Interesting news summary from the Alzheimer's Research Forum:

http://www.alzforum.org/new/detail.asp?id=2544

Common Ground: Is Aβ the Foundation for Multiple Dementias?

27 August 2010. The majority of patients with Parkinson disease eventually develop dementia, but what pathology underlies this decline? In PD, as well as in dementia with Lewy bodies (DLB), intracellular aggregates composed primarily of α-synuclein gum up the specific dopaminergic neurons, but PD patients live with these Lewy bodies for many years before they experience cognitive losses. Intriguingly, scientists have found evidence of amyloid-β (Aβ) pathology in both Parkinson disease dementia (PDD) and DLB, suggesting a role for Aβ in these diseases. Now, two new papers firm up that idea. In the August 18 Neurology online, researchers led by Andrew Siderowf at the University of Pennsylvania, Philadelphia, report on the first longitudinal study to examine changes in the Alzheimer’s marker Aβ42 in the cerebrospinal fluid (CSF) of PD patients. They found that low levels of Aβ42 predicted significant cognitive decline within the next two years, hinting that Aβ pathology is involved in Parkinson’s dementia. Meanwhile, in the August 23 Lancet, scientists led by Murat Emre at Istanbul University, Turkey, describe the largest trial to date studying the efficacy of the N-methyl D-aspartate (NMDA) receptor antagonist memantine, which is approved for treatment of AD, in patients with PDD and DLB. Emre and colleagues found that memantine provides a moderate benefit to DLB patients. Together, these studies raise intriguing questions about the interrelatedness of these disorders, with implications for research, diagnosis, and treatment.

The importance of CSF Aβ as a biomarker has already been demonstrated in AD, with studies showing that in people with mild cognitive impairment, low CSF levels of Aβ and high levels of tau predict cognitive decline and conversion to AD (see, e.g., Hansson et al., 2006 and Shaw et al., 2009). Low CSF Aβ levels are thought to reflect the sequestration of Aβ into amyloid plaques. For PD patients, several cross-sectional studies have shown an association between cognitive impairment and CSF levels of Aβ and tau as well (see Mollenhauer et al., 2005; Bibl et al., 2006; Compta et al., 2009; Alves et al., 2010), but longitudinal data were missing.

[see link for rest of summary]

I'm surprised CSF isn't tested routinely in dementia patients.

I think the issue is three-fold:
* not everyone is willing to get a spinal tap
* researchers are reluctant to tell people "you are going to get Alzheimer's" as there is no current way to slow the progression of AD or stop it in its tracks
* there is reluctance on the part of many to have info like "you are going to get Alzheimer's" in a medical record

I guess that makes sense, Robin. Spinal tap is not without its risks. But it surely would be a good research tool if everyone with dementia had it done and then their progress and outcome compared to the results.