Brain Cells Found to RegenerateMedical science has always presumed that brain cells killed by physical trauma, stroke or other disease cannot regenerate. Victims of such brain injuries faced no hope of growing new cells to fulfill the function of dead cells, leaving their brains permanently impaired.
However, a landmark study in late 1998 by researchers from Sweden and the Salk Institute in La Jolla, Calif., showed for the first time that
brain cells in mature humans can regenerate. The research was reported in the November issue of Nature Medicine.
http://healthlink.mcw.edu/article/926345803.html 2005 Dec;99(4):307-21.
Lithium: potential therapeutics against acute brain injuries and chronic neurodegenerative diseases.Wada A, Yokoo H, Yanagita T, Kobayashi H.
Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan. akihiko@fc.miyazaki-u.ac.jp
In addition to the well-documented mood-stabilizing effects of lithium in manic-depressive illness patients, recent in vitro and in vivo
studies in rodents and humans have increasingly implicated that lithium can be used in the treatment of acute brain injuries (e.g., ischemia) and chronic neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, tauopathies, and Huntington's disease). Consistent with this novel view, substantial evidences suggest that depressive illness is not a mere neurochemical disease, but is linked to gray matter atrophy due to the reduced number/size of neurons and glia in brain.
Importantly, neurogenesis, that is, birth/maturation of functional new neurons, continues to occur throughout the lifetime in human adult brains (e.g., hippocampus); the neurogenesis is impaired by multiple not-fully defined factors (e.g., aging, chronic stress-induced increase of glucocorticoids, and excitotoxicity), accounting for brain atrophy in patients with depressive illness and neurodegenerative diseases. Chronic treatment of lithium, in agreement with the delayed-onset of mood-stabilizing effects of lithium, up-regulates cell survival molecules (e.g., Bcl-2, cyclic AMP-responsive element binding protein, brain-derived neurotrophic factor, Grp78, Hsp70, and beta-catenin), while down-regulating pro-apoptotic activities (e.g., excitotoxicity, p53, Bax, caspase, cytochrome c release, beta-amyloid peptide production, and tau hyperphosphorylation),
thus preventing or even reversing neuronal cell death and neurogenesis retardation.PMID: 16340157
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16340157&query_hl=3&itool=pubmed_docsum2004 Oct;21(10):1457-67.
Dietary omega-3 fatty acids normalize BDNF levels, reduce oxidative damage, and counteract learning disability after traumatic brain injury in rats.Wu A, Ying Z, Gomez-Pinilla F.
Department of Physiological Science, University of California at Los Angeles, 90095, USA.
Omega-3 fatty acids (i.e., docosahexaenoic acid; DHA) regulate signal transduction and gene expression, and protect neurons from death. In this study we examined the capacity of dietary omega3 fatty acids supplementation to help the brain to cope with the effects of traumatic injury. Rats were fed a regular diet or an experimental diet supplemented with omega-3 fatty acids, for 4 weeks before a mild fluid percussion injury (FPI) was performed. FPI increased oxidative stress, and impaired learning ability in the Morris water maze. This type of lesion also reduced levels of brain-derived neurotrophic factor (BDNF), synapsin I, and cAMP responsive element-binding protein (CREB). It is known that BDNF facilitates synaptic transmission and learning ability by modulating synapsin I and CREB. Supplementation of omega-3 fatty acids in the diet counteracted all of the studied effects of FPI, that is, normalized levels of BDNF and associated synapsin I and CREB, reduced oxidative damage, and counteracted learning disability. The reduction of oxidative stress indicates a benevolent effect of this diet on mechanisms that maintain neuronal function and plasticity.
These results imply that omega-3 enriched dietary supplements can provide protection against reduced plasticity and impaired learning ability after traumatic brain injury.PMID: 15672635
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15672635&query_hl=6&itool=pubmed_docsumConsider fish oil.