Blass JP.
Weill Cornell Medical College, White Plains, NY, USA.
Ann N Y Acad Sci 2008;1147:122–8.
[2] Brain glucose hypometabolism and oxidative stress in preclinical Alzheimer’s disease.
Mosconi L, Pupi A, De Leon MJ.
New York University School of Medicine, New York, NY, USA.
Ann N Y Acad Sci 2008;1147:180–95.
Editor’s note: The causes of Alzheimer’s disease (AD) remain uncertain. The disappointing observation that removing brainamyloid through immunological methods did not slow the progression of clinical disability argues strongly against the older theory that amyloid has a “seminal” role in the clinical illness. The cerebral metabolic rate is a neurobiological measure that appears to correlate with the progression of clinical disability; both of these articles summarize and review the current data on the close relationship between the impairment of brain glucose oxidation and the clinical symptoms of AD.