Alzheimer's is not just "senile forgetfulness," but a progressive neurodegenerative disease in which neurons gradually deteriorate, especially in areas of the brain responsible for memory, thinking, and behavior. Even in the early stages, a person may lose the ability to remember new information, confuse dates, forget familiar routes, or even the name of a close person. Over time, this leads to complete dependence on others: the patient stops recognizing relatives, loses self-care skills, and becomes vulnerable to infections and other complications. It is important to understand that Alzheimer's is not a norm of aging, but a disease that requires attention, timely diagnosis, and a comprehensive approach to support.
Classification of the disease according to ICD-11
In the International Classification of Diseases 11th Revision (ICD-11), Alzheimer's disease is coded as **6A04** — "Alzheimer's disease." It belongs to the category "Neurodegenerative disorders," subgroup "Diseases associated with amyloid deposits." Importantly, ICD-11 makes a clear distinction between:
— **6A04.0** — Alzheimer's disease with a pronounced amyloid pattern (i.e., with confirmed beta-amyloid plaques);
— **6A04.1** — Alzheimer's disease without a confirmed amyloid pattern (clinical diagnosis in the absence of biomarkers);
— **6A04.Y** — Other forms of Alzheimer's disease;
— **6A04.Z** — Unspecified form.
This division is fundamental: it allows the doctor not just to state "dementia," but to determine its pathogenetic basis — which directly influences the choice of observation tactics, prevention, and potential therapy. For example, if a patient has beta-amyloid deposits in the cerebrospinal fluid or on PET scans, it refers to the typical form of Alzheimer's disease, whereas in the absence of such markers, other causes of cognitive decline must be excluded — for example, vascular dementia or leukoaraiosis.
History of the disease and interesting historical facts
The clinical picture was first described by German psychiatrist Alois Alzheimer in 1906 — which is why the disease bears his name. He observed a 51-year-old patient named Auguste D., who developed rapid cognitive decline, hallucinations, aggression, and complete loss of orientation. After her death, Alzheimer performed an autopsy and discovered two characteristic signs in the cerebral cortex: **neurofibrillary tangles** and **amyloid plaques** — now considered pathognomonic for the disease.
Interestingly, until the 1970s, Alzheimer's disease was considered a rarity, primarily affecting younger people ("premature dementia"). Only after the demographic transition began in the USA and Europe — an increase in life expectancy — did it become clear: this is the most common cause of dementia in the elderly. In 1984, scientists isolated the beta-amyloid protein from plaques — a key moment that allowed the development of biomarkers and targeted drugs to begin.
Another curious fact: in the 1980s, it was noted in Japan that residents of Okinawa, where there is traditionally a high consumption of fish, greens, and soy, have a lower frequency of dementia than the national average. This became one of the first epidemiological hints at the role of diet and lifestyle in the prevention of neurodegenerative diseases — an idea that today underpins the concept of "brain health."
Epidemiology: how many people suffer from Alzheimer's disease?
According to WHO (2023), about **55 million people** worldwide live with dementia, and approximately **60–70%** of cases are specifically due to Alzheimer's disease. A new case is diagnosed every 3 seconds worldwide. In Russia, according to a study by the Institute of Neurology of the Russian Academy of Sciences (2022), dementia occurs in **7–9%** of people over 65 and in **25–30%** of those over 85. The actual number may be higher due to insufficient diagnosis in regions and stigma.
Here’s how the risk changes with age:
| Age | Risk of developing Alzheimer's disease |
|———|————————————|
| 65–69 years | ~2% |
| 70–74 years | ~5% |
| 75–79 years | ~10% |
| 80–84 years | ~18% |
| 85+ years | ~30–50% |
Note: this does not mean that aging = Alzheimer’s. Age is simply the strongest independent risk factor. However, there are other patterns: women suffer more often than men — likely due to longer life expectancy and the impact of menopause on cholesterol and estrogen metabolism in the brain. Also at risk are people with low levels of education: every additional 2 years of schooling reduces the risk of dementia by 11 % (according to the Lancet Commission, 2020).
Genetic predisposition: which genes "trigger" the disease?
Genetics plays a dual role: in some cases, it is a direct cause, while in others, it only increases susceptibility to external factors. Two forms are distinguished:
1. **Early (hereditary) form** — accounts for less than 1 % of all cases, manifests before the age of 65. It is caused by mutations in three genes:
— **APP** (amyloid precursor protein) — chromosome 21;
— **PSEN1** (presenilin-1) — chromosome 14;
— **PSEN2** (presenilin-2) — chromosome 1.
