Dementia is described as an acquired impairment of cognitive function and worldwide, Alzheimer’s disease [AD] is the most common cause of dementia. Some years back, migraine was also thought to be an unusual disease till awareness of the disease spread and now it is accepted as the most common cause of headache. Similarly, in most households, forgetfulness and behavioural changes in the elderly are attributed to quirkiness and age. In the joint family setting, many such inadequacies get masked as the elderly do not perform daily chores which would challenge their mind. Also, patients do not have awareness of their deficits and deny their presence on questioning, a term called as ‘anosognosia’.
Here we will address some myths and misconceptions regarding the disease.
Myth 1: Only old people get Alzheimer’s disease
Interestingly the first description of the disease was in 1907 when Alois Alzheimer, a German psychiatrist, described the case of a 51-year old woman with memory loss. For nearly half a century the disease was thought to be a rare cause of dementia in the young and only 100 such cases were described in the literature. Pioneering work by researchers in Newcastle in the 60s led to the realisation that Alzheimer’s disease was one of the most common diseases of the ageing population and one of the leading causes of death in the west. While AD can affect younger people too, age is the most important risk factor for developing AD and the prevalence increases as one gets older. The prevalence of the disease may be as high as 40 per cent by 85 years of age.
Myth 2: Memory loss is a normal part of ageing
Many people notice memory impairment as they grow older. However, the memory impairment must not interfere with everyday functioning. Most elderly suffer an occasional difficulty in recalling names and blame it on age to overcome the embarrassment. When the memory loss becomes frequent, causes difficulty in everyday chores and is progressive, then it is not normal and needs to be addressed.
Memory loss is the hallmark and core feature of AD. Patients are not aware of the memory loss and even the relatives may try to protect the patient by giving misleading information so as to assuage the feelings of the patient.
Memory is not a single function and is of different types. Episodic or declarative memory consists of short-term memory [trying to remember a phone number], recent memory [memory of everyday events] and remote memory [childhood events]. In AD, recent memory is affected the earliest. Patients misplace everyday objects and forget recent events and tasks. The relatives are often surprised that the patient could accurately recall details of his/her marriage or work decades ago, but forgot whether s/he had meal or may have spent hours searching for spectacles. The family members often complain that the patient seems to live in the past.
Eventually, remote memory is also affected. It is also important to remember that not all patients with memory loss suffer from AD and there are a number of other causes that need to be investigated. Two such important causes are depression and Vitamin B12 deficiency.
Myth 3: Alzheimer’s is not a fatal disease
AD is the fourth leading cause of death in the west. There is a gradual decline in function with the disease running its course over 7 – 10 years from onset. Patients eventually become bedridden and dependant on the caregiver for all daily activities. Pneumonia is usually the terminal event.
Myth 4: I’m not at risk because no-one in my family has ever suffered with Alzheimer’s disease before
Once a family member is diagnosed with the disease, it is not uncommon for the children or other family members to notice memory loss and worry about inheriting the disease. Familial AD has been described, but is very rare, accounting for less than five per cent of cases.
The commonest risk factor is the Apo E4 gene which increases the risk of AD up to four times in a carrier. Other genetic causes of AD are extremely rare. In most patients, there is no history of a family member being affected previously, thus a negative family history is not protective.
Myth 5: Influenza vaccination increases the risk of AD
There is no evidence that influenza vaccine increases the risk of Alzheimer’s. Doubts that aluminium and mercury content in the vaccine cause AD are unsubstantiated. Elderly patients who have been vaccinated have been shown to be at lesser risk. Similarly, use of aluminium utensils, aspartame [an artificial sweetener] and mercury dental fillings are not associated with AD.
Myth 6: Alzheimer’s disease cannot be prevented
Epidemiological studies have shown certain features to reduce the risk of AD. Higher education, moderate wine consumption and inheritance of apoE2 gene are thought to be protective. Use of cholesterol lowering agents, antioxidants and hormone replacement therapy may also reduce risk. A healthy lifestyle, regular moderate exercise and mental activity should be encouraged. The proverb ‘use it or lose it’ may be true for the mind.
Myth 7 Alzheimer’s disease is curable.
While the disease is not curable, several effective therapeutic options are available. A group of drugs known as acetylcholine esterase inhibitors are available for treatment. These drugs boost the effect of acetyl choline [neurotransmitter] in the brain by inhibiting its breakdown and are available in India. Modest benefit is seen with this class of drugs with improvement or stabilisation of symptoms.
Memantine, an NMDA [N-methyl-D-aspartate] receptor antagonist is also used in moderate to severe dementia. Several other treatment methods like vitamin E, hormone replacement therapy and NSAIDs were tried but have been given up due to minimal benefits or unacceptable side effects.
The behavioural problems can be treated with anti-psychotics and appropriate medication can be used for depression, anxiety and insomnia. It is important to remember that the elderly tolerate medications poorly and over-the-counter medication should not be used.
How is AD diagnosed?
The diagnosis of AD is based on the history, bedside clinical examination and neuropsychological tests. Routine blood investigations and neuroimaging [CT scan or MRI] are done to exclude other causes like vitamin B12 deficiency. Special tests like hippocampal volumetry, PET scan and SPECT are used for research purposes.
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