Alzheimer’s disease is a neurodegenerative brain disorder that leads to progressive loss of cognitive functions, including memory and fact association, and the ability to function in everyday life. It is the most common cause of dementia in the elderly, and its symptoms usually appear after the age of 65, although in rare cases it can occur earlier.

The basis of the pathophysiology of Alzheimer’s disease is the accumulation of abnormal proteins in the brain – beta-amyloid and tau protein. Beta-amyloid forms deposits in the spaces between neurons, which disrupts their communication. In turn, abnormal forms of tau protein lead to the formation of neurofibrillary tangles inside neurons, which contributes to neuron dysfunction and their death. Both of these changes result in the loss of synapses and brain mass. This leads to a gradual loss of brain function.

Early symptoms of the disease include problems with short-term memory, difficulties in performing daily activities, and general disorientation. As the disease progresses, more serious disorders appear, such as speech difficulties, orientation in time and space, and personality changes. In the late stages, patients often become completely dependent on others for care.

There is currently no effective drug that can cure Alzheimer’s disease, but available pharmacological therapies can slow the progression of symptoms, especially in the early stages. These drugs, such as cholinesterase inhibitors (donepezil, rivastigmine) or NMDA receptor antagonists (memantine), aim to improve neuronal transmission.

Alzheimer’s disease research is still ongoing, with the aim of understanding the mechanisms of the disease and developing new therapies that could stop or reverse the process of neurodegeneration. In recent years, special attention has been paid to immune therapies and methods of clearing the brain of pathological proteins.