If you have one of these mutations, the risk of developing the disease is almost 100 %. However, such cases are extremely rare and usually observed in families with multiple generations of affected individuals.
2. **Late (sporadic) form** — 99 % of cases. Here, the key role is played by the gene **APOE**, especially its allele **ε4**. In people with one copy of APOE ε4, the risk increases by 3–4 times, and with two copies — by 8–12 times. However, the presence of ε4 does not mean that the disease will necessarily occur: about 25 % of healthy elderly individuals have this allele but do not have the disease. Conversely, many patients with Alzheimer’s do not have ε4. Therefore, APOE is not a diagnostic marker but rather a "genetic risk modifier."
Important: genetic testing for APOE is recommended only within the framework of scientific research or when there is a clear family history. Self-testing through commercial services can cause unnecessary stress without the possibility of changing the situation.
Risk factors: what can be controlled and what cannot
Uncontrollable factors:
— Age (main),
— Gender (female),
— Genetics (APOE ε4, APP/PSEN mutations),
— Family history,
— Low education level.
Controllable — and there is room for prevention here:
— **Vascular disorders**: hypertension, type 2 diabetes, dyslipidemia. They accelerate neurodegeneration through ischemia and oxidative stress. For example, patients with BP >160/100 mm Hg have a 60% higher risk of dementia.
— **Smoking and alcohol abuse**: nicotine worsens microcirculation in the brain, ethanol leads to hippocampal atrophy.
— **Chronic inflammation**: high levels of C-reactive protein, IL-6, fibrinogen correlate with accelerated cognitive decline.
— **Lack of physical activity**: a sedentary lifestyle reduces neurogenesis and blood flow in the hippocampus.
— **Depression and social isolation**: not just a consequence, but an independent risk factor. People with severe depression in adulthood have an 80% higher risk of Alzheimer's.
— **Poor nutrition**: a deficiency of omega-3, B vitamins, D, E, antioxidants creates "metabolic vulnerability" of the brain.
If your goal is prevention, start with controlling blood pressure and glucose levels. This is more beneficial than any supplement.
Diagnosis: how to distinguish Alzheimer's from other forms of dementia?
The diagnosis is made comprehensively — no single symptom is sufficient on its own. Here are the main stages:
**Clinical signs**:
— Progressive amnesia (especially episodic — forgetting recent events),
— Deficit in executive functions (planning, shifting attention),
— Aphasia (difficulty in word finding),
— Apraxia (inability to perform familiar actions),
— Agnosia (failure to recognize objects or faces).
**Laboratory studies**:
— Complete blood count, biochemistry (glucose, TSH, vitamin B12, folic acid) — to exclude reversible causes (hypothyroidism, B12 deficiency),
— CSF biomarkers (in cerebrospinal fluid):
• ↓ Aβ42 (amyloid-beta 42),
• ↑ p-tau (phosphorylated tau protein),
• ↑ t-tau (total tau).
These three markers provide sensitivity up to 90 % with a confirmed diagnosis.
**Radiological methods**:
— **MRI of the brain**: hippocampal atrophy (volume <5.5 ml in men, <4.5 ml in women), enlargement of the lateral ventricles.
— **PET with ligands to amyloid** (for example, florbetapir): visualization of plaques in the cortex.
— **PET with fluorodeoxyglucose (FDG)**: hypometabolism in the parietal and temporal regions.
**Differential diagnosis** — a mandatory step. Often confused with:
— Vascular dementia (acute cerebrovascular accidents, "stepwise" deterioration),
— Dementia with Lewy bodies (fluctuations in consciousness, hallucinations, parkinsonism),
— Frontotemporal dementia (early personality changes, apathy, not memory),
— Depressive pseudodementia (improvement with antidepressant treatment).
If you notice regular memory lapses in a loved one — do not attribute it to "age." Consult a neurologist or gerontopsychiatrist for screening.
Treatment: what really helps today?
As of today, **there is no medication that stops or reverses Alzheimer's disease**. All available methods aim to slow down progression and improve quality of life. Treatment is divided into three blocks:
**1. Pharmacotherapy**
Based on two mechanisms:
— Acetylcholinesterase inhibitors (donepezil, rivastigmine, galantamine) — increase the level of acetylcholine, a neurotransmitter whose deficiency is associated with cognitive decline.
— Memantine — an NMDA receptor antagonist, protects neurons from the excitotoxicity of glutamate.
Effect — moderate: improvement in cognitive tests by 2–4 points on the MMSE scale over 6–12 months. But importantly: the drugs work only when the brain structure is preserved — in the late stages, the effect is minimal.
