Print

Print


Did anyone asked Dr. Lieberman to confirm the protein information? He is
a leading authority on PD.
Emily
----- Original Message -----
From: "Ray Strand" <[log in to unmask]>
To: <[log in to unmask]>
Sent: Wednesday, June 12, 2002 1:35 PM
Subject: proteins again


>
> news from Reuters
>
>
........................................................................
........................................................
>
>
> [Publication Logo]
>
> Synuclein-Protein Complexes Render Dopamine Neurotoxic
>
>
>
> NEW YORK (Reuters Health) May 31 - Alpha-synuclein forms soluble
> complexes with the anti-apoptotic protein 14-3-3 that appear to cause
> endogenous dopamine to become toxic to neurons in the substantia
nigra,
> according to a study in the June issue of Nature Medicine.
>
> This finding may explain the selective loss of dopaminergic neurons in
> Parkinson's disease, the study authors suggest, and it may ultimately
> lead to new therapies for the disease, as well as for diffuse
Lewy-body
> disease and some variants of Alzheimer's disease.
>
> Dr. Bruce A. Yankner, of the Children's Hospital in Boston, told
Reuters
> Health that "until now, the combination of alpha-synuclein with 14-3-3
> protein was not known to cause neuron degeneration."
>
> Dr. Yankner and associates found that transfection of alpha-synuclein
in
> primary cultures of nondopaminergic human cortical neurons (HCN cells)
> and in human fetal dopaminergic neurons (DAN cells) led to similar
> expression of the protein. Overexpression of alpha-synuclein increased
> survival of the HCN cells, but led to increased apoptosis in the DAN
cells.
>
> They then inhibited endogenous dopamine expression in DAN cells and
> found that apoptosis induced by alpha-synuclein and potentiated by
> oxidative stress was completely blocked.
>
> Autopsy studies showed that alpha-synuclein in the substantia nigra
was
> complexed with 14-3-3 protein. This inactivates the anti-apoptotic
> effect of 14-3-3 protein, and dopamine metabolism subsequently
promotes
> apoptosis by acting as a source of reactive oxygen species, the
authors
> suggest. They believe that the complexes may also increase neuronal
> vulnerability to other pro-oxidative agents, such as amyloid
beta-protein.
>
> "It is too early to make any clear predictions regarding treatment,"
> said Dr. Yankner. "However, if the findings of this paper prove to be
> important for Parkinson's disease, then preventing alpha-synuclein
from
> getting together with the 14-3-3 protein could be a new therapeutic
> approach to the disease."
>
> Nat Med 2002;8:600-606.
>
>
>
>
>
>
........................................................................
..........................................................
>
>  Ray Strand
>                                      Prairie Sky Design
>  -----------------(   on  the Edge of the Prairie
byss  )---------------
>                                 when  the  sky  is  clear
>                                   the ground is visible
> 50/47dx PD/40? onset
> http://folding.stanford.edu
> join  MSA TEAM CURE
> #2508
> }
>
>

----------------------------------------------------------------------
To sign-off Parkinsn send a message to: mailto:[log in to unmask]
In the body of the message put: signoff parkinsn