I have been involved in AD related research before, so I know more about it, here is a detailed introduction:From the neuropathology, Alzheimer's disease (AD) is mainly a damage to neurons and synapses in the brain and specific subcortical areas. This damage results in significant atrophy of brain regions, including the temporal and parietal lobes, as well as parts of the prefrontal lobe and cingulate gyrus, and patients with AD have significant amyloid deposits and neurofibrillary tangles in the brain regions, which are thought to be the primary cause of neuronal damage. Because of this significant amyloid deposition and neurofibrillary tangles, AD is thought to be a disease of protein misfolding, caused mainly by the accumulation of abnormally folded A-beta and tau proteins in the brain. There is a membrane protein called amyloidophorin (APP) on the nerve cell membrane, which plays a key role in neuronal growth, survival and post-traumatic repair. In AD patients, lesions cause APP to be broken down by enzymes into small molecular fragments - one of which is beta amyloid, which accumulates and deposits on the outside of the neuron, causing neuronal death. The pathogenesis of AD is still under investigation. There is no evidence that the disease is inherited, but there are a number of genes that may be potentially risky. However, 0.1% of AD patients show familial autosomal inheritance (i.e., gender-neutral), and this type of AD usually develops before the age of 65 years, so it is called early-onset familial Alzheimer's disease. Most cases of early-onset familial AD are associated with mutations in one of three genes: the previously mentioned APP gene (amyloid precursor protein) and presenilins 1 and 2. However, the majority of AD patients do not have autosomal inheritance but are sporadic, so mutations in many genes may contribute to this outcome. For example, the most studied gene is APOE (a serum apolipoprotein). However, this mutation is not necessarily the primary cause of the disease; it may be a superimposed effect of the environment. I know of a study where mice with a specific knockout of a glutamate receptor protein showed symptoms of AD, so abnormalities in the glutamate system may also contribute to AD. The diagnosis of AD is usually based on the patient's medical history, relatives' histories, and clinical observations, etc. CT, MRI, SPECT, or PET can all be used to help diagnose brain lesions and types of dementia. They can also help predict the transition from generalized memory impairment to AD. Some cardiovascular risk factors, such as hypercholesterolemia, high blood pressure, diabetes, and cigarette smoking, are thought to have a potential impact on the development of AD. Certain foods may potentially reduce the incidence of AD, such as fruits, vegetables, bread, wheat, olive oil, fish, and red wine (although I personally feel that this is more a matter of maintaining good health through healthy living and diet rather than targeting the prevention of AD). There is no evidence that vitamins play a significant role in preventing or treating AD. A phenomenon known as "environmental enrichment" may be effective in treating AD: People who engage in regular intellectual activities, such as reading, playing chess, crossword puzzles, playing a musical instrument, or engaging in regular social activities, show a lower risk of AD. So activities that are good for cognitive enhancement clearly have a positive effect on cognitive impairment as well - even learning a second foreign language has been shown to be effective in delaying the onset of AD. Similarly, physical activity is also effective in reducing the risk of AD. Currently there are five approved medications for the treatment of AD (mainly in the US and the EU): four are acetylcholinesterase inhibitors (tacrine, ristigmine, galantamine, and donepezil), and one is an NMDA receptor (a type of glutamate receptor) antagonist (memantine). There is also an NMDA receptor (a type of glutamate receptor) antagonist (Memantine). However, these medications only relieve symptoms and do not slow down the progression of the disease. Psychotropic drugs are also sometimes prescribed to AD patients to relieve behavioral problems. My personal opinion: If you have an elderly family member who is experiencing significant memory loss, you should seek medical attention as soon as possible to check for the risk of AD (there are many behavioral methods of diagnosing dementia that can be found on the Internet, and you should be able to do this yourself). Although there is no effective treatment for AD, it is always better to take measures as soon as possible. It is our filial duty to pay more attention to the elderly at home and to our parents who are over 60 years old, and to pay attention to their health and memory problems. P. I realized that I had written so much without realizing it, and decided to post this paragraph to the "From Neuron to Brain" group for archival purposes. I hope more people will pay attention to Alzheimer's disease and their parents' health.
Thanks for the comment!