Underlying cause of Gulf War illness confirmed (Medical X press)
- Thread starter ahimsa
- Start date
Chandelier
Senior Member (Voting Rights)
Decadelong low basal ganglia NAA/tCr from elevated tCr supports ATP depletion from mitochondrial dysfunction and neuroinflammation in Gulf War illness
Abstract
Abstract Reduced N-acetylaspartate (NAA)/total creatine (tCr) ratio found with long echo-time proton magnetic resonance imaging ( 1 H-MRS) of deep brain structures in a Seabees Battalion in 1997–1998 was soon replicated by two studies but not in a later one using intermediate echo time.
We undertook this study in 2008–2009 to repeat the previous long echo-time 1 H-MRS study with 1 H-MRS at both long (TE = 270 ms) and short (TE = 30 ms) echo time and higher field strength (3T) to test whether the abnormality of NAA/tCr affecting this Battalion had normalized or been obscured by effects of the T 2 decay curve.
Under investigator blinding, 39 Seabees in the three GWI variant groups and 16 Seabees controls prospectively underwent 1 H-MRS at both short (TE = 30 ms) and long (TE = 270 ms) echo time to measure metabolites and at five TE values between 60 ms and 270 ms to measure transverse relaxation time (T 2 ) in the basal ganglia.
A mixed-effects linear model adjusting for age tested group differences. Findings supported the observations of the prior studies, demonstrating that veterans with GWI no longer had reduced NAA/tCr at long echo time but had significantly lower basal ganglia NAA/tCr than controls at short echo time (left: 1.22 ± 0.02 vs. 1.38 ± 0.03, P < 0.0001; right: 1.12 ± 0.02 vs. 1.18 ± 0.03, P = 0.059). The group differences were mainly due to higher [tCr] (left: 14.1%, P = 0.0001; right: 9.1%, P = 0.009) rather than lower [NAA] in the ill groups.
Longer echo time substantially reduced the sensitivity of 1 H-MRS. Chronic metabolite abnormalities persisted in GWI for 10 more years but remained detectable only at short echo time.
That reduced NAA/tCr is due primarily to increased [tCr] rather than decreased [NAA] supports recent studies implicating mitochondrial dysfunction with ATP depletion and neuroinflammation as causative factors and therapeutic targets in GWI.
Web | DOI | PMC | PDF | Scientific Reports
Cheshkov, Sergey; Krishnamurthy, Lisa C.; Chang, Audrey; Baek, Hyeon-Man; Ganji, Sandeep; Babcock, Evelyn; Spence, Jeffrey S.; Briggs, Richard W.; Haley, Robert W.
Abstract
Abstract Reduced N-acetylaspartate (NAA)/total creatine (tCr) ratio found with long echo-time proton magnetic resonance imaging ( 1 H-MRS) of deep brain structures in a Seabees Battalion in 1997–1998 was soon replicated by two studies but not in a later one using intermediate echo time.
We undertook this study in 2008–2009 to repeat the previous long echo-time 1 H-MRS study with 1 H-MRS at both long (TE = 270 ms) and short (TE = 30 ms) echo time and higher field strength (3T) to test whether the abnormality of NAA/tCr affecting this Battalion had normalized or been obscured by effects of the T 2 decay curve.
Under investigator blinding, 39 Seabees in the three GWI variant groups and 16 Seabees controls prospectively underwent 1 H-MRS at both short (TE = 30 ms) and long (TE = 270 ms) echo time to measure metabolites and at five TE values between 60 ms and 270 ms to measure transverse relaxation time (T 2 ) in the basal ganglia.
A mixed-effects linear model adjusting for age tested group differences. Findings supported the observations of the prior studies, demonstrating that veterans with GWI no longer had reduced NAA/tCr at long echo time but had significantly lower basal ganglia NAA/tCr than controls at short echo time (left: 1.22 ± 0.02 vs. 1.38 ± 0.03, P < 0.0001; right: 1.12 ± 0.02 vs. 1.18 ± 0.03, P = 0.059). The group differences were mainly due to higher [tCr] (left: 14.1%, P = 0.0001; right: 9.1%, P = 0.009) rather than lower [NAA] in the ill groups.
Longer echo time substantially reduced the sensitivity of 1 H-MRS. Chronic metabolite abnormalities persisted in GWI for 10 more years but remained detectable only at short echo time.
That reduced NAA/tCr is due primarily to increased [tCr] rather than decreased [NAA] supports recent studies implicating mitochondrial dysfunction with ATP depletion and neuroinflammation as causative factors and therapeutic targets in GWI.
Web | DOI | PMC | PDF | Scientific Reports
Wirth saw it coming:
mitodicure.com
Pipeline – Mitodicure
mitodicure.com
Utsikt
Senior Member (Voting Rights)
Wirth saw it coming:
Pipeline – Mitodicure
MDC002 is targeting skeletal muscles, not the brain.
There is evidence (from their model) that MDC002 has vascular / perfusion-improving effects in the brain, too.
That said, the brain effects are more about blood flow and edema, not necessarily the same molecular ionic processes that they target in muscle.
It took 16 years to analyze and publish?
Yann04
Senior Member (Voting Rights)
I think it’s long term longitudinal. Like they mention measurments at “10 years”.
But still 6 years is a massive amount of time to wait before publishing if they think they’re publishing something that will advance the field.
It seems to me like "10 years" refers to the span between the 1998 study and this study:
Utsikt
Senior Member (Voting Rights)
So purely hypothetical?
Is there any evidence of cerebral edema in GWI, ME/CFS, FM, etc?