A stereotaxic atlas of the rat brain

In some patients with major depressive disorder (MDD), individual illness characteristics appear consistent with those of a neuroprogressive illness. Features of neuroprogression include poorer symptomatic, treatment and functional outcomes in patients with earlier disease onset and increased number and length of depressive episodes. In such patients, longer and more frequent depressive episodes appear to increase vulnerability for further episodes, precipitating an accelerating and progressive illness course leading to functional decline. Evidence from clinical, biochemical and neuroimaging studies appear to support this model and are informing novel therapeutic approaches. This paper reviews current knowledge of the neuroprogressive processes that may occur in MDD, including structural brain consequences and potential molecular mechanisms including the role of neurotransmitter systems, inflammatory, oxidative and nitrosative stress pathways, neurotrophins and regulation of neurogenesis, cortisol and the hypothalamic–pituitary–adrenal axis modulation, mitochondrial dysfunction and epigenetic and dietary influences. Evidence-based novel treatments informed by this knowledge are discussed.

The neuroprogressive nature of major depressive disorder: pathways to disease evolution and resistance, and therapeutic implications.

This review provides details on the phytochemicals in green coffee beans and the changes that occur during roasting. Key compounds in the coffee beverage, produced from the ground, roasted beans, are volatile constituents responsible for the unique aroma, the alkaloids caffeine and trigonelline, chlorogenic acids, the diterpenes cafestol and kahweol, and melanoidins, which are Maillard reaction products. The fate of these compounds in the body following consumption of coffee is discussed along with evidence of the mechanisms by which they may impact on health. Finally, epidemiological findings linking coffee consumption to potential health benefits including prevention of several chronic and degenerative diseases, such as cancer, cardiovascular disorders, diabetes, and Parkinson's disease, are evaluated.

Coffee: biochemistry and potential impact on health

Molecular mechanisms behind the biological effects of hesperidin and hesperetin for the prevention of cancer and cardiovascular diseases.

Synaptic plasticity confers environmental adaptability through modification of the connectivity between neurons and neuronal circuits. This is achieved through changes to synapse-associated signaling systems and supported by complementary changes to cellular morphology and metabolism within the tripartite synapse. Mounting evidence suggests region-specific changes to synaptic form and function occur as a result of chronic stress and in depression. Within subregions of the prefrontal cortex (PFC) and hippocampus structural and synapse-related findings seem consistent with a deficit in long-term potentiation (LTP) and facilitation of long-term depression (LTD), particularly at excitatory pyramidal synapses. Other brain regions are less well-studied; however the amygdala may feature a somewhat opposite synaptic pathology including reduced inhibitory tone. Changes to synaptic plasticity in stress and depression may correlate those to several signal transduction pathways (e.g. NOS-NO, cAMP-PKA, Ras-ERK, PI3K-Akt, GSK-3, mTOR and CREB) and upstream receptors (e.g. NMDAR, TrkB and p75NTR). Deficits in synaptic plasticity may further correlate disrupted brain redox and bioenergetics. Finally, at a functional level region-specific changes to synaptic plasticity in depression may relate to maladapted neurocircuitry and parallel reduced cognitive control over negative emotion.

Synaptic plasticity in depression: molecular, cellular and functional correlates.

Protective effect of naringin against ischemic reperfusion cerebral injury: possible neurobehavioral, biochemical and cellular alterations in rat brain.

http://if-pan.krakow.pl/pjp/pdf/2010/4_635.pdf

Hesperidin pre-treatment attenuates NO-mediated cerebral ischemic reperfusion injury and memory dysfunction

Nitric oxide mechanism in the protective effect of naringin against post-stroke depression (PSD) in mice.

Venlafaxine involves nitric oxide modulatory mechanism in experimental model of chronic behavior despair in mice.

Protective effect of desipramine, venlafaxine and trazodone against experimental animal model of transient global ischemia: possible involvement of NO-cGMP pathway.

Vaibhav Gaur

Papers

Protective effect of naringin against ischemic reperfusion cerebral injury: possible neurobehavioral, biochemical and cellular alterations in rat brain.

Hesperidin pre-treatment attenuates NO-mediated cerebral ischemic reperfusion injury and memory dysfunction

Nitric oxide mechanism in the protective effect of naringin against post-stroke depression (PSD) in mice.

Venlafaxine involves nitric oxide modulatory mechanism in experimental model of chronic behavior despair in mice.

Protective effect of desipramine, venlafaxine and trazodone against experimental animal model of transient global ischemia: possible involvement of NO-cGMP pathway.