to have genetic causes. First-degree relatives of FTD patients (who had twice the risk of dementia before age 80 compared with relatives of controls) were much more likely to develop dementia early: age of onset of dementia in affected first-degree relatives of FTD patients averaged was just under 61, compared to 72.3 for affected first-degree relatives of controls.

The genes implicated in familial cases of FTD are on chromosome 17, in the gene for the tau protein, and in the gene for the progranulin protein. Research4 has now confirmed that people with these hereditable defects produce only half of the normal amount of progranulin, and recently a simple test for measuring the quantity of progranulin in the blood was developed. The test reveals whether someone has the mutations that carry an increased risk of FTD.

A recent study5 involving 225 FTD patients found 41.8% of patients had some family history, although only 10.2% had a clear autosomal dominant history (at least 3 cases within the last 2 generations). However, the importance of genes varied across the different clinical subtypes of the disease, with the behavioral variant being the most heritable and FTD–motor neuron disease and the language syndromes (particularly semantic dementia) the least heritable.

For more information:

http://emedicine.medscape.com/article/1135164-overview

http://memory.ucsf.edu/ftd/

References: 

  1. Rosso, S.M. et al. 2003. Frontotemporal dementia in The Netherlands: Patient characteristics and prevalence estimates from a population-based study. Brain, 126, 2016-22. Full text available at http://brain.oxfordjournals.org/cgi/content/full/126/9/2016
  2. Ratnavalli, E., Brayne, C., Dawson, K. & Hodges, J.R. 2002. The prevalence of frontotemporal dementia. Neurology, 58, 1615-1621.
  3. Stevens, M. et al. 1998. Familial aggregation in frontotemporal dementia. Neurology, 50(6), 1541-5.
  4. Sleegers, K. et al. 2009. Serum biomarker for progranulin-associated frontotemporal lobar degeneration. Annals of Neurology, Published online March 13.
  5. Rohrer, J.D. et al. 2009. The heritability and genetics of frontotemporal lobar degeneration. Neurology, 73(18), 1451-1456.

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Dementia: A general introduction

alence of dementia

Dementia is estimated1 to afflict over 35.5 million people worldwide -- this includes nearly 10 million people in Europe, nearly 4.4 million in North America, nearly 7 million in South and Southeast Asia, about 5.5 million in China and East Asia and about 3 million in Latin America.

The estimated prevalence for over 60s is 4.7% worldwide. Because this is a disorder of age, prevalence is of course greatly affected by the proportion of people reaching their senior years. Hence the prevalence is higher in the more developed countries: the estimated prevalence in Western Europe and North America is 7.2% and 6.9% respectively, compared to 2.6% in Africa.

What kinds of dementia are most common?

The prevalence of the various dementia types is a complicated story. Certainly Alzheimer's disease is by far the most common type of dementia, accounting for perhaps 70% of all dementias (although a 2006 study13 suggested that non-Alzheimer dementias were as common as Alzheimer's — however this was based on dementia among military veterans). The second most common dementia is almost certainly vascular dementia, which may account for some 17% of dementias. However, the actual numbers are made uncertain by the fact that these two dementias often occur together.

At minimum, around a quarter of Alzheimer's cases have been found, on autopsy, to also have vascular pathology; this proportion reaches higher levels when the samples are not restricted to dementia clinics. One such community-based study2, for example, found 45% of the Alzheimer's cases also showed significant vascular pathology. Another, U.K., study3 found a similar proportion (46%).

Another, large long-running, study14 has found that only 30% of people with signs of dementia had Alzheimer’s disease alone. 42% had Alzheimer’s disease with cerebral infarcts (strokes) and 16% had Alzheimer’s disease with Parkinson’s disease (including two people with all three conditions). Infarcts alone caused another 12% of the cases. Vascular dementia caused another 12%.

Although there are other types of dementia that also co-occur with Alzheimer's, mixed dementia generally refers to the co-occurrence of Alzheimer's and vascular dementia.