**2. Non-drug support**
This is not an "auxiliary" part — it is the foundation of therapy:
— Cognitive stimulation (puzzles, reading, learning something new),
— Physical activity (walking 30 minutes a day reduces the rate of hippocampal atrophy by 2 % per year),
— Social interaction (group activities, volunteering),
— Sleep correction (sleep disorders accelerate the accumulation of beta-amyloid),
— Management of behavioral symptoms through the environment (for example, using labels on doors, light indicators).
**3. Experimental approaches**
Since 2021, two drugs aimed at amyloid have been approved:
— Aducanumab (Aduhelm®) — a monoclonal antibody against amyloid. Approved by the FDA, but not in the EU and RF due to weak evidence and the risk of ARIA (amyloid-related imaging abnormalities).
— Lecanemab (Leqembi®) — a more effective antibody, showed a slowdown in cognitive decline by 27 % over 18 months. Not yet registered in the RF, but used in clinical trials.
Important: these drugs are prescribed only with a confirmed amyloid pattern and at an early stage — they are ineffective and dangerous at already pronounced atrophy.
List of drugs used in Alzheimer's disease
Here is the current list of medications approved for use in the Russian Federation (according to the State Register of Medicines, 2025):
| Drug | Group | Dosage | Features |
|———-|———|————|————-|
| **Donepezil** (Aricept, Donepezil-Teva) | AChE inhibitor | 5–10 mg/day | First choice for mild and moderate forms. Start with 5 mg, increase to 10 mg after 4–6 weeks. |
| **Rivastigmine** (Exelon) | AChE inhibitor | 3–12 mg/day (oral) or patch 4.6–9.5 mg/day | Well tolerated in gastrointestinal disorders. The patch reduces side effects. |
| **Galantamine** (Reminyl) | AChE inhibitor + nicotinic receptor modulator | 8–24 mg/day | May improve attention better than others. Requires taking with food. |
| **Memantine** (Akamin, Memantine-SZ) | NMDA antagonist | 5–20 mg/day | Prescribed for moderate and severe forms. Often combined with donepezil. |
| **Cerebrolysin** | Peptide neuroprotector | 5–30 ml/day (iv or im) | Has no proven efficacy in large RCTs, but is used in the Russian Federation for clinical reasons. |
| **Piracetam** | Nootropic | 2.4–4.8 g/day | Efficacy not confirmed in Cochrane meta-analyses. Used rarely, mainly in combination. |
Note: all medications require monitoring of liver and kidney function. Donepezil and rivastigmine may cause nausea, bradycardia, seizures in predisposed individuals. Memantine — less frequently, but dizziness and drowsiness are possible.
Disease monitoring: how to track progress and adjust therapy.
Control must be regular and standardized. Recommended timelines:
— **Every 3 months** — assessment using scales: MMSE (mini-mental status), ADL (activities of daily living), NPI (neuropsychiatric inventory for behavioral symptoms).
— **Every 6–12 months** — repeat MRI to assess hippocampal atrophy and lateral ventricle volume.
— **In case of deterioration** — therapy review: it may be necessary to increase the dose of memantine or add non-pharmacological interventions.
The prognosis depends on the age of onset and the rate of progression:
— If onset is before 65 years — average life expectancy after diagnosis: 8–10 years;
— If onset is after 80 years — 3–5 years.
Complications that often lead to fatal outcomes:
— Pneumonia (due to aspiration),
— Pressure sores and sepsis,
— Injuries (falls due to coordination disorders),
— Dehydration and exhaustion.
Early detection and comprehensive support can extend independent living by 2–3 years — and this is a huge gain for the patient and family.
Age-related features: how the disease manifests in different groups
**Young patients (up to 65 years)** — rare (<1 %). Most often — hereditary form. Symptoms may begin with speech disorders (logopedic form), visual perception issues (posterior cortical atrophy), or executive function problems (frontal form). Progression is faster than in the elderly. Diagnosis is complicated — doctors often think of depression or stress.
**Elderly (65–80 years)** — classic picture: amnesia, disorientation, apathy. Often combined with vascular changes (“mixed dementia”). Respond better to AChE inhibitors.
**Old age (80+)** — often a “quiet” course: first — apathy and slowing down, then — loss of self-care skills. Often masked as “natural aging.” In this group, fall and infection prevention is especially important.
An interesting nuance: in people over 90 years old, Alzheimer's disease may progress “more gently” — likely due to the selection of survivors with more resilient brains (the “survivor effect”). But this does not mean that symptoms can be ignored — the approach to therapy should simply be gentle.
Questions and answers: the most common inquiries from patients and their families
Question 1: Can Alzheimer's disease be prevented with vitamins?
