Alzheimer's Disease: Synapses Gone Cold
Author Information
Author(s): Koffie Robert M, Hyman Bradley T, Spires-Jones Tara L
Primary Institution: Massachusetts General Hospital, Harvard Medical School
Hypothesis
Alzheimer's disease is primarily a disease of synaptic dysfunction.
Conclusion
Oligomeric amyloid beta is a key player in the induction of synaptic failure in Alzheimer's disease.
Supporting Evidence
- Alzheimer's disease is characterized by synapse loss, which correlates with cognitive decline.
- Oligomeric amyloid beta has been shown to induce synapse loss and cognitive impairment in animal models.
- Recent studies suggest that oligomeric amyloid beta is toxic to synapses and impairs memory formation.
Takeaway
Alzheimer's disease affects how brain cells connect and communicate, leading to memory problems. A specific form of a protein called amyloid beta can harm these connections.
Methodology
The review summarizes recent findings concerning Alzheimer's disease pathogenesis, focusing on the impact of amyloid beta on synapses.
Limitations
The review does not provide original experimental data and relies on existing literature.
Digital Object Identifier (DOI)
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