The other important dementia type that co-occurs with Alzheimer's at a high rate is dementia with Lewy bodies, also considered to be one of the most common dementias (although, due to inconsistent criteria, estimates of its actual prevalence vary wildly). It is estimated to co-occur with Alzheimer's pathology around half the time. At a lesser frequency, but still high, is Parkinson's disease dementia — about 20% of Alzheimer's patients also have Parkinson's disease.

But it is probably fair to say that the distinction between these dementia types is not clear-cut. Lewy bodies are found in a high proportion of both Alzheimer's and Parkinson's patients — the number of cases of 'pure' Lewy body dementia is much smaller. It's been said, in fact, that the main difference between Lewy body dementia and Parkinson's disease dementia lies in the timing — Parkinson's disease dementia will be preceded by at least a year and more likely a number of years, by full-blown Parkinson's disease.

Regardless of the difficulties in establishing clear clinical criteria, however, there is no doubt that Alzheimer's co-occurs with vascular pathology or Lewy body pathology at a startlingly high rate.

One of the problems with clearly distinguishing between these types of dementia is a happy one: vascular and Alzheimer's pathology can be found, at autopsy, in many elderly brains that have not shown symptoms of dementia.

For example, in one community-based study4, in which the median age at death was around 85 for the 209 individuals, 48% had had dementia, of whom 64% showed Alzheimer's pathology. However, 33% of those who had not had dementia showed similar levels of Alzheimer's plaques. Similarly, some amount of tau tangles (another aspect of Alzheimer's pathology) was found in 61% of the demented and 34% of the non-demented individuals. Finally, multiple vascular pathology was found in 46% of the demented group and 33% of the non-demented, and vascular lesions were equally common in both.

And in the large long-running study mentioned earlier14, in those without dementia, brain autopsy revealed the presence of Alzheimer’s in 24% of cases, and infarctions in 18%.

How likely am I to develop dementia?

The question of how likely any person is to develop dementia must begin with estimates of prevalence, but this of course is only the very beginning of the story.

Estimating prevalence is complicated by the fact that dementia is greatly affected by lifestyle, environmental, and genetic factors, and consequently prevalence varies a lot depending on geographic region.

Different dementia sub-types have different causes, and some give a much greater weight to genetic or environmental factors than others. However, the finding that dementia risk is much greater in those with more than one pathology, and that Alzheimer’s pathology with cerebral infarcts is a very common combination, adds to growing evidence that dementia risk might be reduced with the same tools we use for cardiovascular disease such as control of blood cholesterol levels and hypertension.

Age as a factor

The first American study to use nationally representative data5 (rather than extrapolating from regional data) came up with a figure of 13.9% of those aged 71 and older (one in seven). But age of course makes all the difference in the world. The study found 5% of those aged 71 to 79, rising to 37.4% of those age 90 and older.

Although all the dementia types show an increase with age, Alzheimer's is particularly a disorder of age: although the study found only 46.7% of those with dementia in their 70s had Alzheimer's, for those in their 90s, Alzheimer's was the dementia type for 79.5% of them.

An Italian study of over 2000 seniors over 80 years old6 confirms that dementia does indeed keep increasing with age (it had been thought that risk leveled off for those who reached their 90s). The study found that 13.5% of those aged 80 to 84 had dementia, rising sharply to 30.8% of those 85 to 89, 39.5% of those 90 to 94, and 52.8% among those older than 94.

Gender as a factor

A number of studies have found differences between men and women, or between difference ethnicities, but this large, nationally representative study found that, although on the face of it there were race and gender differences, these differences disappeared once age, years of education, and presence of at least one "Alzheimer's gene" was taken into account.

However, an American study of over 900 seniors over 90 years old7 found that women of this age were much more likely to have dementia than men (some 45% of them, compared to 28% of the men), and that the likelihood of having dementia kept increasing with age for the women, but not for the men. Of course, more women than men survive to this age (some two-thirds of the participants were women).

Interestingly, education was protective for the women (the risk of dementia decreasing the more years of education the individual had had) but not for the men. The study participants were not, however, a random sampling -- they all came from the same retirement community, and most were white and of high socioeconomic status. Given that, and considering the times in which they were born, it seems likely that there would be far more variability in educational level among the women than the men. The men, while less likely to develop dementia, did tend to decline faster if they did develop it.

