promising biomarker for parkinson’s disease: PPMI results

Parkinson’s disease is typically characterized in a clinical setting by the present of tremor, rigidity, bradykinesia (slow movement), and in the later stages, postural instability (balance).

Researchers from the University of Pennsylvania report ( JAMA Neurology) that the appearance of proteins in the spinal fluid may be the key to identifying affected patients early in the disease process, long before symptoms set in. The study results, which came from the Parkinson’s Progression Markers Initiative (PPMI) study. PPMI is sponsored by the Michael J Fox Foundation and aims to take biological measurements from 400 patients and 200 healthy controls to better understand the onset and progression of the disease.

The study found that people with early stage Parkinson’s had lower levels of the biomarker proteins amyloid beta and alpha synuclein.

It also distinguished between people with different disease presentations:

  • those with higher levels of motor dysfunction,  had lower levels of tau and alpha synuclein,
  • those whose muscles tended to freeze, or people who had difficulty walking, showed lower levels of amyloid beta and tau.

These promising results suggest we may be able to detect Parkinson’s with spinal fluid earlier, which could change the way it is diagnosed and treated. It also suggests for the first time that there may be different types of the disease with different potential treatments. This seems to support the hypothesis that Parkinson’s disease is a “spectrum”, and that people are diagnosed and face different disease along the “dopamine spectrum”.

This is definitely a step in the right direction. Having a biomarker to enable earlier detection and better disease management will improve the quality of life of all those involved. Really exciting! much love.

Read more…

slowing Parkinson’s progression: a research update

alpha-synuclein is a protein encoded by the SNCA gene.

Although we are still not certain of what it does, we do know it makes up Lewy Bodies, clusters of proteins that are a pathological hallmark of Parkinson’s disease and other dementias (lewy body dementias). It is thought that in Parkinson’s disease, the variability in alpha-synuclein gene produces either too much alpha-synuclein protein or causes it to malfunction — which may be toxic to brain cells and to result in neuron dysfunction.

Some of the ways in which research is targeting alpha-synuclein is by:

  • a vaccine that binds to alpha-synuclein and clears it from the brain
  • compounds to stop alpha-synuclein from clumping (avoiding lewy body formation)
  • compound to break up alpha-synuclein clumps (breaking up formation of lewy bodies)

Recent research developments include a chemical compound that slows down the onset and progression of Parkinson’s disease in mice. Griese and Griesinger in Gottingen have developed a substance which, in mouse models of the disease, reduces the rate of growth of the alpha-synuclein deposits and delays nerve cell degeneration. As a consequence, mice treated with this agent remain disease-free for longer than non-medicated controls. The current gold-standard, Levodopa, controls Parkinson’s symptoms by enhancing the function of the surviving nerve cells in the substantia nigra. This compound shows promise in slowing down the progression, according to their lab results; the earlier the onset of treatment, the longer the animals remained disease free.

(Max-Planck-Gesellschaft (2013, April 22). Putting the brakes on Parkinson’s.ScienceDaily. Retrieved May 12, 2013, from­/releases/2013/04/130422111147.htm#.UXa4E78jkGQ)

Another research effort looking to halt Parkinson’s disease progression involves GM1 glanglioside. GM1 impacts neuron plasticity, repair mechanisms, and neurotrophin release.

A study published in November 2012 showed that GM1 ganglioside improved symptoms and slowed disease progression during a two and a half-year trial in persons with Parkinson’s. Dr. Jefferson, published in the Journal of the Neurological Sciences, followed 77 subjects over a 120-week period and 17 control subjects as comparison.  GM1 group had significant improvement in UPDRS motor scores and maintained much of the initial benefit of GM1 treatment, (i.e. showed relatively minor symptom progression compared to patients using standard anti-Parkinson medications).

(Jay S. Schneider, Stephen M. Gollomp, Stephanie Sendek, Amy Colcher, Franca Cambi, Wei Du. A randomized, controlled, delayed start trial of GM1 ganglioside in treated Parkinson’s disease patients. Journal of the Neurological Sciences, 2012; DOI:10.1016/j.jns.2012.10.024)

… some very interesting drug developments on the horizon. it’s a long process from developing compounds, animal testing, clinical testing etc. … but nice to know there are possibilities on the horizon! much love

From research to real life: smell, sleep, constipation and Parkinson’s

… what do these 3 things have in common? Early detection of PD.

New research shows that hyposmia (loosing sense of smell), rapid eye movement sleep behavior disorder (RBD), and constipation, may be early Parkinson’s disease manifestations that reflect the underlying alphasynuclein pathology (the degeneration that is happening in the brain!) as well as predict subsequent onset of motor manifestations (Ravina & Aarsland, Mov Disord 2013).

Also, recent prospective (it means the researchers followed patients for 4-years) study shows that patients with RBD have increased cognitive impairment on neuropsychological testing (Postuma et al., Mov Disord 2012). The results showed that 48% of persons with RBD developed some cognitive impairments (especially hallucinations and some cognitive fluctuations), compared to 0% of patients who did not have RBD. This gives us an indication that we should watch RBD diagnosis in Parkinson’s disease closely as RBD may be a good marker of cognitive impairment subtypes associated with Parkinson’s.

A typical sleep cycle (

A typical sleep cycle (

what RBD can often look like! Yikes! ... and often dangerous to your bedmate (

what RBD can often look like! Yikes! … and often dangerous to your bedmate

… so ask your bedmate and talk to your doctor about how do you sleep at night. much love.

from research to real life – curcumin attacks proteins related to Parkinson’s disease

is a natural compound in the Indian spice, Turmeric, part of the ginger family.

The main idea: In Parkinson’s disease, abnormal clumping of the protein alpha-synuclein occurs. New research shows curcumin may bind to the alpha-synuclein proteins and prevent the abnormal folding and clumping that may be the first steps to Parkinson’s disease.

Research: Curcumin prevents aggregation in α-synuclein by increasing reconfiguration rate

Real life: Curcumin shows promise in attacking Parkinson’s disease

chick pea curry with turmeric

However, turmeric doesn’t go directly to the brain where this clumping occurs, so don’t go out and fill up on curry’s just yet (or do, it’s pretty delicious!). much love.

from research to real life – calcium may advance Parkinson’s disease

I’m starting a new regular post… from research to real life. There’s so much information out there, it’s hard to keep track of it all! I will present new (and exciting!) research in both a scientific and news media format, so the ideas come across in whatever way you choose to get your information!

I thought this was an interesting article on calcium and dopaminergic neurons.

The main idea: calcium stresses dopamine neurons, leading to premature aging and cell death. There is ongoing research into drugs that shut down Cav1.3 (a membrane protein that controls calcium release) to relieve stress on dopamine cells… and may slow disease progression.

ResearchCaV1.3-selective L-type calcium channel antagonists as potential new therapeutics for Parkinson’s disease

Real lifeParkinson’s breakthough could slow disease progression – Dementia News – –.

enjoy! much love.