Memory problems in mid-life

grandson helping grandfather with computer

Dr. Martin Zarate

Department of Rehabilitation and Geriatrics HUG, Geneva and Clinique de Genolier, Genolier

November 15, 2022

Memory problems can occur at any time, even in our mid-life. The issues can be small or big, depending on the severity of the memory problems. There are a couple of different memory types that can be affected. Short-term and long-term memories can both cause problems. Mild cognitive impairment is an early stage of memory loss and can lead to bigger issues. It’s considered to be a precursor to Alzheimer’s disease. The risk factors for dementia include age, gender, and lifestyle. This is preventable by changing your lifestyle, eating healthier, exercising often, taking your medicine, and more. 

Want to learn more? Keep reading the article by Dr. Martin Zarate.

My memory fails me….

What’s his name again? Wait a minute, wait a minute! I have it on the tip of my tongue… What did I mean? What did I come here for? Have you seen my glasses by any chance? What did we talk about? My appointment was yesterday, I forgot to put it in my diary! How many times has your memory playing tricks on you?

“A place of predilection for our knowledge, skills and know-how, but also a place of intimacy, available or not to the conscience, the memory constitutes a cement for our identity… it allows us to access our past and to prepare the future… it is synonymous with activity, social role, availability to the world…” Pierre-Yves Jonin & Virginie Matteo

Memory disorders are common and of less concern to older people because the gradual decline in memory performance is considered an integral part of the ageing process. On the other hand, when younger people experience the first memory difficulties, the fear of seeing these disorders evolve into a dementia process immediately comes to mind.

The memory complaint affects up to 50% of people over 50 years of age. For people in their fifties, the difficulty in fixing the attention, retaining recent information, and acquiring new data, because they no longer have the same cognitive performance as twenty years ago, is a major source of concern.

Subjective memory complaints can range from simple attentional problems during periods of stress, overwork, emotional conflict, temporary depression, or sleep disturbance, to a more worrisome condition called MCI (mild cognitive impairment).

How does our memory work?

The relationship between brain and mind, between material and abstract entities, is currently the subject of intense scientific activity. The neurobiological bases of consciousness, cognitive functions, and in particular the cerebral processing of information, are only partially elucidated. We know that the brain processes the information it receives by simultaneously activating multiple networks of neurons, involving the activity of different cell populations.

In the nervous system, memory is a highly hierarchical process, consisting of several successive stages. Thus, information first undergoes a phase of acquisition (encoding), followed by a phase during which the information is stored (storage and consolidation) and later recalled and played back (retention, decoding and playback). A brain structure deep in the brain called the hippocampus underlies this process. It is part of a more complex brain circuit called the Papez circuit.

Memory defects can occur during acquisition (difficulties in learning or storing new information) or during retrieval of stored information.

Neurobiologically, the acquisition of memory is associated with the constitution of a trace of the memorised information, called a memory trace, which is materialised by modifications of the neuronal terminations called dendrites, by the synthesis of new proteins and by the solicitation or creation of new neuronal circuits involved in the construction of memory.

The different types of memory

When we receive information through our sensory organs, it can either be ignored and disappear almost instantly, or it can be perceived and integrated into the storage system.

This information will first be held in a short-term memory system that allows storage for a very short time (less than a minute). This type of memory is used, for example, when we dial a new telephone number. Active effort can still maintain it, otherwise, it fades away. Keeping a memory in the short-term memory allows it to be transferred to another, more durable, long-term storage system.

Long-term memory includes recent, still fragile memories, and old, usually well-consolidated facts. Once entered into the long-term storage system, the encoded information can be kept for a long time, even for life if it is well consolidated. How easy or difficult it is to retrieve or restore this information depends on the length of time between the event and its subsequent reuse (recollection), its integration into other memories and knowledge, and its emotional charge. The more well coded, well organised and well structured a memory is, the easier it is to retrieve. Thus, forgetting can be caused by poor stages of encoding (acquisition), consolidation or retrieval of information.