Answer: Vitamins themselves do not prevent disease, but a deficiency of some of them accelerates its development. Especially critical are:
— Vitamin B12 and folic acid — their deficiency causes hyperhomocysteinemia, which damages the brain's blood vessels.
— Vitamin D — a level below 20 ng/ml correlates with a 2-fold risk of dementia.
— Vitamin E (alpha-tocopherol) — at a dose of 2000 IU/day in one large study (DATATOP) slowed progression by 6 months, but did not improve survival and increased the risk of cardiovascular events. Therefore, it is not recommended as monotherapy now.
The best strategy is a balanced diet (Mediterranean diet), rather than taking individual vitamins "just in case."
Question 2: Is fish oil and omega-3 suitable for Alzheimer's?
Answer: Yes, but with caveats. DHA (docosahexaenoic acid) is the main component of neuron membranes. In people with mild cognitive impairment (MCI), taking 1–2 g of DHA per day may slow memory decline. However, in already diagnosed Alzheimer's, the effect is minimal — because the neurons are already damaged. The key point: it should be taken **early**, before significant atrophy. And preferably — from food: salmon, sardines, flaxseed oil.
Question 3: What products are really beneficial for the brain?
Answer: Based on data from the FINGER and MIND studies, the most proven are:
— Green leafy vegetables (spinach, kale) — 1–2 servings a day reduce the rate of cognitive decline by 40%.
— Berries (blueberries, raspberries) — anthocyanins protect against oxidative stress;
— Nuts and seeds (especially walnuts, pumpkin seeds) — a source of vitamin E and magnesium;
— Extra virgin olive oil — polyphenols reduce inflammation;
— Dark chocolate (>70% cocoa) — flavonoids improve blood flow in the brain.
The rule is simple: the more diverse the diet, the higher the "cognitive reserve."
Question 4: Is it necessary to have an MRI if a relative is diagnosed with Alzheimer's?
Answer: Not necessarily — if you have no symptoms. But if you notice regular memory lapses, difficulties with planning or orientation — yes, an MRI will help rule out a tumor, hydrocephalus, or stroke. It is also worth getting tested for APOE only in the context of a genetic counselor consultation — the result alone does not provide a clear prognosis.
Question 5: Can Alzheimer's be treated at home without a doctor?
Answer: No. Self-medication is dangerous. For example, taking high doses of vitamin B6 without supervision can cause polyneuropathy. And some "nootropics" can increase anxiety or aggression in patients with dementia. A doctor is always needed — they will select a safe regimen, consider comorbidities, and prescribe adequate monitoring.
Typical mistakes to avoid
1. **"I just forget — it's age"**
→ Error: ignoring the first symptoms.
→ What to do: undergo screening — MMSE or MoCA (Montreal Cognitive Assessment). Both tests can be done for free at the clinic.
2. **Taking "vitamin cocktails" without analysis**
→ Error: combining B6 + B12 + folic acid without checking homocysteine levels can be useless or harmful.
→ What to do: get tested for B12, folate, homocysteine, 25-OH vitamin D — and only then make adjustments.
3. **Fascination with "miracle supplements" from the internet**
→ Error: taking ginkgo biloba, piracetam, or "neuroprotectors" without evidence.
→ What to do: trust only medications included in the clinical guidelines of the Ministry of Health of the Russian Federation or the European Dementia Society (EFNS).
4. **Complete exclusion of the patient from life**
→ Error: "He doesn't understand anything — why lead him?"
→ What to do: even at a late stage, a person feels emotions, music, touches. Engage in simple rituals — shared meals, walks, listening to childhood songs.
5. **Start treatment only when "everything is bad"**
→ Error: waiting until a person no longer recognizes relatives.
→ What to do: at the first signs — consult a neurologist. Early intervention gives the maximum effect.
The result: what works and what is just an illusion
Alzheimer's disease is not a sentence, but a challenge that requires a systematic approach. Today we cannot cure it, but we can:
— Slow down progress by 1–3 years with donepezil + memantine,
— Maintain quality of life through physical activity, social engagement, and proper nutrition,
— Prevent development in 40 % people through control of vascular factors and cognitive stimulation.
Vitamins are not medicine, but their deficiency exacerbates the situation. The best "supplement" for the brain is not a capsule, but daily walking, talking with your grandson, reading a book, and the confidence that you are not alone. If you are reading these lines, you are already taking a step in the right direction. Don't wait until it is "too late." Start today: make an appointment with a neurologist, check your blood pressure, add spinach and walnuts to your diet. The brain appreciates care—even if it temporarily forgets how to receive it.
