It is sometimes difficult for people to understand that dementia is not a mental disease as such. This is particularly confusing because the diagnosis of dementia is most often (though not always) made by a psychiatrist. Research also shows that some forms of mental illness are risk factors for dementia.

Alzheimer’s disease is a physical disease which affects the brain. Actual physical changes take place in the tissues of the brain which alter the way that the brain works. In the advanced stages of Alzheimer’s disease, the atrophy of the brain can be measured. As far as is known, it is not the result of any other disease.

Vascular dementia is caused by changes in the circulatory and the vascular system which result in a lack of adequate blood supply to the brain. Some doctors think that a vascular ‘event’ such as a stroke may also trigger Alzheimer’s disease (see chapter 1) and that the two forms of dementia are more closely connected than was previously thought to be the case.

These two diseases are the most common forms of dementia, although there are many other more rarely seen types which appear to develop as primary diseases.

At the same time, it is also known that there are many rare physical diseases that may lead to dementia, including progressive HIV/AIDS, Creutzfeldt−Jakob disease (CJD), supranuclear palsy, Korsakoff’s syndrome, and Binswanger’s disease. Some people with multiple sclerosis, motor neurone disease, Parkinson’s disease or Huntington’s disease may develop dementia as a result of the progression of one of these diseases.

Because we are used to modern medicine being able to treat many conditions, and even to cure some of them, and because in the developed world we no longer fear the scourges of the past such as contagious diseases and disease caused by poor sanitation, there is a tendency to see illness as something which has only a short-term effect and which, after a cure has been effected, will not leave any residual problem in the human body. People have tended to become quite blasé about even very serious illness, such as pneumonia. The need to convalesce is no longer considered necessary and even taking extra rest after an illness is slightly frowned upon as ‘malingering’ or making a fuss.

In fact all illness leaves its mark upon the body. People live longer now and medical practitioners are beginning to see the residual effects of illness manifesting itself in later life. For example, we now know that there is a connection between polio and symptoms of lassitude, weakness and muscle fatigue in later life, known as ‘post polio syndrome’. The viral illness chickenpox, which many people contract as children, can resurface in later life as shingles, an extremely painful condition.

An analysis reported in the Journal of Social Science and Medicine examined whether childhood illness had a long-term effect on the appearance of chronic disease in later life. The authors reported that poor childhood health increases ‘morbidity’ (the likelihood of becoming ill) in later life. An association with poor health in childhood was found for cancer, lung disease, cardiovascular conditions, and arthritis/rheumatism. Non-infectious diseases were associated with higher rates of cancer and arthritis or rheumatism in later life, while infectious diseases were strongly associated with lung conditions, such as emphysema and bronchitis. The writers stated that: ‘Our results point to the importance of an integrated health care policy based on the premise of maximizing health over the entire life cycle’.1

Such findings do not mean that we should be anxious about trivial illness or worry about past medical history. There is, however, ample evidence for making sure that we give our bodies time to recover after illness and that we make every effort not to allow neglect of our health to cause problems in later life.

We will see in the course of this chapter that some illnesses, both physical and mental, and some traumatic events predispose people towards dementia in later life. There are indeed chronic diseases and disorders which are known to have a ‘connection’ with dementia. The most well documented of these are cardiac and vascular disease (including stroke) and diabetes.

Stroke

Many people who suffer a stroke which causes temporary cognitive, as well as neurological, problems make a considerable, if not a full, recovery. They do not develop dementia and may go on to live comfortable and active lives. However, the fact is that suffering a stroke does increase your chances of developing dementia. Atrial fibrillation in someone who has suffered an ischemic stroke seems to be associated with an increased risk of developing dementia.2 If you have a stroke and are discovered to suffer from atrial fibrillation, you will be offered medical treatment to reduce the chances of a further stroke.

Someone who has suffered a stroke will normally be subject to a number of tests and investigations to discover the ostensible cause. Health issues such as high blood pressure or cardiac disease will hopefully be addressed by the attending medical team. If you have had a stroke you can help yourself by making full use of all the physical therapy offered to you and by adopting a positive ‘can do’ attitude. Cognitive and physical recovery can happen over a number of months or years. The part of the brain which has effectively ‘died’ following the loss of blood supply will not recover (it is known as an infarct) but other parts of the brain may, and frequently do, take over the functions of the dead cells and remarkable recovery can be made.

