Abstract: AD is a serious neurological disorder worldwide that affects about 26 million people, and whose prevalence has been calculated to quadruple by 2050, thus reaching over 1% of the total population, with the highest prevalence occurring in both adults and elderly (Pluta et al., 2018). Neurodegenerative processes of the sporadic form of AD probably start 20 years before the clinical onset of the disorder (Pluta et al., 2018). This disease is the most important cause of dementia in world aged society (~75%). AD is a disorder that affects not only patients but also their caregivers. The social and economic burden associated with AD was calculated as an example in the United States alone; 600 billion dollars annually is spent on caring for AD patients (Pluta et al., 2018). AD is the one of the great health-care challenges of the 21st century. The incidence of AD, a chronic and progressive neurodegenerative disorder, is increasing, as well as the need for efficient methods of diagnosis, prevention and treatment (Pluta et al., 2018). The characteristic clinical and neuropathological hallmarks of AD are: dementia as the main clinical symptom and in post-mortem neuropathological examination, the presence of amyloid plaques as well as neurofibrillary tangles and loss of neurons in the brain of AD patients. The role of amyloid and tau protein is questioned in the etiology of AD and other causes such as ischemic etiology are being considered (Pluta and Ułamek-Kozioł, 2019). There are several treatments that are not causal but symptomatic that are not effective, especially for advanced disease. To date, only a few drugs are approved, such as acetylcholinesterase inhibitors and memantine. Drugs that regulate partly the activity of neurotransmitters and partly alleviate behavioral symptoms. Other treatment options include active and passive immunization, anti-aggregation specifics, and secretase inhibitors. The road to clarity AD etiology, early final ante mortem diagnosis and treatment has been one fraught with a wide range of complications and numerous revisions with a lack of a final solution. Research has recently been launched to identify new mechanisms underlying AD that could be the target of new prevention strategies (Pluta and Ułamek-Kozioł, 2019). Therefore, other treatment options can be recommended, and the ketogenic diet seems to be an interesting last resort solution at the moment (Rusek et al., 2019). The diet contains large amounts of fat and low carbohydrates with vitamin supplementation. New scientific articles suggest that a low-carbohydrate and high-fat ketogenic diet may help alleviate the brain damage in AD (Ota et al., 2019; Rusek et al., 2019). A ketogenic diet can alleviate the effects of impaired glucose metabolism in AD by providing ketones as an additional source of energy. Here, based on new data, we have presented that a ketogenic diet can be effective in preventing and treating AD, but both ketone bodies production and carbohydrate reduction are needed to achieve this.