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This study shows that tau accumulation in Alzheimer's disease drives synaptic loss over two years, correlating with cognitive decline. This finding suggests a potential therapeutic window for tau-targeting treatments.

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Area of Science:

  • Neuroscience
  • Neuropathology
  • Radiology

Background:

  • Synaptic loss is a key Alzheimer's disease (AD) hallmark linked to cognitive decline.
  • While tau pathology is suspected to cause synaptic loss, in vivo experimental evidence is lacking.

Purpose of the Study:

  • To experimentally verify in vivo if tau accumulation drives synaptic loss in Alzheimer's disease.
  • To investigate the longitudinal relationship between tau progression, synaptic density changes, and cognitive function in MCI patients.

Main Methods:

  • A 2-year longitudinal study involving 12 amnestic mild cognitive impairment (MCI) patients.
  • Dual tracer positron emission tomography-magnetic resonance imaging (PET-MR) using 18F-MK-6240 for tau and 11C-UCB-J for synaptic vesicle protein 2A (SV2A) as a synaptic density proxy.

Main Results:

  • Tau accumulation was observed in the neocortex at baseline, progressing to Braak V/VI stages at follow-up.
  • Synaptic loss, initially limited to limbic regions, spread to tau-affected areas (Braak stages IV/V) over two years.
  • Changes in synaptic density significantly correlated with changes in cognitive function.

Conclusions:

  • This study provides the first in vivo evidence that regional synaptic loss follows tau accumulation over time in Alzheimer's disease.
  • The findings suggest that tau spread is a potential driver of synaptic vulnerability.
  • A disease-modifying window of opportunity may exist for combined tau-targeting therapies.