The Italian oldest-old study, too, found more women than men had dementia: across all ages, 25.8% of the women and 17.1% of the men.

These figures don't of course tell us how many develop dementia at those ages. Obviously, survival rates are a factor, and as we saw in the other study, male and female survival rates do vary. The figures for new cases of dementia developing in these age bands were:

  • 6% at 80 to 84 years;
  • 12.4% at 85 to 89 years;
  • 13.1% from 90 to 94 years; and
  • 20.7% among those over 94.

These figures make even more clear what was apparent in the earlier figures: dementia jumps suddenly in the later half of the 80s, and again in the later half of the 90s.

Importantly, however, the incidence of new cases shows us how important the gender difference in survival rates is: the difference in prevalence is much smaller in these terms --9.2% among women and 7.2% among men.

The study, which canvassed everyone in the age group within a specific geographical area and had an 88% response rate, had a ratio of 74 women to 26 men. Because the number of men at the very highest ages was so small, we can't draw any firm conclusions about gender differences at those ages.

The Italian study involves a very different population from that of the American study: Varese is in a heavily industrialised part of northern Italy, with a high immigrant population, and the average amount of education was only 5.1 years.

A review of 26 studies looking at dementia prevalence in Europe8 confirmed rates for men rising from 1.8% in the 65-69 years age range up to 30% in the over 90 years age group, and for women rising from 1.5% to 30% in the 80-85 years age band. However (and confirming the American study), rates in the oldest old for women rose to over 50% in those over 95 years.

Early onset of dementia

The average age at the onset of dementia is around 80 years. Early-onset dementia is defined arbitrarily (and variably) as occurring before 60-65. Early-onset cases have been estimated to make up about 6-7% of all cases of Alzheimer's disease, and though a lot of attention has been given to them, only about 7% of early-onset cases are in fact familial9.

Familial cases involve mutations in specific genes (the APP or presenilin genes); they do not include what is popularly referred to as the "Alzheimer's gene" — variants of APOE. A 1995 study10 calculated that a person with no family history of Alzheimer's disease who has an e4 allele has a lifetime risk of 29%, compared to a risk of 9% if they don't have an e4 allele. In other words, if you don't have any of the Alzheimer's risk genes, or any family history, you only have a 9% risk of developing Alzheimer's, and even if you do have the "Alzheimer's gene", your chance of not getting Alzheimer's is still over 70%. Your risk does, however, go up dramatically if both your APOE alleles are e4.

A large study11 found, however, that there were both ethnic and gender differences for the risk of this genetic factor. The effect of having an e4 allele was much greater among Japanese compared to Caucasian, and greater for Caucasian compared to African American and Hispanic. Additionally, the effect of having an e4 allele becomes less significant after 70.

There is evidence12 that the age of onset for both Alzheimer's and Parkinson's diseases, for those genetically disposed, is controlled by genes on chromosome 10.

References: 