There are two main types of vascular dementia known to be related to stroke: ‘multi-infarct dementia’ (MID) and ‘single-infarct dementia’.

Multi-infarct dementia (MID) is the result of multiple, small strokes and is a common form of dementia. It develops when blockages in the blood supply to the brain occur frequently over a period of time in the smaller blood vessels, giving rise to many tiny and widespread areas of damage. These small strokes are commonly known as transient ischaemic attacks (TIAs). Often someone can suffer a TIA without any major symptoms and they may even be unaware that it has happened. Sometimes the only symptoms are fleeting, such as a few moments dizziness or a slurring of speech which rights itself in moments, or a weakness and numbness in a limb which passes off and may be put down to cramp or to sitting too long in one position. These continuing small strokes can go on for years, causing gradual loss of function and leading to confusion and intellectual deterioration. A feature of this type of vascular dementia is that some people experience periods of relative stability before another TIA causes further significant and abrupt worsening of the symptoms.

Single-infarct dementia results from a single stroke that is extremely severe or affects a particular area of the brain to which the damage is limited.

Sub-cortical vascular dementia (also known as ‘small vessel disease related dementia’) is a further form of vascular dementia. It is not caused by stroke but may be experienced by somebody who has also had a stroke. It is caused by injury to small blood vessels that are deep within the brain. The onset of this type of dementia is more gradual than stroke-related dementia, and so it appears more like the onset of Alzheimer’s disease rather than the ‘stepped’ deterioration common to multi-infarct vascular dementia.

If you have suffered a stroke you can make every effort to recover your physical abilities, and making adjustments to your lifestyle and co-operating with medical teams will help to prevent further strokes. This will help to preserve your cognitive abilities.

If you have been diagnosed with vascular dementia (as a result of several minor strokes/TIAs, for example), you may be given medication aimed at preventing further strokes. Treatment of vascular dementia is aimed at preventing more damage and capitalising on the cognitive abilities which are retained. Therefore, the suggestions in the chapters on exercise, social and cognitive stimulation, and nutrition are all relevant.

You can reduce your risk of suffering a stroke by taking regular exercise, refraining from smoking and controlling your blood pressure. You cannot usually anticipate a stroke, although there is evidence that a transient ischaemic attack is a serious warning sign of stroke and should not be ignored.

Up to 40 per cent of all people who have experienced a TIA will go on to have an actual stroke. Most studies show that nearly half of all strokes occur within the first two days after a TIA. Within two days after a TIA, 5 per cent of people will have a stroke. Within three months after a TIA, 10 to 15 per cent of people will have a stroke. If you believe that you have suffered a TIA, you should see your doctor without delay.

Diabetes

Diabetes is an increasingly common health condition. There are 2.9 million people diagnosed with diabetes in the UK and an estimated 850,000 people who have the condition but do not know it.3

Diabetes is the term used for a condition where the amount of glucose in the blood is too high because the body cannot metabolise it properly. When the body is working as it should, the organ called the pancreas produces a hormone called ‘insulin’ that allows blood sugar (glucose) to enter the body’s cells, where it is used as fuel. Problems arise when the pancreas either does not produce any insulin, or does not produce enough. It may also be that the body’s response to insulin becomes gradually weaker so that the pancreas has to produce more and more insulin without it ever being enough; this is called ‘insulin resistance’.

There are two main types of diabetes: type 1 (often called juvenile-onset diabetes because it usually develops in childhood) and type 2 (sometimes called maturity-onset diabetes). Type 1 diabetes develops when the insulin-producing cells in the body have been destroyed and the body is unable to produce any insulin. Type 2 develops when the body can still make some insulin, but not enough, or when the body is unable to use the insulin being produced.

Diabetes is a serious condition and should not be treated lightly. If uncontrolled, it can lead to problems with blood circulation which can affect the eyes, heart and peripheral parts of the body (hands and feet, especially fingers and toes).

