Decoding Synaptic Imbalance In Neurodegenerative Diseases: From Pathological Analysis To Targeted Intervention
Our brains rely on tiny connections called synapses to transmit, integrate, and store information. These crucial communication points are essential for everything we think, feel, and do. However, in conditions like Alzheimer’s, Parkinson’s, Huntington’s disease, and ALS, these vital connections begin to falter and break down early in the disease process.
This damage to synapses, known as synaptic dysfunction, often occurs even before brain cells themselves start to die or before individuals experience clear symptoms. The specific areas of the brain where this synaptic damage occurs and how severe it is can significantly influence how a disease progresses.
Researchers have identified that this synaptic trouble is closely tied to abnormal proteins specific to each neurodegenerative disorder. Furthermore, several key processes contribute to this synaptic breakdown. These include the harmful effects of these abnormal proteins, problems with how synaptic proteins are maintained, an overstimulation of brain cells (excitotoxicity) coupled with an imbalance in calcium levels, damaging oxidative stress and inflammation, and a lack of essential growth factors that support nerve cells.
By understanding these underlying mechanisms, scientists aim to develop new treatments that can specifically target and intervene in these early stages of synaptic damage, potentially slowing or even preventing the progression of these devastating diseases.
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