Curcumin treatment leads to better cognitive and mood function in a model of Gulf War Illness with enhanced neurogenesis, and alleviation of inflammation and mitochondrial dysfunction in the hippocampus.

by | Functional & Integrative Medicine, Mast Cell Activation Syndrome

https://www.ncbi.nlm.nih.gov/pubmed/29454881

Comment; Curcumin is a well known antioxidant/anti-inflammatory that’s been used in Ayurvedic medicine for >7,000 years.  Our current system in which natural compounds cannot be patented encourages the pharmaceutical industry to pay little if any attention to these compounds, thus “mainstream medicine” is largely ignorant of them.

 

Other ISEAI practitioners have also weighed in;

From: Sandeep Gupta, MD
Sent: Wednesday, February 21, 2018 3:23 AM

Seeking Health Liposomal Curcumin is one I have just started using. There are a few papers on curcumin’s effect on TGF-beta and also MMP-9 levels if people would like to see these? This should mean in theory, that it would be a key agent for treating increased BBB permeability.

From: Mary Ackerley, MD, Wednesday, Feb 21st, 10:59 am
I use Neuroprotek and Quercenase extensively.  Several of my patients feel Neuroprotek is much more helpful than Vasoactive Intestinal Peptide (VIP), including a Type 3 Alzheimer patient.

Kodali M1, Hattiangady B1, Shetty GA1, Bates A1, Shuai B1, Shetty AK2.

Abstract

Diminished cognitive and mood function are among the most conspicuous symptoms of Gulf War Illness (GWI). Our previous studies in a rat model of GWI have demonstrated that persistent cognitive and mood impairments are associated with substantially declined neurogenesis, chronic low-grade inflammation, increased oxidative stress and mitochondrial dysfunction in the hippocampus. We tested the efficacy of curcumin (CUR) to maintain better cognitive and mood function in a rat model of GWI because of its neurogenic, antiinflammatory, antioxidant, and memory and mood enhancing properties. Male rats were exposed daily to low doses of GWI-related chemicals, pyridostigmine bromide, N,N-diethyl-m-toluamide (DEET) and permethrin, and 5-minutes of restraint stress for 28 days. Animals were next randomly assigned to two groups, which received daily CUR or vehicle treatment for 30 days. Animals also received 5′-bromodeoxyuridine during the last seven days of treatment for analysis of neurogenesis. Behavioral studies through object location, novel object recognition and novelty suppressed feeding tests performed sixty days after treatment revealed better cognitive and mood function in CUR treated GWI rats. These rats also displayed enhanced neurogenesis and diminished inflammation typified by reduced astrocyte hypertrophy and activated microglia in the hippocampus. Additional studies showed that CUR treatment to GWI rats enhanced the expression of antioxidant genes and normalized the expression of multiple genes related to mitochondrial respiration. Thus, CUR therapy is efficacious for maintaining better memory and mood function in a model of GWI. Enhanced neurogenesis, restrained inflammation and oxidative stress with normalized mitochondrial respiration may underlie better memory and mood function mediated by CUR treatment.

 

 

 

 

Dr. Raymond Oenbrink
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