A growing body of research links diabetes with both Alzheimer’s disease and vascular dementia. There is even a school of thought which suggests that Alzheimer’s disease is actually a third type of diabetes.4

Non-insulin dependent diabetes has specifically been identified as a significant risk factor for age-related cognitive impairment, cognitive decline and dementia.5 It has been demonstrated that people with mild cognitive impairment (MCI) who also have diabetes are three times more likely to develop dementia than those who have MCI alone.6 The term MCI is used to describe someone who has memory impairment but no impairment in other cognitive functions or problems with the activities of daily living. (For more information about mild cognitive impairment see chapter 2.) There is evidence that patients who have diabetes are more likely to suffer cognitive impairment following a stroke7 than those patients who do not have diabetes.

If you refer to chapter 6, on nutritional factors and dementia, it becomes clear that the problem lies in the metabolism of glucose and the effect this has on the brain. The brain uses glucose as its sole food (although it cannot store glucose), making use of almost a quarter of the glucose and oxygen which the body takes in. Because the brain uses glucose as its main source of energy it might be thought that a high level of glucose in the blood would be good for the brain, making it work better. In actual fact, fluctuations in blood glucose level, such as are caused by a diet high in carbohydrate (which the body breaks down into glucose, its absorbable form) and sugar including the sugar found in fruit (fructose), are detrimental. The brain needs a sustained and balanced supply of glucose, and this is best obtained from eating foods which cause blood glucose levels to rise more slowly and to be sustained for longer. Uncontrolled diabetes can lead to excessive high and low levels of glucose.

What does this mean in terms of avoiding dementia? Firstly, the risk factors for maturity-onset diabetes are well known. Do not assume that because many people are developing the condition it is not serious. You should take strenuous steps to avoid becoming diabetic. Whilst some of the risk factors may not be under your control, others, like excessive weight gain, lack of exercise and high blood pressure are likely to be within your control. Further information about risk factors is readily available on the Diabetes UK website and in their literature.3 Remember that, aside from the risk of dementia, diabetes increases the risk of experiencing many other health problems too.

If you have been diagnosed with type 2 diabetes, you may be able to reverse the process by losing weight and addressing other health issues. If this is not possible, take the condition seriously. Adjust your diet, attend for medical screening and take your doctor/diabetic nurse’s advice.

Diabetics who have been diagnosed with early stage dementia need special attention from their carer to watch blood glucose levels and take medication in a timely manner.

Other physical conditions

A number of other physical conditions have been linked with dementia especially in people known to carry the ApoE4 gene (for further information about ApoE4 see chapter 2), but research into these is still ongoing. Information about some of these conditions and the current state of research is included here for those who are interested. It is important to remember that, because we do not know the actual cause(s) of dementia, some of these lines of research may later be proved not to be relevant.

Herpes simplex

Ruth F Itzhaki, from the University of Manchester, UK, has done a substantial amount of research which suggests that a common virus, the herpes simplex virus type 1 (HSV1), acting in combination with the APoE gene, may have a major causative role. This is the virus which causes the common cold sore. Ruth Itzhaki presents evidence that the virus is, indeed, a factor in Alzheimer’s disease (AD). However, her research, published in the Lancet, cautions that: ‘the combination of HSV1 in brain and carriage of an APOE-epsilon 4 allele [gene] is a strong risk factor for AD, whereas either of these features alone does not increase the risk of AD.’8 In other words, you should not necessarily worry just because you are prone to develop ‘cold sores’. Other factors may play a more important part in the possibility of developing dementia.

Age-related macular degeneration

Scientists have known for some time that there is a connection between Alzheimer’s disease and age-related macular degeneration (AMD) – the deterioration of the part of the retina called the ‘macular’, which provides our central field of vision. This condition is a major cause of sight problems in older people.

One of the early signs of Alzheimer’s disease is the presence of ‘extracellular senile plaques’ in the brain – deposits of a protein called amyloid that disrupt communication between brain cells. These plaques are akin to deposits of cellular debris that are responsible for age-related macular disease; they build up between the retina and choroid layers at the back of the eyeball and disrupt vision.