  1. From the 2009 World Alzheimer's Report: http://www.alz.co.uk/research/worldreport/
  2. Lim A, Tsuang D, Kukull W, et al. 1999. Cliniconeuropathological correlation of Alzheimer’s disease in a community-based case series. Journal of the American Geriatric Society, 47, 564-569.
  3. Neuropathology Group of the Medical Research Council Cognitive Function and Ageing Study (MRC CFAS). 2001. Pathological correlates of late-onset dementia in a multicentre, community-based population in England and Wales. Lancet, 357, 169-175.
  4. Langa, K.M., Foster, N.L. & Larson, E.B. 2004. Mixed Dementia: Emerging Concepts and Therapeutic Implications. JAMA, 292(23), 2901-2908.
  5. Plassman, B.L. et al. 2007. Prevalence of Dementia in the United States: The Aging, Demographics, and Memory Study. Neuroepidemiology, 29, 125-132. 
  6. Lucca, U. et al. 2009. Risk of dementia continues to rise in the oldest old: The Monzino 80-plus Study. Presented on July 14, 2009, at the annual International Conference on Alzheimer's Disease in Vienna. http://www.alz.org/icad/documents/abstracts/abstracts_prev_ICAD09.pdf
  7. Corrada, M.M. et al. 2008. Prevalence of dementia after age 90: Results from The 90+ Study. Neurology, 71 (5), 337-343.
  8. Reynish, E. et al. 2009. Systematic Review and Collaborative Analysis of the Prevalence of Dementia in Europe. Presented on July 14, 2009, at the annual International Conference on Alzheimer's Disease in Vienna. http://www.alz.org/icad/documents/abstracts/abstracts_prev_ICAD09.pdf
  9. Nussbaum, R.L. & Ellis, C.E. 2003. Alzheimer's Disease and Parkinson's Disease. New England Journal of Medicine, 348 (14), 1356-1364. http://content.nejm.org/cgi/content/full/348/14/1356#R23
  10. Seshadri S, Drachman DA, Lippa CF. 1995. Apolipoprotein E epsilon 4 allele and the lifetime risk of Alzheimer's disease: what physicians know, and what they should know. Archives of Neurology, 52, 1074-1079. http://tinyurl.com/ya7vss7
  11. Farrer LA, Cupples LA, Haines JL, et al. Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease: a meta-analysis. JAMA 1997;278:1349-1356. http://tinyurl.com/yb9tdju
  12. Li, Y. et al. 2002. Age at Onset in Two Common Neurodegenerative Diseases Is Genetically Controlled. American Journal of Human Genetics, 70, 985-993. Press release
  13. Ross, E.D. et al. 2006. Changing Relative Prevalence of Alzheimer Disease versus Non-Alzheimer Disease Dementias: Have We Underestimated the Looming Dementia Epidemic? Dementia and Geriatric Cognitive Disorders, 22 (4), 273-277.
  14. Schneider, J.A., Arvanitakis, Z., Bang, W. & Bennett, D.A. 2007. Mixed brain pathologies account for most dementia cases in community-dwelling older persons. Neurology, published ahead of print June 13.

 

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Older adults' distractability can be used to help put a face to a name

  • A small study has used older adults’ inability to ignore irrelevant information to improve their memory for face-name pairs.

One important reason for the greater cognitive problems commonly experienced as we age, is our increasing difficulty in ignoring distracting and irrelevant information. But it may be that in some circumstances that propensity can be used to help memory.

The study involved 25 younger (17-23) and 32 older adults (60-86), who were shown the faces and names of 24 different people and told to learn them. The names were written in bright blue text and placed on the forehead, and each photo was shown for 3 seconds. After the learning session, participants were immediately tested on their recall of the name for each face. The test was self-paced. Following a 10 minute interval, during which they were given psychological tests, they were shown more photos of faces, but this time were told to ignore the text — their task was to push a button when they saw the same face appear twice in a row. The text was varied: sometimes names, sometimes words, and sometimes nonwords. Ten of the same faces and names from the first task were repeated in the series of 108 trials; all items were repeated three times (thus, 30 repeated face-name pairs; 30 other face-name pairs; 24 face-word pairs; 24 face-nonword pairs). The photos were each displayed for 1.5 seconds. A delayed memory test was given after another 10 minutes of psychological testing. A cued-recall test was followed by a forced-choice recognition test.

Unsurprisingly, overall younger adults remembered more names than older adults, and both groups remembered more on the second series, with younger adults improving more. But younger adults showed no benefit for the repeated face-name pairs, while — on the delayed recall task only — older adults did.

Interestingly, there was no sign, in either group, of repeated names being falsely recalled or recognized. Nor did they significantly affect familiarity.

It seems that this sort of inadvertent repetition doesn’t improve memory for items (faces, names), but, specifically, the face-name associations. The study builds on previous research indicating that older adults hyperbind distracting names and attended faces, which produces better learning of these face-name pairs.

