Synaptic Dysfunction without Neurodegeneration

Recent research suggests that brain dysfunction precedes cell death in several neurodegenerative diseases including Alzheimer’s disease. Two hallmarks of Alzheimer’s disease are senile plaques and neurofibrillary tangles. Senile plaques are associated with amyloid beta and neurofibrillary tangles are associated with tau. The new paper “Tau Mislocalization to Dendritic Spines Mediates Synaptic Dysfunction Independently of Neurodegeneration” (published December 22, 2010 in Neuron) investigates how tau may diminish brain function before neurodegeneration becomes evident. More specifically, the research team “investigated how tau induces early memory deficits and disrupts synaptic plasticity, prior to overt synaptic or neuronal degeneration.”

The team showed that abnormally phosphorylated (hyperphosphorylated) tau accumulates in dendritic spines. This accumulation disrupts the targeting or anchoring of glutamate receptors (AMPA and NMDA receptors) in the postsynaptic dendritic spine membrane. The significantly decreased number of postsynaptic glutamate receptors results in disrupted long term potentiation (LTP) which probably underlies the loss of synapses and deterioration of memory in patients with a neurodegenerative disease resulting from the pathological aggregation of tau protein (tauopathy).

Other related blog posts:

Alzheimer’s Disease and the New Age-Based Hypothesis

Decreased Clearance of Amyloid Beta from the Central Nervous System in Alzheimer’s Disease

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  1. Pingback: Reversing Learning and Memory Deficits in Alzheimer’s Disease | Dr. Donald Doherty's Blog

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