Because of these parallels, researchers were prompted to study the appearance of the two diseases together within a major population study, the ‘Rotterdam study’. This study was set up in the Netherlands to investigate factors that determine the occurrence of cardiovascular, neurological, ophthalmological, endocrinological and psychiatric diseases in elderly people. In a paper published in the American Journal of Epidemiology the researchers reported that subjects who had advanced AMD when the study began showed an increased risk of developing Alzheimer’s disease. Their conclusion was that the neural degeneration occurring in AMD and that in AD might have a common pathogenesis, or underlying disease process.9 However, the association was only significant for the most severe stages of AMD and the authors pointed out that this depended also on smoking and atherosclerosis (hardening of the arteries). Smoking is an established risk factor for AMD. (For further information on research results connecting smoking with incidence of dementia, see chapter 3 on personality and lifestyle.)

Hearing impairment

Hearing impairment may seem a strange factor to associate with dementia. However, a piece of research published in 1989 found that untreated hearing impairment was more prevalent in those with dementia and that the risk of dementia increased with the degree of hearing loss. The researchers did point out that there was no suggestion that hearing loss was a cause of dementia; rather that hearing loss might reveal or exacerbate the symptoms. Hearing impairment can cause social isolation and can also contribute to a general loss of understanding of the environment as well as, perhaps, contributing to depression.10

People with dementia are often reluctant to wear hearing aids even when they have been prescribed and carers sometimes find it difficult to ensure that they are worn consistently. A person who has dementia who also has a severe hearing loss will be likely to be more confused if he/she cannot hear what is going on around him/her.

Infection

Along with the evidence around HSV1 (Herpes simplex), there is emerging discussion of the possibility of some forms of dementia (as well as other chronic conditions, such as heart disease) resulting from infection. Chlamydophila pneumoniae and several types of bacteria, collectively known as ‘spirochetes’, have been suggested as possible causes.11 Evidence to date has been inconsistent, however.

Scientists at the University of Texas Medical School in Houston did some research which involved injecting brain tissue from a confirmed Alzheimer’s patient into mice and compared the results with a control group. Those mice injected with the Alzheimer’s brain extracts developed plaques and other alterations to the brain typical of Alzheimer’s disease. This research raises the possibility that some cases of Alzheimer’s disease may arise from an infectious process similar to diseases like Creutzfeldt-Jakob disease.12

What is known is that infections of any kind are likely to accelerate neurodegeneration in someone who has dementia or mild cognitive impairment. Urinary and chest infections, in particular, are known to exacerbate symptoms in people with dementia and there is a school of thought which believes that inflammation is the prime ‘culprit’ in the development of dementia, particularly inflammation caused by infections.

Systemic inflammation – inflammation of the whole body – is known to have direct effects on brain function. Recently a number of observational studies linked the intake of non-steroidal anti-inflammatory drugs (NSAIDs) with a lowered risk of developing Alzheimer’s disease,13 and for a while this looked like a very promising research route. Unfortunately, randomised controlled trials so far have not confirmed any beneficial effect from taking NSAIDs. However, scientists are still following up this line of research, and it is possible that a different dose than that used in the randomised controlled trials, or the use of NSAIDs at an earlier stage of disease or for a different length of time, might show benefit.

There are a number of (mostly rare) infectious and inflammatory conditions which can lead to dementia and that can be treated leading to the improvement or stability of any dementia symptoms. These diseases include Hashimoto’s encephalitis, syphilis, Lyme disease (later stages) and HIV/AIDs. Usually other (non-dementia) symptoms will be evident and lead to a correct diagnosis and treatment.

Episodes of delirium, in which elderly and demented patients become extremely disoriented and confused, are frequently caused by infections, injury or surgery (see below). Urinary tract infections, which are usually caused by bacteria, appear to be particularly common inducers of psychiatric symptoms which can sometimes mimic dementia.

