Amyloid-β Associated Cortical Thinning in Clinically Normal Elderly
2010

Amyloid-β and Brain Thinning in Healthy Older Adults

Sample size: 119 publication Evidence: moderate

Author Information

Author(s): Becker J Alex PhD, Hedden Trey PhD, Carmasin Jeremy BA, Maye Jacqueline BS, Rentz Dorene M PsyD, Putcha Deepti BA, Fischl Bruce PhD, Greve Douglas N PhD, Marshall Gad A MD, Salloway Stephen MD, Marks Donald MD, Buckner Randy L PhD, Sperling Reisa A MD, Johnson Keith A MD

Primary Institution: Massachusetts General Hospital, Harvard Medical School

Hypothesis

Aβ deposition would be associated with local cortical thickness reductions in regions associated with the default network at early stages of the pathophysiological process, prior to cognitive impairment.

Conclusion

Aβ deposition is associated with a pattern of cortical thickness reduction consistent with Alzheimer's disease prior to the development of cognitive impairment.

Supporting Evidence

  • PiB retention in CN subjects was age-related and associated with cortical thickness reductions.
  • Significant Aβ-associated cortical thickness reductions were observed in the posterior cingulate and precuneus.
  • Thickness decreases in CN+ relative to CN− ranged up to 0.19mm.
  • Aβ deposition in normal individuals may represent preclinical Alzheimer's disease.
  • Longitudinal follow-up is ongoing to determine if Aβ burden and volumetric loss predict cognitive decline.

Takeaway

This study found that older adults without dementia who have amyloid-β in their brains also show signs of brain thinning, which is similar to what happens in Alzheimer's disease.

Methodology

119 older individuals underwent PiB PET and high-resolution structural MRI, with regression models used to relate PiB retention to cortical thickness and hippocampal volume.

Potential Biases

Potential biases may arise from the selection of participants from memory clinics and the exclusion of those with notable medical or neurological illnesses.

Limitations

The study's findings are based on cross-sectional data, and longitudinal data will be required to evaluate the strength and timing of the link between Aβ deposition and neurodegeneration.

Participant Demographics

87 clinically normal older individuals and 32 patients with mild Alzheimer's disease, with a mean age not specified.

Statistical Information

P-Value

p < 1 × 10−5

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1002/ana.22333

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