Long-term memory is made up of different entities:

  • Explicit or declarative memory allows us to consciously recall facts; it requires an effort to remember (a list of objects for example) in order to be retrieved verbally. This explicit memory is expressed in two distinct forms:

1) Episodic or autobiographical memory allows us to remember events experienced in a given place and time (for example I remember where and with whom I celebrated my 40th birthday…).

2) Semantic memory stores knowledge about the world, rules, ideas and concepts. It is an easily accessible knowledge base (for example; Paris is the capital of France, I remember the colour and smell of a banana…).

Unlike episodic memory, semantic memory is independent of the temporal and spatial context of its acquisition.

  • An implicit, non-declarative, unconscious memory, which is recalled automatically, without effort. It is a form of memory in which we do not retain the experience that gave rise to it. It also has two components:

1) procedural memory allows the acquisition of skills and the improvement of performance. It is the support of automatisms of which we are almost no longer aware (for example; eating, walking, riding a bicycle, driving a vehicle).

2) Associative learning, emotions and conditioned reflexes (a sound, a scent, an image, can awaken an emotion or even a behaviour) call upon an unconscious memory which is said to be located in a brain structure called the amygdala.

What is mild cognitive impairment (MCI)?

Mild cognitive impairment (MCI) refers to memory complaints usually confirmed by a third party and objectified by memory tests, but with preserved global cognitive functioning, without dementia. MCI can occur in the single domain of memory or in other domains (language, executive functions, visual-spatial domain, etc.). The term applies to individuals whose cognitive performance is impaired compared to people of the same age and education level. It is therefore not the classic decline in cognitive performance with advancing age, which is not, as a rule, pathological in nature. LTC is considered to be an intermediate state between normal cognitive performance and a pathological process that may develop into dementia.

Does MCI presage dementia?

Mnesic MCI (memory impairment) is considered a precursor to Alzheimer’s disease. The prevalence of memory impairment is 2-30% in the population over 65. According to published studies, people with MCI are three times more likely to develop Alzheimer’s disease. However, other studies looking at the evolution of MCI over a 3-year period have shown that 10-40% of those affected improve and return to normal. Age appears to be the main factor in the progression to dementia. TCL does not appear to be a pre-dementia state in people under 50.

What are the risk factors for dementia?

  • Age is the main risk factor for dementia due to Alzheimer’s disease. The annual incidence of this disease increases from 0.5% before the age of 70 to 8.5% at the age of 85. A dementia process is thus observed in 50% of people over the age of 90.
  • Women appear to be more frequently affected than men.
  • Lifestyle: maintaining physical, intellectual and social activities is associated with a reduced risk of dementia, although the protective mechanism is not yet clear. A high level of education has also been linked to a reduced risk. On the other hand, other factors such as head injuries, depression, exposure to solvents and alcoholism appear to favour the appearance of dementia.

Heredity: a positive family history, especially if the disease occurred early, is a risk factor for Alzheimer’s disease. For direct descendants, there is a 10-30% increase in the risk of developing the disease. Inherited genetic mutations in chromosomes 21 (amyloid precursor peptide), 14 (presenilin1), or 1 (presenilin2), can cause familial Alzheimer’s disease. In non-familial forms, a variant (epsilon 4) of the apolipoprotein E gene is thought to promote the development of Alzheimer’s disease-related brain damage. Carriers of the epsilon 4 form of the gene have rapidly worsening memory problems, generally occurring before the age of 60. – Other risk factors for dementia are identical to those involved in the development of cardiovascular disease. Thus, hypercholesterolemia, hyperhomocysteinemia, atherosclerosis, high blood pressure, and diabetes increase the risk of dementia.

How to recognize and assess LTC? A medical consultation will allow the detection of certain psychological (anxiety, anguish, overwork, depression, insomnia, etc.) and/or medical conditions (in particular a poor nutritional state) likely to influence cognitive abilities and in particular memory. The search for drugs with negative side effects on memory such as tranquilizers, anxiolytics, hypnotics, beta-blockers, and other molecules with an anticholinergic effect is essential.

