Groundbreaking Approaches in the Battle Against Alzheimer’s Disease

Groundbreaking Approaches in the Battle Against Alzheimer’s Disease

Alzheimer’s disease is a degenerative brain disorder that develops in mid-to late adulthood. This results in a progressive and irreversible loss of memory and deterioration of various other cognitive abilities. This disease is caused by the destruction of nerve cells and nerve connections in the cerebral cortex of the brain and a significant loss of brain mass.

The disease was first described in 1906 by the German neuropathology Alois Alzheimer. By the early 21st century it was recognized as the most common form of dementia in the elderly.

                                 Alzheimer disease Stages

There are three stages of Alzheimer’s disease: early stage, mild cognitive impairment (MCI) and Alzheimer’s disease. The two most relevant stages for clinical diagnosis are MCI and dementia. Early-stage recognition recognizes that the Alzheimer’s disease process begins before symptoms appear and anticipates advances in diagnostic testing that may eventually enable diagnosis at a clinical stage.

MCI is often divided into different types, namely amnestic and nonmonastic. One of the first signs of the transition from normal aging to Alzheimer’s disease is forgetfulness. This transitional stage represents amnestic MCI and is characterized by marked impairment in memory with retention of normal cognitive ability in judgment, reasoning, and cognition. In atypical MCI, impairments in cognitive functions related to attention, perception, and language predominate over deficits in memory. However, as MCI progresses to Alzheimer’s disease, memory loss becomes more severe, and language, cognition, and motor skills deteriorate. Mood becomes unstable, and the individual becomes irritable and more sensitive to stress and may be intermittently angry, anxious, or depressed. These changes mark the transition to Alzheimer’s dementia, which in its advanced stages is characterized by unresponsiveness and loss of movement and control of body functions. Death occurs after a disease course of 2 to 20 years.

About 10 percent of those diagnosed with the disease are under 60 years of age. These cases, initially called familial Alzheimer’s disease, appear to be the result of an inherited genetic mutation. Most cases of Alzheimer’s disease, however, develop after age 60 (late-onset) and are usually sporadic—that is, in people with no family history of the disease. Although a genetic factor has been identified that is thought to predispose them to some disease. Rosacea, a chronic inflammatory skin condition, is also linked to an increased risk of Alzheimer’s disease, especially in people aged 60 and older.

               Neuritic plaques and neurofibrillary tangles

The presence of plaques and neurofibrillary tangles in the brain is used to diagnose Alzheimer’s disease at autopsy. Neuronal plaques—also called senile, dendritic, or amyloid plaques—consist of degenerative nerve material surrounded by deposits of a sticky protein called amyloid beta (or beta-amyloid). This protein is derived from a large molecule called amyloid precursor protein, which is a normal component of nerve cells. Neurofibrillary tangles are twisted protein fibers in nerve cells. These fibers are composed of a protein, called tau, which is normally found in neurons. When processed incorrectly, tau molecules clump together and become tangled.

Both neural plaques and neurofibrillary tangles, which are found in small amounts even in the brains of healthy elderly individuals, are thought to somehow interfere with normal cellular function. However, it is not known whether plaques and tangles are the cause or the result of the disease. Animal research shows that amyloid-beta plaques form naturally in the brain in response to infection, acting to trap microorganisms. The idea that amyloid beta acts as a natural antibiotic means that Alzheimer’s disease may be somehow linked to brain infections, plaque formation, or excessive plaque formation in older people. is or is otherwise abnormal in individuals who eventually develop Alzheimer’s disease.

Other features have been noted in the brains of many people with Alzheimer’s disease. One such condition is a deficiency of the neurotransmitter acetylcholine. Neurons containing acetylcholine play an important role in memory.

                                 Treatment of Alzheimer’s disease

There is no cure for Alzheimer’s disease. However, there are many therapeutic agents that can be used to slow disease progression or alleviate symptoms. In about 50 percent of patients, the progression of amnestic MCI can be delayed for up to a year with drugs called acetylcholinesterase inhibitors (or anticholinesterases). These drugs, including galantamine, donepezil and rivastigmine work by slowing the breakdown of acetylcholine. Common side effects of acetylcholinesterase inhibitors include nausea, vomiting, and diarrhea. Alzheimer’s disease symptoms can be reduced in some patients with a drug called memantine, which reduces abnormal brain activity by blocking the binding of glutamate (an excitatory neurotransmitter) to certain receptors in the brain. Although this drug can improve cognition and enable patients to engage more in daily activities, it can make some patients unusually agitated or delusional. Other treatments are aimed at controlling the depression, behavioral problems, and insomnia that often accompany the disease.

                                          Experimental Drugs

There are also several experimental drugs for Alzheimer’s disease in early and late-stage clinical trials. One drug that has shown some success is methylthioninium chloride (Rambar), commonly known as methylene blue (an organic dye), targeting the tau protein of neurofibrillary tangles. In clinical trials, methylthioninium chloride either stopped or significantly slowed the progression of cognitive decline in patients with Alzheimer’s disease. It is the first drug capable of dissolving tau protein fibers and preventing the formation of neurofibrillary tangles.

                                Example of experimental theory

Another example of an experimental therapy is the monoclonal antibody lecanimab, which has the ability to inhibit the formation of amyloid deposits as well as clear them. In clinical trials lecanemab was found to slow disease progression in human patients with early-stage Alzheimer’s disease; The drug was approved by the US Food and Drug Administration in 2023 for the treatment of early-stage Alzheimer’s disease. In animal studies, derivatives of the naturally occurring flavonoid fisetin, particularly found in onions, cucumbers and fruits such as strawberries and apples, have been shown to reverse memory loss in people with Alzheimer’s disease symptoms.