Post-operative cognitive impairment

Following an operation under general anaesthetic some people develop a severe (and temporary) form of confusion often termed post-operative delirium. It is known that people who suffer postoperative delirium are more likely to suffer from dementia at a later date.14 This has been noticed more particularly in patients undergoing coronary bypass grafting. For more detail on postoperative cognitive impairment see chapter 7 on trauma.

Physical disease as a trigger

Clearly physical disease and the risk of dementia are not unconnected.15 Whilst not suggesting that you should become over-concerned about minor illness, the evidence implies that as we grow older we should take care of our physical health, be sensible about minor infections or injuries, and not allow minor health problems to become major ones through self-neglect. If you have a long-standing health problem you should not become blasé about the way you manage it. Whilst the human body has huge recuperative powers, you should respect the potential for future damage and protect against this as far as possible.

The family and carers of people who have been diagnosed with dementia often state that they date the appearance of symptoms from a severe illness, the beginning of a physical health problem or a stay in hospital for a surgical operation. Some doctors tend to dismiss this anecdotal evidence, suggesting that there is no robust research which proves such incidents precipitate early symptoms of dementia. Others, including consultant psychiatrists who specialise in elderly care, are more cautious. If you notice symptoms of cognitive loss following a major physical illness or surgical intervention, do not allow yourself to be dismissed as neurotic.

Other causes of memory loss and confusion

It is important to remember that there are some physical problems – one example is a vitamin B12 deficiency – which may cause memory problems and mild confusion. When people present to their doctor with suspected dementia, the doctor will normally conduct tests to screen out the possibility of such a cause. If you are worried about the possibility of a vitamin deficiency you can check this with your doctor.

There are also some drugs, or combinations of drugs, which may cause these symptoms. Sometimes the symptoms may arise even after you have been taking the drug for some time without problems.

Memory loss and confusion do not always mean dementia. If you suspect a deficiency or a drug interaction you should mention this to your doctor or pharmacist. Pharmacists are often more knowledgeable about drug interactions than GPs.

Depression

Depression is linked to dementia and often accompanies the diagnosis, although it is not clear whether the depression is part of the illness or is caused by the diagnosis. Many of us might consider that such a diagnosis might make us depressed. It is also not clearly understood whether depression precedes the development of dementia or is a causal effect. Depression is particularly common in people diagnosed with vascular dementia or with dementia due to Parkinson’s disease.

Most of the symptoms of depression are generally well known. They include feelings of hopelessness and sadness, loss of interest in daily activities, feelings of worthlessness and possibly guilt, feelings of isolation, loss of appetite and difficulty with sleeping, problems with concentration and decision making, and tiredness and loss of energy.

You may recognise from chapter 2 that many of these symptoms are similar to those experienced by someone with dementia. Indeed, it is not uncommon for someone who has dementia and retains insight to believe that they are suffering from a form of depression and to visit the doctor believing this to be their problem. It is unfortunately quite common for people actually to be treated for depression for some time before the possibility of a diagnosis of dementia is considered, especially in people under the age of 65.

*******

I believed that my difficulties in concentrating and my confusion were because I was depressed. I put this down to the fact that I had recently retired and that two close friends had died in the past six months. Initially I felt a little better when I was given an anti-depressant medicine but the confusion and memory problems did not get better. It was almost a relief to have a proper diagnosis and at this point my GP explained that I was probably suffering from depression alongside the dementia.

*******

Josh Woolley and colleagues studied the likelihood of those with emerging dementia being diagnosed initially with depression or other psychiatric problems. Their investigation involved 252 patients with a neurodegenerative disease diagnosis seen between 1999 and 2008. Of these, 28.2 per cent (nearly a third) had received a prior psychiatric diagnosis. Depression was the most common in all groups, but those with fronto-temporal dementia received a psychiatric diagnosis more often than those with Alzheimer’s disease. The researchers concluded that dementia is often misclassified as psychiatric disease, with patients that had behavioural-variant fronto-temporal dementia at highest risk of misdiagnosis. The authors of this paper pointed out that the study could not rule out the possibility that psychiatric disease is an independent risk factor for dementia (see more research below). However, if misdiagnosed, then patients may receive ‘delayed, inappropriate treatment and be subject to increased distress’.16

Depression can make the behavioural symptoms of someone suffering from dementia worse, and treating the depression will mean that both the person with dementia and his/her carers will be better able to cope, although some medical opinion suggests that conventional anti-depressant treatment does not work to lift depression in those with dementia.