It’s suggested that repetition as distraction might act as a sort of covert retrieval practice that relies on a nonconscious process specifically related to the priming of relational associations. Perhaps older adults’ vulnerability to distraction is not simply a sign of degeneration, but reflects a change of strategy to one that increases receptiveness to environmental regularities that have predictive value. Younger adults have narrowed attention that, while it allows them greater focus on the task, also stops them noticing information that is immediately irrelevant but helpful further down the track.

The researchers are working on a training program to help older adults with MCI use this benefit to better remember faces and names.

https://www.eurekalert.org/pub_releases/2018-03/bcfg-oad031618.php

Reference: 

Biss, Renée K., Rowe, Gillian, Weeks, Jennifer C., Hasher, Lynn, Murphy, Kelly J. 2018. Leveraging older adults’ susceptibility to distraction to improve memory for face-name associations. Psychology and Aging, 33(1), 158-164.

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Rigorous exercise does not slow dementia decline

  • A study involving nearly 500 people with dementia has found that a rigorous physical exercise program did nothing to slow their decline.

A number of studies have found that physical exercise can help delay the onset of dementia, however the ability of exercise to slow the decline once dementia has set in is a more equivocal question. A large new study answers this question in the negative.

The study involved 494 people with mild-to-moderate dementia (average age 77; 61% male), of whom 329 were randomly assigned to a four-month aerobic and strength exercise programme and 165 were assigned to usual care. The exercise program was personalized, and involved two 60-90 minute gym sessions every week, plus a further hour at home. Nearly two-thirds of the exercise group attended more than three-quarters of the gym sessions.

While the exercise group did get physically fitter, their cognitive fitness (as measured by ADAS-cog score) actually worsened slightly.

The researchers emphasize that this was a specialized and intense exercise program, and in no way should it be taken to mean that gentle exercise, which is good for dementia sufferers, should be avoided.

https://www.theguardian.com/society/2018/may/16/rigorous-exercise-makes-dementia-worse-study-concludes

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Gist memory may be why false memories are more common in older adults

  • Gist processing appears to play a strong role in false memories.
  • Older adults rely on gist memory more.
  • Older adults find it harder to recall specific sensory details that would help confirm whether a memory is true.

Do older adults forget as much as they think, or is it rather that they ‘misremember’?

A small study adds to evidence that gist memory plays an important role in false memories at any age, but older adults are more susceptible to misremembering because of their greater use of gist memory.

Gist memory is about remembering the broad story, not the details. We use schemas a lot. Schemas are concepts we build over time for events and experiences, in order to relieve the cognitive load. They allow us to respond and process faster. We build schemas for such things as going to the dentist, going to a restaurant, attending a lecture, and so on. Schemas are very useful, reminding us what to expect and what to do in situations we have experienced before. But they are also responsible for errors of perception and memory — we see and remember what we expect to see.

As we get older, we do of course build up more and firmer schemas, making it harder to really see with fresh eyes. Which means it’s harder for us to notice the details, and easier for us to misremember what we saw.

A small study involving 20 older adults (mean age 75) had participants look at 26 different pictures of common scenes (such as a farmyard, a bathroom) for about 10 seconds, and asked them to remember as much as they could about the scenes. Later, they were shown 300 pictures of objects that were either in the scene, related to the scene (but not actually in the scene), or not commonly associated to the scene, and were required to say whether or not the objects were in the picture. Brain activity was monitored during these tests. Performance was also compared with that produced in a previous identical study, involving 22 young adults (mean age 23).

As expected and as is typical, there was a higher hit rate for schematic items and a higher rate of false memories for schematically related lures (items that belong to the schema but didn’t appear in the picture). True memories activated the typical retrieval network (medial prefrontal cortex, hippocampus/parahippocampal gyrus, inferior parietal lobe, right middle temporal gyrus, and left fusiform gyrus).

Activity in some of these regions (frontal-parietal regions, left hippocampus, right MTG, and left fusiform) distinguished hits from false alarms, supporting the idea that it’s more demanding to retrieve true memories than illusory ones. This contrasts with younger adults who in this and previous research have displayed the opposite pattern. The finding is consistent, however, with the theory that older adults tend to engage frontal resources at an earlier level of difficulty.

