Alzheimer’s disease is the most common form of dementia, affecting over 44 million people worldwide. Inside the brain, Alzheimer’s disease is characterized by loss of neurons, and presence of abnormal tangles and plaques in the brain. Now, researchers from the University of Toronto have found that molecules that are strongly associated with Alzheimer’s disease are important players in a process called long-term depression (LTD).
The team state that long-term depression is a process through which the strength of synapses, the connections between neurons, is selectively reduced. The current study suggests improperly regulated long-term depression could cause the degeneration of the connections between neurons that is a core feature of Alzheimer’s and other neurodegenerative diseases. The results of the study were presented at the 9th Annual Canadian Neuroscience Meeting.
The results showed that tau has a key physiological role in the process of long-term depression. Tau aggregates to form the hall-mark tangles of Alzheimer’s disease and serves as the best marker of disease progression. The finding that tau has a normal function at synapses adds considerable weight to the argument that Alzheimer’s disease is triggered by a mis-regulation of a normal synaptic mechanism. The researchers state that they have also recently identified a novel and very rapid synaptic action of Abeta, a protein fragment that forms the senile plaques and is strongly implicated in the aetiology of Alzheimer’s disease.
Previous studies show that learning and memory involve modifications in the distribution and strength of synapses, which are the points of connection between neurons. The two most studied forms of such modification are long-term potentiation, which is a strengthening of a synapse, by an increase in the transmission of signals through a synapse, and long-term depression, which is a weakening of the synapse. These modifications, also called synaptic plasticity, are a major process used for information storage in the brain and spinal cord.
Over the past decade, researchers have realized that aberrant synaptic plasticity may lie at the heart of many brain disorders. The current study focuses on a brain region called the hippocampus, which is important for memory storage, to identify the key players in LTD. Once identified, the group state that these will become potential therapeutic targets, as new drugs could be designed specifically to activate or inhibit them.
The team surmise that Alzheimer’s disease is an incurable and chronic disease, and current treatments bring only modest improvements to symptoms, and do not work for all patients. They go on to conclude that a better understanding of the process affected in the brain will lead to identification of new drug targets, and potentially, life-changing preventive therapies or treatments.
Source: University of Toronto
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