There are a number of links between clinical depression during adulthood and dementia in later life but it is difficult to draw definite conclusions. Robert S Wilson, PhD, of Rush University Medical Center, Chicago, and colleagues, studied 917 older Catholic nuns, priests and monks who did not have dementia, beginning in 1994. Those with more symptoms of depression at the beginning of the study were more likely to develop Alzheimer’s disease. For each depressive symptom registered at the beginning of the study, the risk of developing Alzheimer’s disease increased by an average of 19 per cent, and the annual rate of cognitive decline increased by an average of 24 per cent. In this study, those who developed Alzheimer’s disease did not show any increase in depressive symptoms in the period just before the diagnosis was made. These researchers therefore concluded that symptoms of depression might be associated with changes in the brain that reduce its resistance to dementia.17

Looking at the connection another way, research reported in the European Journal of Epidemiology suggests that there may be a genetic link between a susceptibility to depression and a higher than normal risk of dementia.18 In this study of 6596 subjects, researchers looked at the association of self-reported depression which required treatment by a psychiatrist, to family history of psychiatric disease, dementia and Parkinson’s disease. Not surprisingly perhaps, a family history of psychiatric disease was significantly associated with overall depression. In addition, people who had two or more first-degree relatives, such as parents, siblings or children, with dementia had a higher risk of depression. Those with only one relative with dementia had no increased risk. The researchers suggested that this study indicates that there might be ‘shared susceptibility gene(s) underlying these diseases’. Of course it might be concluded that the stress of caring for two or more relatives with dementia could be a cause of depression.

Depression, and additionally bipolar disorder, are also associated with a higher than average risk of dementia in another piece of research which looked at all hospital admissions for primary affective disorder (low mood and depression) in Denmark during 1970–1999. A total of 18,726 patients with depressive disorder and 4248 patients with bipolar disorder were included in the study. Risk of a later diagnosis of dementia was significantly increased according to the number of times patients had been admitted to hospital previously. It was calculated that every admission for depression increased the possibility of later dementia by 13 per cent and every admission for bipolar disorder increased the possibility of dementia by 6 per cent. The researchers concluded that the risk of later dementia increased with the number of episodes of hospitalisation with depression.19

This is not an easy conclusion to interpret, however. Is one to conclude that hospital admission makes dementia more likely or that a more severe experience of bipolar disorder (therefore involving hospital admission) is the risk factor?

Mood disorders in general may be risk factors for the development of dementia. A study involving 455 people with mood disorders, including major depression and bipolar disorder, compared with 1003 ‘normal’ controls, showed that cognitive decline developed faster in people with mood disorders after the age of 65 than in the control group. The authors concluded that not only might depression in later life be an early manifestation of dementia but that those who develop depression or fail to recover from an earlier depression may have a higher risk of developing dementia. The researchers did, however, point out that the results could equally show that changes resulting from past disease or injury might cause both mood disorders and dementia.20

This sample of the research into a possible causal link between dementia and depression indicates both the difficulties which researchers encounter and the lack of robust conclusions from research to date. The only clear conclusion appears to be that there is some connection between clinical depression and a later diagnosis of dementia. Clinicians also know that people diagnosed with dementia are often also depressed.

Schizophrenia

Schizophrenia is a mental illness characterised by a breakdown in thought processes and by poor emotional responsiveness. It commonly manifests itself as ‘hearing voices’ (auditory hallucinations), paranoia, strange delusions, and disorganised patterns of speech and thought, and it is accompanied by significant social and/or occupational dysfunction. It is a completely different disorder from dementia and the onset of symptoms generally occurs in young adulthood.

