SSRI's v alternative

[Guest guest]

While I am sure some believe you can do this with natural stuff you can NOT it

has never changed a spect scan

SSRI's are found to be neuroprotective

Elyse Goldberg

J Neurosci Res. 2009 Mar;87(4):1037-45.

Fluoxetine affords robust neuroprotection in the postischemic brain via its

anti-inflammatory effect.

Lim CM, Kim SW, Park JY, Kim C, Yoon SH, Lee JK.

Department of Anatomy, Inha University School of Medicine, Inchon, Korea.

Abstract

Fluoxetine is a selective serotonin reuptake inhibitor that is widely used in

the treatment of major depression including after stroke. In this study, we

tested whether fluoxetine protects neuronal death in a rat cerebral ischemia

model of middle cerebral artery occlusion (MCAO). The administration of

fluoxetine intravenously (10 mg/kg) at 30 min, 3 hr, or 6 hr after MCAO reduced

infarct volumes to 21.2+/-6.7%, 14.5+/-3.0%, and 22.8+/-2.9%, respectively, of

that of the untreated control. Moreover, the neuroprotective effect of

fluoxetine was evident when it was administered as late as 9 hr after

MCAO/reperfusion. These neuroprotective effects were accompanied by improvement

of motor impairment and neurological deficits. The fluoxetine-treated brain was

found to show marked repressions of microglia activation, neutrophil

infiltration, and proinflammatory marker expressions. Moreover, fluoxetine

suppressed NF-kappaB activity dose-dependently in the postischemic brain and

also in lipopolysaccharide-treated primary microglia and neutrophil cultures,

suggesting that NF-kappaB activity inhibition explains in part its

anti-inflammatory effect. These results demonstrate that curative treatment of

fluoxetine affords strong protection against delayed cerebral ischemic injury,

and that these neuroprotective effects might be associated with its

anti-inflammatory effects.

PMID: 18855941 [PubMed - indexed for MEDLINE]

Publication Types, MeSH Terms, Substances

Neurobiol Dis. 2008 Jun;30(3):312-22. Epub 2008 Mar 10.

Sertraline slows disease progression and increases neurogenesis in N171-82Q

mouse model of Huntington's disease.

Duan W, Peng Q, Masuda N, Ford E, Tryggestad E, Ladenheim B, Zhao M, Cadet JL,

Wong J, Ross CA.

Division of Neurobiology, Department of Psychiatry and Behavioral Sciences,

s Hopkins University School of Medicine, CMSC 8-121, 600 North Wolfe Street,

Baltimore, MD 21287, USA. wduan2@...

Abstract

Huntington's disease (HD) is an inherited progressive neurodegenerative disorder

resulting from CAG repeat expansion in the gene that encodes for the protein

huntingtin. To identify neuroprotective compound (s) that can slow down disease

progression and can be administered long term with few side effects in

Huntington's disease, we investigated the effect of sertraline, a selective

serotonin reuptake inhibitor (SSRI) which has been shown to upregulate BDNF

levels in rodent brains. We report here that in HD mice sertraline increased

BDNF levels, preserved chaperone protein HSP70 and Bcl-2 levels in brains,

attenuated the progression of brain atrophy and behavioral abnormalities and

thereby increased survival. Sertraline also enhanced neurogenesis, which

appeared to be responsible for mediating the beneficial effects of sertraline in

HD mice. Additionally, the effective levels of sertraline are comparable to the

safe levels achievable in humans. The findings suggest that sertraline is a

potential candidate for treatment of HD patients.

PMID: 18403212 [PubMed - indexed for MEDLINE]

Brain Res. 2009 Jul 24;1281:108-16. Epub 2009 May 7.

Fluoxetine attenuates kainic acid-induced neuronal cell death in the mouse

hippocampus.

Jin Y, Lim CM, Kim SW, Park JY, Seo JS, Han PL, Yoon SH, Lee JK.

Department of Anatomy and Center for Advanced Medical Education (BK21 project),

Inha University School of Medicine, Incheon, Republic of Korea.

Abstract

Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) and one of the

commonly prescribed antidepressants. Numerous clinical observations and animal

studies indicate that fluoxetine enhances the anticonvulsant potencies of

several antiepileptic drugs. In the previous report, we showed that fluoxetine

strongly protects against delayed cerebral ischemic injury. In the present

study, the authors investigated whether fluoxetine has a beneficial effect on

KA-induced neuronal cell death. An intracerebroventricular (i.c.v.) injection of

0.94 nmol (0.2 microg) of KA produced typical neuronal cell death both in CA1

and CA3 regions of the hippocampus. Although, there was no significant

difference in the time course or severity of epileptic behavior, the systemic

administration of fluoxetine 30 min before KA administration significantly

attenuated this neuronal cell death. Fluoxetine was found to suppress neuronal

cell loss when injected at 10 mg/kg and the effect was enhanced at 50 mg/kg.

Furthermore, this fluoxetine-induced neuroprotection was accompanied by marked

improvements in memory impairment, as determined by passive avoidance tests.

KA-induced gliosis and proinflammatory marker (COX-2, IL-1beta, and TNF-alpha)

inductions were also suppressed by fluoxetine administration. It is interesting

to note here that fluoxetine treatment suppressed NF-kappaB activity

dose-dependently in KA-treated mouse brains, suggesting that this explains in

part its anti-inflammatory effect. Together, these results suggest that

fluoxetine has therapeutic potential in terms of suppressing KA-induced

pathogenesis in the brain, and that these neuroprotective effects are associated

with its anti-inflammatory effects.

PMID: 19427844 [PubMed - indexed for MEDLINE]