# Alzheimer's disease | Symptoms, Causes, Tests and Treatment | OSANG

> Alzheimer's disease is a degenerative disease in which nerve cells gradually disappear as amyloid beta and hyperphosphorylated tau protein accumulate in the brain. It is…

- Official page: https://osns.co.kr/en/encyclopedia/alzheimers-disease
- Organization: OSANG Neurosurgery

## Page content

Dementia/Cognition

## Alzheimer's disease

Alzheimer's Disease · G30

Alzheimer's disease is a degenerative brain disease that begins with a decline in recent memory due to the gradual loss of nerve cells due to abnormal accumulation of amyloid beta and tau proteins, and is the most common cause of overall dementia.

## At a glance

Alzheimer's disease is a degenerative disease in which nerve cells gradually disappear as amyloid beta and hyperphosphorylated tau protein accumulate in the brain. It is the most common, accounting for 60-70% of all dementia causes, and begins with recent memory decline and progresses to language, visuospatial, and executive dysfunction. Diagnosis uses neuropsychological tests and biomarkers such as amyloid PET and cerebrospinal fluid according to NIA-AA standards. In the CLARITY-AD study, the anti-amyloid antibody lecanemab slowed the worsening of Clinical Dementia Scale (CDR-SB) by 27% compared to placebo at 18 months.

- 01Definition and Overview

- 02Causes and Pathophysiology

- 03symptoms

- 04diagnosis

- 05treatment

## Definition and Overview

Alzheimer's disease is a degenerative brain disease in which nerve cells gradually disappear due to abnormal accumulation of amyloid beta and hyperphosphorylated tau protein in the brain. It begins slowly with a decline in recent memory and progresses to impairment in various cognitive areas such as language, visuospatial ability, and executive function, ultimately making independent daily living difficult.

Alzheimer's disease is the most common cause, accounting for 60-70% of all dementia cases. The older people are, the higher the prevalence is, and the number of patients is rapidly increasing along with the aging population. In ICD-10, it is classified as G30.

## Causes and Pathophysiology

The core pathology of Alzheimer's disease is the abnormal accumulation of two proteins.

- Amyloid beta: It deposits outside nerve cells and forms senile plaques. It is known that accumulation begins years to decades before onset.

- Tau protein: Hyperphosphorylated, creates neurofibrillary tangles within nerve cells, breaks down the skeleton of nerve cells, and leads to cell death.

These changes start in the medial temporal lobe (hippocampus), which is responsible for memory, and gradually spread throughout the cerebral cortex. The most important risk factor is old age, and the APOE ε4 genotype increases susceptibility to disease. Vascular risk factors such as high blood pressure, diabetes, obesity, hearing loss, and social isolation are also analyzed as correctable factors that increase the risk.

## symptoms

Symptoms progress in stages.

- Early: Recent memory decline is prominent. They repeat the same questions, forget appointments or where they left things, and cannot recall even when given hints.

- Middle stage: Language difficulties (difficulty finding words), visuospatial difficulties (wandering on familiar paths), and decreased executive function (difficulties with calculations and money management) become evident. It may also be accompanied by behavioral and psychological symptoms such as delusions, depression, and agitation.

- Late stage: Full assistance is required for all aspects of daily life, communication is difficult, and basic functions such as walking and swallowing are impaired.

The speed of progress varies greatly from person to person.

## diagnosis

Diagnosis aims to objectively confirm cognitive decline and identify Alzheimer's pathology, and the NIA-AA (National Institute on Aging-Alzheimer's Association) criteria are widely used.

- History taking: Confirmation of onset time, progression pattern, and accompanying symptoms through guardian

- Neuropsychological test: Evaluation of cognitive areas such as memory, language, visuospatial, and executive function

- Brain imaging: MRI confirms atrophy of the hippocampus and medial temporal lobe, excludes other causes such as vascular lesions

- Biomarker: Direct confirmation of Alzheimer's pathology through amyloid PET and cerebrospinal fluid amyloid beta and tau tests

- Blood test: exclude correctable causes such as thyroid function and vitamin B12

Using biomarkers, it is possible to identify Alzheimer's pathology even in the mild cognitive impairment stage, which helps in early diagnosis and treatment decisions.

## treatment

### medication

Cholinesterase inhibitors (donepezil, rivastigmine, galantamine) relieve cognitive symptoms by inhibiting the breakdown of acetylcholine and are used in mild to moderate stages. In moderate to severe stages, the NMDA receptor antagonist memantine is added. These drugs do not stop the progression of the disease but control the symptoms.

Recently, anti-amyloid antibodies that directly remove amyloid were introduced for the purpose of suppressing the progression of early Alzheimer's disease. In the CLARITY-AD study, lecanemab slowed the worsening of the Clinical Dementia Scale Summated Score (CDR-SB) by 27% compared to placebo at 18 months. However, monitoring of side effects such as amyloid-related imaging abnormalities (cerebral edema and microhemorrhage) is necessary.

### Non-drug treatment

Cognitive stimulation training, regular exercise, social activities, and lifestyle management contribute to maintaining cognitive function. For behavioral and psychological symptoms, environmental adjustments and non-pharmacological approaches are given priority.

### Risk Factor Management

Managing high blood pressure, diabetes, and dyslipidemia, quitting smoking, abstaining from drinking, correcting hearing, and maintaining social activities help lower the risk of developing the disease and slow its progression.

## Frequently asked questions

### Q01What are the earliest symptoms of Alzheimer's disease?

Deterioration of recent memory occurs first, often forgetting recent events and repeating the same questions or words. It differs from simple forgetfulness in that it forgets promises or where things are placed and is unable to recall even when given hints. As the disease progresses, language, navigation, calculation and management skills become impaired.

### Q02Is Alzheimer's disease inherited?

Most are not inherited. Familial Alzheimer's disease caused by a specific genetic mutation accounts for less than 1%, and the remainder is caused by a combination of age, lifestyle, and vascular risk factors. The APOE ε4 gene is a susceptibility factor that increases the risk of developing the disease, but having it does not necessarily mean that you will develop the disease.

### Q03When is an amyloid PET test performed?

When it is unclear whether the cause of memory decline is Alzheimer's disease, it is performed to check for amyloid deposition in the brain. If the test is positive, it supports Alzheimer's pathology, and if it is negative, it serves as a basis for finding other causes. It is also used to select anti-amyloid antibody treatment targets.

### Q04Is Alzheimer's disease curable?

There is currently no cure, and the goal of treatment is to control symptoms and slow progression. Cholinesterase inhibitors and memantine relieve cognitive symptoms, and in early stage patients, antibody treatment to remove amyloid is used to inhibit progression.

### Q05For whom is anti-amyloid antibody such as lecanemab used?

The target patients are patients with mild cognitive impairment or mild Alzheimer's disease in the early stage and confirmed to have amyloid deposition. In the CLARITY-AD study, cognitive and functional deterioration was slowed by 27% at 18 months compared to placebo, but side effects such as cerebral edema and microhemorrhage need to be monitored, so decisions are made after expert evaluation.

### Q06What can I do to lower my risk of Alzheimer's disease?

Management of high blood pressure, diabetes, and dyslipidemia, smoking cessation, abstinence from drinking, regular exercise, hearing correction, social activities, and cognitive stimulation help lower the risk. Although lifestyle modification alone cannot completely prevent the onset, it contributes to delaying the onset and slowing the progression.

## Related articles

- Dementia Overview

- vascular dementia

- Lewy body dementia

- frontotemporal dementia

This article provides general medical information and does not replace an individual diagnosis or treatment plan. Please seek a medical assessment if symptoms persist.

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