Some research has been done on the connection of an extracellular matrix protein which may be involved in the pathologic changes in both schizophrenia and Alzheimer’s disease.21 The cells which secrete this protein are reduced in the brain of someone with schizophrenia and they are also reduced in the brain of someone with Alzheimer’s disease. As with Alzheimer’s disease though, the causes of schizophrenia are unclear. Where dementia develops in people with schizophrenia it seems to be similar to fronto-temporal dementia22 (see chapter 2).

Recently a particular study has been made of the association of the drug benzodiazepine with the development of dementia. Benzodiazepine is primarily used for treating the symptoms of anxiety and sleep disorders over short periods. It is widely prescribed in developed countries. It is known that the drug impairs free recall and the recognition of information. Studies focusing on the association between benzodiazepine use and dementia or cognitive decline in elderly people have previously shown conflicting results. Some found an increased risk of dementia or cognitive impairment in benzodiazepine users,23,24 whereas others reported a potential protective effect.25

In 2012 a large, prospective, population-based study of elderly people who were free of dementia and did not use benzodiazepines until at least the third year of follow-up was reported in the British Medical Journal. This research concluded that new use of benzodiazepines ‘was associated with a significant, approximately 50% increase in the risk of dementia’. The researchers reported that this result remained stable after adjustment for potential confounding factors, including any cognitive decline before starting benzodiazepine and clinically significant symptoms of depression.26

Precautions

If you have been diagnosed with any form of dementia, or if you are caring for someone with dementia, you should remember that it is a serious disease. In the early days, especially, there are often no obvious physical signs and people are apt to forget how serious the condition is. If you have dementia you should consider that your immunity is compromised. Every effort should be made to protect someone with dementia from catching infections, even such minor things as the common cold, and especially such illnesses as chest and urinary infections. If any elective surgery is required it should be carefully planned and efforts should be made to ensure that the person with dementia reaches the hospital in the best possible state of physical health. Sometimes doctors themselves do not appear to take these precautions seriously so it is up to carers to do their best. Keep people with colds away from a person with dementia, take colds seriously and do your best to make sure that no complications develop. Any infection may result in a (sometimes temporary) worsening of dementia so be aware of this.

If the person you care for suffers from diabetes you should make absolutely certain that his/her blood sugar is kept regulated. People with dementia (even if previously self-medicating) may forget to check their blood sugar levels and to take their medication or may become confused about time and dosages. Unregulated blood sugar levels will cause a person with dementia to become more confused and disorientated.

If the person you are caring for has vascular dementia you should familiarise yourself with the symptoms of small stroke (TIA) and be alert for any signs of this; a deterioration in cognitive ability may result.

If the person you are caring for has been prescribed medication such as anti-depressants or mood-controlling drugs, and once they have been stabilised on these drugs, you should not discontinue or reduce (or increase) the dose without checking with the doctor first, even if you think the medication is causing other symptoms. The doctor can help to find the dose which will give most benefit with the least side effects. Discontinuing or giving medication erratically can make someone’s symptoms worse.

References

1. Blackwell DL, Hayward MD, Crimmins EM. Does childhood health affect chronic morbidity in later life? Social Science & Medicine 2001; 52(8): 1269–1284.

2. Mizrahi EH, Waitzman A, Arad M, Adunsky A. Atrial fibrillation predicts cognitive impairment in patients with ischemic stroke. American Journal of Alzheimer’s Disease and Other Dementias 2011; 26(8): 623-626. DOI: 10.1177/1533317511432733.

3. Information from Diabetes UK http://www.diabetes.org.uk

4. Zhao WQ, De Felice FG, Fernandez S, et al. Amyloid beta oligomers induce impairment of neuronal insulin receptors. FASEB Journal 2008; 22: 246-260.

5. Logroscino G, Kang JH, Grodstein P. Prospective study of type 2 diabetes and cognitive decline in women aged 70-81 years. British Medical Journal 2004; 328(7439): 548-503.

6. Velayudhan L, Poppe M, Archer N et al. Risk of developing dementia in people with diabetes and mild cognitive impairment. British Journal of Psychiatry 2010; 196(1): 36-40.