Older adults also displayed greater activation in the medial prefrontal cortex for both schematic and non-schematic hits than young adults did.

While true memories activated the typical retrieval network, and there were different patterns of activity for schematic vs non-schematic hits, there was no distinctive pattern of activity for retrieving false memories. However, there was increased activity in the middle frontal gyrus, middle temporal gyrus, and hippocampus/parahippocampal gyrus as a function of the rate of false memories.

Imaging also revealed that, like younger adults, older adults also engage the ventromedial prefrontal cortex when retrieving schematic information, and that they do so to a greater extent. Activation patterns also support the role of the mediotemporal lobe (MTL), and the posterior hippocampus/parahippocampal gyrus in particular, in determining true memories from false. Note that schematic information is not part of this region’s concern, and there was no consistent difference in activation in this region for schematic vs non-schematic hits. But older adults showed this shift within the hippocampus, with much of the activity moving to a more posterior region.

Sensory details are also important for distinguishing between true and false memories, but, apart from activity in the left fusiform gyrus, older adults — unlike younger adults — did not show any differential activation in the occipital cortex. This finding is consistent with previous research, and supports the conclusion that older adults don’t experience the recapitulation of sensory details in the same way that younger adults do. This, of course, adds to the difficulty they have in distinguishing true and false memories.

Older adults also showed differential activation of the right MTG, involved in gist processing, for true memories. Again, this is not found in younger adults, and supports the idea that older adults depend more on schematic gist information to assess whether a memory is true.

However, in older adults, increased activation of both the MTL and the MTG is seen as rates of false alarms increase, indicating that both gist and episodic memory contribute to their false memories. This is also in line with previous research, suggesting that memories of specific events and details can (incorrectly) provide support for false memories that are consistent with such events.

Older adults, unlike young adults, failed to show differential activity in the retrieval network for targets and lures (items that fit in with the schema, but were not in fact present in the image).

What does all this mean? Here’s what’s important:

  • older adults tend to use schema information more when trying to remember
  • older adults find it harder to recall specific sensory details that would help confirm a memory’s veracity
  • at all ages, gist processing appears to play a strong role in false memories
  • memory of specific (true) details can be used to endorse related (but false) details.

What can you do about any of this? One approach would be to make an effort to recall specific sensory details of an event rather than relying on the easier generic event that comes to mind first. So, for example, if you’re asked to go to the store to pick up orange juice, tomatoes and muesli, you might end up with more familiar items — a sort of default position, as it were, because you can’t quite remember what you were asked. If you make an effort to remember the occasion of being told — where you were, how the other person looked, what time of day it was, other things you talked about, etc — you might be able to bring the actual items to mind. A lot of the time, we simply don’t make the effort, because we don’t think we can remember.

https://www.eurekalert.org/pub_releases/2018-03/ps-fdg032118.php

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Lifestyle changes can prevent cognitive decline even in genetically at-risk individuals

  • A large study indicates that lifestyle changes, together with advice and support for managing vascular health, can help prevent cognitive decline even in carriers of the Alzheimer's gene.

A Finnish study involving over 1000 older adults suggests that a counselling program can prevent cognitive decline even among those with the Alzheimer’s gene.

The study involved 1,109 older adults (aged 60-77) of whom 362 were carriers of the APOE4 gene. Some of the participants received regular lifestyle counselling (general health advice), while the rest received “enhanced” lifestyle counselling, involving nutrition counselling, physical and cognitive exercises, and support in managing the risk of cardiovascular diseases.

Earlier findings from the FINGER (Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability) trial showed that the regular lifestyle counselling group had a significantly increased risk of cognitive and functional impairment compared to the group receiving enhanced counselling. This analysis shows that this holds true even for those with the Alzheimer's gene, and indeed, might even be more helpful for carriers of the risky gene.

The findings emphasize the importance of early prevention strategies that target multiple modifiable risk factors simultaneously.

https://www.eurekalert.org/pub_releases/2018-01/uoef-lcp012518.php

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