New Hope for Alzheimer’s Treatment: Restoring Energy Production in Brain Cells

New Hope for Alzheimer’s Treatment: Restoring Energy Production in Brain Cells

Researchers from the Scripps Research Institute have made a breakthrough in understanding the energetic reactions within brain cells that contribute to neurodegeneration in Alzheimer’s disease. By targeting the malfunctioning mitochondria, which are responsible for energy production in cells, they were able to restore many neuron-to-neuron connections in nerve cell models derived from patients with Alzheimer’s. This discovery suggests that improving mitochondrial metabolism could be a promising therapeutic approach for Alzheimer’s and related disorders.

The team identified a dysfunction in the enzymes that produce energy due to an abnormal chemical reaction called S-nitrosylation. This reaction, characterized by the attachment of nitrogen and oxygen atoms to a sulfur atom, forms a dysfunctional “SNO” enzyme. Using brain tissue samples from individuals with and without Alzheimer’s disease, as well as nerve cells derived from patient stem cells, the researchers observed unique deficits in the energy production of Alzheimer’s neurons compared to healthy cells.

Further investigation revealed a disruption in the Krebs cycle, a cellular process in mitochondria that generates ATP, the body’s main source of molecular energy. The researchers identified a bottleneck in the production of succinate, a key molecule in the Krebs cycle that drives ATP production. By supplying the missing succinate molecules using an analog that could penetrate nerve cell membranes, the researchers successfully restored up to 75% of the lost synapses and prevented further decline.

While this study provides proof-of-concept that the Krebs cycle can be re-energized, the researchers acknowledge the need for a more effective compound to develop a drug for human use. Their goal is to develop an energy-preserving drug that can restore neuronal connectivity in Alzheimer’s patients, halting disease progression and enhancing cognitive function.

The findings offer new hope for Alzheimer’s treatment by targeting the underlying energy deficits that contribute to the loss of neuron-to-neuron connections. With further research and development, this novel therapeutic approach could potentially revolutionize the treatment of Alzheimer’s and related neurodegenerative disorders.

FAQ

1. What did the researchers at the Scripps Research Institute discover?
The researchers discovered that targeting malfunctioning mitochondria, which are responsible for energy production in cells, can restore neuron-to-neuron connections in nerve cell models derived from patients with Alzheimer’s disease.

2. What is the significance of this discovery?
This discovery suggests that improving mitochondrial metabolism could be a promising therapeutic approach for Alzheimer’s and related disorders.

3. What specific dysfunction did the researchers identify in the enzymes that produce energy?
The researchers identified a dysfunction called S-nitrosylation, which is characterized by the attachment of nitrogen and oxygen atoms to a sulfur atom and leads to the formation of a dysfunctional “SNO” enzyme.

4. How did the researchers observe deficits in energy production in Alzheimer’s neurons?
The researchers used brain tissue samples from individuals with and without Alzheimer’s disease, as well as nerve cells derived from patient stem cells, to observe unique deficits in energy production in Alzheimer’s neurons compared to healthy cells.

5. What cellular process in mitochondria did the researchers discover a disruption in?
The researchers discovered a disruption in the Krebs cycle, a cellular process in mitochondria that generates ATP, the body’s main source of molecular energy.

6. What molecule in the Krebs cycle was identified as a bottleneck for ATP production?
The researchers identified succinate as a key molecule in the Krebs cycle that drives ATP production and found a bottleneck in its production.

7. How did the researchers restore lost synapses in the nerve cell models?
By supplying missing succinate molecules using an analog that could penetrate nerve cell membranes, the researchers successfully restored up to 75% of the lost synapses and prevented further decline.

8. What is the researchers’ ultimate goal?
The researchers’ goal is to develop an energy-preserving drug that can restore neuronal connectivity in Alzheimer’s patients, halting disease progression and enhancing cognitive function.

Definitions

– Mitochondria: Organelles responsible for energy production in cells.
– Neurodegeneration: The progressive loss of structure or function of neurons, often leading to diseases such as Alzheimer’s.
– S-nitrosylation: A chemical reaction characterized by the attachment of nitrogen and oxygen atoms to a sulfur atom, resulting in the formation of a dysfunctional enzyme.
– ATP: Adenosine triphosphate, the main source of molecular energy in the body.
– Krebs cycle: A cellular process in mitochondria that generates ATP.
– Synapses: Junctions between nerve cells that allow for communication and transmission of signals.
– Analog: A compound that is similar in structure or function to another compound.

Suggested Related Links
Scripps Research Institute
Alzheimer’s Association

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