7. Mizrahi EH, Waitzman A, Blumstein T, Arad M, Adunsky A. Diabetes mellitus predicts cognitive impairment in patients with ischemic stroke. American Journal of Alzheimer’s Disease and Other Dementias 2010; 25(4): 362-366. DOI: 10.1177/1533317510365343.

8. Itzhaki RF, et al. Herpes simplex virus type 1 in brain and risk of Alzheimer’s disease. Lancet 1997; 349(9047): 241-244.

9. Klaver CCW, et al. Is age related maculopathy associated with Alzheimer’s disease? American Journal of Epidemiology 1999; 150(9): 963-968.

10. Uhlmann RF, et al. Relationship of hearing impairment to dementia and cognitive dysfunction in older adults. Journal of the American Medical Association 1989; 261(13): 1916-1919.

11. Ewald PW. Plague Time: The new germ theory of disease. Anchor Books; 2002.

12. Morales R, et al. De novo induction of amyloid-B deposition in vivo. Molecular Psychiatry 2012; 17: 1347–1353. DOI: 10.1038/mp.2011.120.

13. In ‘t Veld BA, Ruitenberg A, Hofman A, et al. Nonsteroidal anti-inflammatory drugs and the risk of Alzheimer’s disease. New England Journal Medicine 2001; 345: 1515-1521. DOI: 10.1056/NEJMoa010178.

14. Hanning CD. Postoperative cognitive dysfunction. British Journal of Anaesthesia 2005; 95(1): 82-87.

15. Holmes C, et al. Systemic inflammation and disease progression in Alzheimer disease. Neurology 2009; 73(10): 768-774.

16. Woolley JD, Khan BK, Murthy NK, Miller BL, Rankin KP. The diagnostic challenge of psychiatric symptoms in neurodegenerative disease: rates of and risk factors for prior psychiatric diagnosis in patients with early neurodegenerative disease. Journal of Clinical Psychiatry 2011; 72(2); 126-133.

17. Wilson et al. Depressive symptoms, cognitive decline, and risk of AD in older persons. Neurology 2002; 59(3): 364-370. DOI: 10.1212/WNL.59.3.364

18. Fahim S, et al. A study of familial aggregation of depression, dementia and Parkinson’s disease. European Journal of Epidemiology 1998; 14(3) 233-238. DOI: 10.1023/A:1007488902983

19. Kessing LV, Andersen PK. Does the risk of developing dementia increase with the number of episodes in patients with depressive disorder and in patients with bipolar disorder? Journal of Neurology Neurosurgery and Psychiatry 2004; 75: 1662–1666. DOI: 10.1136/jnnp.2003.031773

20. Gualtieri CT, Johnson LG. Age related cognitive decline in patients with mood disorders. Progress in Neuro-Psychopharmacology & Biological Psychiatry 2008; 32(4): 962-967; 0278-5846.

21. Aoki T, Mizuki Y, Terashima T. Relation between schizophrenia and Alzheimer’s disease: the reelin signalling pathway. Psychogeriatrics 2005; 5: 42-47.

22. de Vries PJ, Honer W, Kemp P, McKenn P. Dementia as a complication of schizophrenia. Journal of Neurology Neurosurgery and Psychiatry 2001; 70: 588-596.

23. Gallacher J, Elwood P, Pickering J, Bayer A, Fish M, Ben-Shlomo Y. Benzodiazepine use and risk of dementia: evidence from the Caerphilly Prospective Study (CaPS). Journal of Epidemiology and Community Health 2012; 66: 869-873.

24. Wu CS, Wang SC, Chang IS, Lin KM. The association between dementia and long-term use of benzodiazepine in the elderly: nested case-control study using claims data. American Journal of Geriatric Psychiatry 2009; 17: 614-620.

25. Fastbom J, Forsell Y, Winblad B. Benzodiazepines may have protective effects against Alzheimer disease. Alzheimer’s Disease and Associated Disorders 1998; 12: 14-17.

26. Billioti de Gage S, Bégaud B, Bazin F, Verdoux H, Dartigues J-F, Pérès K, Kurth T, Pariente A. Benzodiazepine use and risk of dementia: prospective population based study. British Medical Journal 2012; 345: e6231.