http://www.sciencewa.net.au/topics/h...-activity.html

Looks like even more reason to stay active, and if able, to do the "forced exercise" cycling routine (or some equivalent).

Looks like Amyloid-β (mentioned in the Alzheimer's article in soccertese's post) is also likely associated with Parkinson's dementia.

http://www.ncbi.nlm.nih.gov/pubmed/18219254

"Dementia is common in Parkinson disease (PD), although its anatomic and pathologic substrates remain undefined. Recently, striatal abnormalities in Lewy body diseases have been described, but their clinical relevance is not clear. Thirty PD cases from the United Kingdom Parkinson's Disease Society Tissue Bank were grouped as demented (PDD; n = 16) and nondemented (PD; n = 14) based on a review of clinical records. The extent of alpha-synuclein, tau, and amyloid beta peptide (Abeta) deposition in the caudate nucleus, putamen, and nucleus accumbens was assessed. All cases showed severe dopaminergic striatal terminal denervation based on tyrosine hydroxylase immunohistochemistry. Alpha-synuclein and tau deposition in the striatum were rare in both groups, but the Abeta burden was significantly greater in the striatum of PD cases with dementia than present in the nondemented PD group. Striatal Abeta deposition was type-independent of Alzheimer disease changes in the cortex and was minimal in nondemented PD cases. We conclude that Abeta deposition in the striatum strongly correlates with dementia in PD."

one more paper that has positive info:f
mouse brain cells rapidly recover after Alzheimer's plaques are cleared
Brain cells in a mouse model of Alzheimer's disease have surprised scientists with their ability to recuperate after the disorder's characteristic brain plaques are removed. Researchers at Washington University School of Medicine in St. Louis injected mice with an antibody for a key component of brain plaques, the amyloid beta (Abeta) peptide. In areas of the brain where antibodies cleared plaques, many of the swellings previously observed on nerve cell branches rapidly disappeared.

"These swellings represent structural damage that seemed to be well established and stable, but clearing out the plaques often led to rapid recovery of normal structure over a few days," says senior author David H. Holtzman, M.D., the Charlotte and Paul Hagemann Professor and head of the Department of Neurology. "This provides confirmation of the potential benefits of plaque-clearing treatments and also gets us rethinking our theories on how plaques cause nerve cell damage." Prior to the experiment, Holtzman and some other scientists had regarded plaque damage to nerve cells as a fait accompli--something that the plaques only needed to inflict on nerve cells once. According to Holtzman, the new results suggest that plaques might not just cause damage but also somehow actively maintain it. The study, will appear in the Feb. 5 issue of the Journal of Clinical Investigation. Lead author Robert Brendza, Ph.D., research instructor, began the experiment with one key question: how did clearance of brain plaques, made possible by the development of Abeta antibodies, affect the progression of Alzheimer's disease? Through collaborations with researchers at other institutions, he had acquired several key techniques and technologies that allowed him to closely track changes in live brain cells in mice with an Alzheimer's-like condition. The mice he used for the study had two mutations. One, utilized by scientists at Eli Lilly, causes amyloid plaques to build up, creating the Alzheimer's-like condition. The second, developed by scientists at Washington University, causes some of the mouse brain cells to produce a dye that allowed Brendza to obtain detailed images of nerve cell branches. To correlate brain cell changes with plaque development, Brendza injected another dye, developed by scientists at the University of Pittsburgh, that temporarily sticks to amyloid. He showed that as the plaques appeared, nearby branches of nerve cells developed bumps and swellings. "If you look under the electron microscope at these swellings, they are filled with abnormal amounts of different types of cellular parts known as organelles," Holtzman explains. "Normally any given segment of a nerve cell branch would have only very small amounts of these organelles." Nerve cells move organelles along their branches as a part of their regular function. Holtzman suspects that this transport breaks down in the mice, leading to pileups that become swellings. Scientists have previously demonstrated that such swellings make it difficult or impossible for nerve-cell branches to send signals. After showing that the swellings were mostly stable in number and size over the course of three to seven days, Brendza injected Abeta antibodies directly onto the surface of the mouse brains. In the region of the injection, the antibodies cleared the plaques, confirming earlier research results. Then Brendza closely monitored the swellings for three days. "We thought that clearing the plaques would halt the progression of the damage--stop the development of new swellings," says Brendza. "But what we saw was much more striking: in just three days, there were 20 to 25 percent reductions in the number or size of the existing swellings." The nerve cells' rapid ability to regain normal structure has Holtzman and Brendza wondering if the nerve cells are constantly trying to restore their normal structure. If so, that recuperative effort must somehow be countered on an ongoing basis by the effects of the plaques. More research is needed to determine if similar effects will occur in humans. Abeta antibodies are currently being considered for use in Alzheimer's patients in clinical trials. In the mice, the largest swellings were least likely to heal. Brendza plans to look into whether additional treatment can prompt their recovery. Holtzman and Brendza plan to continue using the mouse model to study disease treatments and the cellular abnormalities caused by their Alzheimer's-like condition. "For example, we'd like to know what's going wrong in the nerve cell branches that get these swellings," Holtzman says. "Is it really a cellular transport problem, or do the swellings result from the plaques' effects on nearby support cells? Or is it something else?"

http://www.theparkinsonsgroup.com/webcasts.asp
2011 webcasts very interesting, especially on agonists.