A neuropsychological interview will specify the nature of the complaint and the use of psychometric tests will be essential to characterize the memory defect and attempt to identify the memory mechanisms involved. A cognitive profile is then drawn up, taking into account the patient’s individuality. Thus, the memory complaint is confronted with possible biological, physio-pathological, and/or social modifications, at the origin of psychic rearrangements likely to affect memory capacities. Anxiety, powerlessness, illness, loneliness, bereavement often lead to a dynamic of loss invading the memory domain.

Biological tests carried out in blood, urine or cerebrospinal fluid are currently of little interest in the diagnosis of memory disorders. Some biological markers (phosphorylated tau protein, beta-amyloid substance) and genetic markers (presenilins) are still in the field of research or cannot be used in practice for ethical reasons (ApoE epsilon4), in the absence of effective medical treatment. On the other hand, certain vitamin and nutritional deficiencies (vitamin B12, folic acid, etc.), biological abnormalities (sodium, calcium, etc.), and the production of certain hormones (thyroid and parathyroid hormones, testosterone, etc.), whose imbalance may affect memory, must be detected.

Brain imaging (brain MRI) can provide information on the organic state of the brain, measure hippocampal atrophy, and eliminate another cause such as a tumor or cerebral vascular lesion. New techniques known as functional neuroimaging are currently being evaluated and will undoubtedly be of great use in the near future. These techniques make it possible, for example, to measure a decrease in cerebral metabolism or to quantify specific lesions (plaques) found in the brains of patients with Alzheimer’s disease. In carriers of the epsilon 4 genetic variant, studies using this technology have shown that their brain metabolism was already reduced 5 to 10 years before the onset of symptoms.

Can cognitive impairment be prevented?

– Lifestyle: In general, physical and mental activity and social interaction help to maintain cognitive function during aging. Constantly maintaining memory through reading, crossword puzzles and intellectual activity appears to prevent the effects of non-pathological aging on cognitive performance.

– Diet: regular consumption of fish and foods rich in omega-3 fatty acids appears to decrease the risk of cognitive decline, while cholesterol and saturated fats increase it. Similarly, a diet rich in fruit and vegetables reduces cardiovascular risk, appears to reduce the risk of dementia, and may even improve cognitive performance in older people.

– Vitamins and food supplements: if we accept the theory that oxidative stress is involved in the onset of neurodegenerative diseases, then logically anti-oxidant vitamins (vitamin A, E, C…) should have a preventive effect. Although some studies have shown that a diet rich in antioxidants can slow the progression of Alzheimer’s disease, its usefulness in preventing dementia remains controversial. Vitamin E supplementation does not appear to influence long-term cognitive performance. Chronic deficiency of group B vitamins (B1, B6, B12) is generally associated with poor cognitive performance and an increased risk of dementia. However, vitamin supplements do not appear to reduce the risk of Alzheimer’s disease. Nevertheless, foods rich in vitamin B9 and B12 (cereals, spinach, shellfish, lentils, etc.), magnesium (cocoa, sunflower, sesame, wheat, almonds, etc.), and zinc (oysters, cheese, red meat, etc.) are recommended Supplements to improve memory are legion.

– Medicines: statins, medicines designed to reduce blood cholesterol levels, are said to have a significant effect in preventing dementia. This product acts directly by reducing the amyloid load that causes the brain lesions found in Alzheimer’s disease and indirectly by reducing vascular cholesterol deposits and the risk of stroke. Chronic use of anti-inflammatory drugs also appears to reduce the risk of dementia. Hormone replacement therapy for menopause, if started early, may delay the onset of age-related cognitive disorders.

In general, it seems that the various interventions proposed are likely to slow down the cognitive decline associated with normal aging but are unable to prevent the onset of a neurodegenerative pathological process.

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