Those of you interested in advances in imaging for neurodegenerative disorders and the correlations between imaging studies (while a patient is alive) and brain pathology (seen on post-mortem autopsy) will LOVE this news.
The PET is a type of brain scan. Currently, nearly all PET scans employ FDG, which picks up on glucose in the brain. For the last several years, the latest in PET scans for Alzheimer’s or other dementia patients employs PIB, Pittsburgh Compound B. PIB picks up on amyloid plaques. (The dye is retained by the insoluble amyloid protein.) Alzheimer’s disease is a disorder of two proteins — amyloid (which forms plaques) and tau (which forms tangles).
Hopefully, one day, we’ll have PET scans that can detect tau tangles (which would help diagnose PSP and CBD). Also, PSP and CBD can co-occur with Alzheimer’s Disease, so this news may be relevant to some in the PSP/CBD community also. (I’ve forgotten the exact percentage but it’s something like 20-30% of the time.)
The Alzheimer Research Forum has a (mostly-understandable) summary of a recently published article in the December 13th issue of the journal Brain about a woman with Alzheimer’s Disease who “volunteered for the first PET-PIB scan ever performed. She received another PIB scan two years later, and over the course of her disease also got an MRI and three PET scans using fluorodeoxyglucose (FDG), a marker for glucose use and therefore brain metabolism.” The woman died at the age of 61. She donated her brain for autopsy.
“Over the eight years she was studied, the woman’s score on the Mini-Mental State Examination declined from a near-normal score of 27 down to five. The FDG data showed that her brain’s glucose metabolism decreased in parallel with her cognitive powers. By contrast, PIB retention, already high at first examination, showed little change over two years during which her cognition declined steeply. The amount of amyloid deposition seen at autopsy three years later also looked similar to PIB estimates…suggesting no further change in amyloid between the second PIB scan and death three years later. This pattern matches the data from numerous previous studies, in which PIB retention increases during mild cognitive impairment, then seems to plateau during AD.”
“Autopsy results confirmed the patient’s diagnosis of pure AD. … The results confirmed that in vivo PIB retention correlates quite well with amyloid deposits, but does not correlate closely with tau and neurofibrillary tangles, as previous studies have found. … In addition, the authors performed detailed studies not done before and turned up intriguing correlations between amyloid accumulation and synaptic receptor density, as well as a surprising lack of correlation with markers of inflammation.”
The summary on the Alzheimer Research Forum discusses four clinical trials with compounds targeting amyloid in Alzheimer’s patients. The trials were all negative. This PET-PIB study gives additional insight as to why that may be the case.
Here’s the summary on ARF about the recently-published study:
http://www.alzforum.org/new/detail.asp?id=2653
Note that some of the comments are well worth reading, though harder to understand than the summary. Some of the comments (posted in 2004) give historical info on PIB.
The recently-published study is available at no charge through the journal Brain. See:
http://brain.oxfordjournals.org/content/134/1/301.long (for HTML version)