Alzheimer’s disease is the most prevalent type of dementia. Dementia is a disease affecting the brain, caused by an interplay of genetic and environmental factors over time. Age is the main risk factor for developing Alzheimer’s disease.
Neurons die gradually as Alzheimer’s disease progresses over several years, due to buildups of otherwise safe proteins including amyloid and tau. Amyloid forms plaques between neurons while tau forms tangles inside them. These structures result in the death of brain cells.
The first area of the brain affected by Alzheimer’s disease is the hippocampus. The hippocampus controls memory formation. A decreasing ability to form new memories results in the early symptoms of the disease, namely short term memory loss. Pre-existing memories are not as affected during this time. Emotion is also not affected initially, as this rests with the amygdala.
Once the amygdala becomes affected too, emotional symptoms arise, such as sudden mood changes, aggression or suspicion. In addition to brain cell death, Alzheimer’s disease presents a loss in essential brain neurotransmitters including acetylcholine, serotonin and norepinephrine. This impairs the connections between neurons.
Deterioration in brain function in the rest of the brain causes other symptoms, such as inability to plan and coordinate movements, loss of vision and hearing, changed perception of reality or hallucination, impaired language and ability to communicate, walking about, aggression, depression or anxiety, memory loss and others.
The genetic causes of Alzheimer’s disease are diverse. In familial Alzheimer’s disease (early onset around 40 years old), a single mutation in one of three different genes can be associated with a much higher incidence of Alzheimer’s disease.
These are very rare, so most cases of the disease are not explained by this simple genetic factor. However, there are many other genes whose variants act as risk factors for developing Alzheimer’s disease (late onset, after 65 years old). These interact with each other, and with lifestyle (environmental) factors to give an overall predisposition to developing the disease. Over 20 different variations of genes exist that act in subtle ways to increase the risk of developing Alzheimer’s disease to varying degrees.
Environmental factors that have been shown to be involved in the likelihood of developing Alzheimer’s disease include mental activity, physical exercise, diet high in polyunsaturated fat, fruit and vegetables and low in sugar and processed meats, having an optimal weight, and removing alcohol and tobacco smoke from the diet if applicable.
Hearing, vision and memory loss
The damage and debris accumulated over time results in multiple age-related diseases of the nervous system. Key ones are hearing loss, vision loss and memory loss.
Age-related hearing loss (presbyacusis) occurs in almost all people as they get older, mainly due to damage incurred to the hair cells on the cochlea in the inner ear. These hair cells are responsible for converting the vibrations in the cochlea fluid caused by sound waves into electric signals carried away by the auditory nerve to the brain to process sound.
Sound waves captured in the outer ear travel down the ear canal and reach the eardrum and the three smallest bones in the body (malleus, incus and stapes) where the air vibrations are transmitted to the fluid inside the cochlea, creating waves that are picked up by the hair cells lining the base. These cells themselves have many tiny hair-like projections called stereocilia which bend as a result. This movement stimulates the opening of pores which take up neurotransmitters and generate electric signals in the cells. Finally, these are carried by the auditory nerve to the brain to create hearing.
Therefore, the death of these hair cells (they’re cells not hairs) impairs hearing. The way they die over time can be affected by other factors such as genetics, exposure to loud noise for long periods of time, and separate conditions such as diabetes and chemotherapy treatment.
The death of these cells cannot be undone. Common symptoms of presbyacusis occur slowly and include difficulty hearing things clearly in loud environments, asking others to repeat themselves often, and listening to audio media on very high volumes. Treatment involves getting a hearing aid which comes in varying placements (behind the ear, inside the ear, etc.), or taking up a different communication method such as sign language if hearing is lost. Hearing aids are fitted for each person individually, and work through complex processing of environmental sound to pick up voices, remove wind, etc.
Age-related vision loss has multiple causes, the most prevalent of which are age-related macular degeneration (AMD) and glaucoma. Dry AMD occurs as cellular debris accumulates in the eye’s retinal pigment epithelial (RPE) cells, resulting in drusen deposits which damage the eye’s photoreceptor cells. Dry AMD differs from wet AMD. In wet AMD, blood vessels start forming under the macula, resulting in them bursting and releasing blood and other fluids into the eye, damaging the macula.
The condition progresses gradually, and affects the central vision of the patient. Glaucoma on the other hand is caused by damage to the optic nerve due to high pressure inside the eye, or poor blood flow. It presents no symptoms until vision loss has already started occurring, which cannot be reversed from that point.
Less severe vision loss conditions include presbyopia, dry eyes, decreased vision in low light, decreased colour perception, and more floaters and flashes. With ageing, the probability of developing these conditions as well as cataracts, goes up. More specifically, the nuclear type of cataract is associated with ageing. Nuclear cataracts form deep in the central zone of the eye’s lens. The clumping of proteins normally present here causes cataract formation. This clouds the lens and can lead to vision loss.
The lack of predictability and irreversible nature of some of these conditions makes regular vision testing crucial to maintaining good vision for as long as possible.
Age-related memory loss may occur as a result of lost brain cells and connections due to poor blood flow to the brain and accumulation of tau protein aggregates, and has other risk factors such as general health and mental activities undertaken.
It is not necessarily related to dementia such as Alzheimer’s disease (previously covered), but it can be a risk factor, and the beginning stage for it. Age-related memory loss is not severe, as it does not impair functioning. It manifests through symptoms such as occasional forgetting of information, actions or places.
An intermediary state where someone may frequently experience amnesia (memory loss) is termed mild cognitive impairment (MCI). The line between age-related memory loss and MCI is not clear-cut. However, MCI still does not involve the severe mental impairment that comes with dementia.
People with MCI can still function without having to rely on others for support in their everyday activities. The degree of severity of MCI is an indication of whether the person will progress onto dementia. If it is not severe or getting worse, it may simply plateau there without becoming dementia.
Practical investigations into the reaction time of people, as well as memory, reveal decreasing function with age. Some aspects of memory, however, may not suffer.
Experimental designs for these studies include computer tests, word and numbers tests, spatial skill testing, recall, etc.