Brain neurodegenerative diseases

Many studies have recently been conducted in the area of gene therapy. GABA may change the neuron excitability. GABA content in the brains and blood of people with brain neurodegenerative disease was lower than that of individuals without disease. In addition, researchers have used the adeno-associated virus (AAV) vector to deliver GAD into the brain cells of animals in order to adjust the synthesis of GABA and increase the stability of the athletic control system. These results show that... 

Cartier L, Hartley O, Dubois-Dauphin M, Krause KH (2005) Chemokine receptors in the central nervous system role in brain inflammation and neurodegenerative diseases. Brain Res Brain Res Rev 48 16-42... 

Endogenous estrogens are known to be active in a number of areas of the brain. There are indications that estrogens may play a role in mood, locomotor activity, pain sensitivity, vulnerability to neurodegenerative diseases and cognition (McEwan, 1999). In humans, the blood brain barrier is not fiilly developed at birth and, for this reason, the central nervous system (CNS) may be more sensitive to phytoestrogens in utero or at birth. As ERs are expressed in the CNS, phytoestrogens may also be active in this area. 

Mechanisms from Cell to Brain 352 Neurodegenerative Diseases 353 Huntington s Disease 353 Parkinson s Disease 358 Perspectives on the Pharmacogenomics of Neurodegenerative Processes 361 Conclusions 362 References 363... 

Neurotrophic factors Mainly conditions caused by/associated with neurodegeneration, including peripheral neuropathies, amyotrophic lateral sclerosis and neurodegenerative diseases of the brain... 

IGF-I is widely expressed in the central nervous system. IGF-II is also present, being produced mainly by tissues at vascular interfaces with the brain. Both growth factors, along with insulin, play a number of important roles in the nervous system. They stimulate the growth and development of various neuronal populations and promote neurotrophic effects (discussed later) and may, therefore, be of potential use in the treatment of various neurodegenerative diseases. 

Phospholipids in synaptic membranes are an important target in seizures, head injury, neurodegenerative diseases and cerebral ischemia. Synaptic membranes are excitable membranes enriched in phospholipids esterified with the polyunsaturated fatty acids AA and DHA which form a significant proportion of the FFAs rapidly released during ischemia, seizure activity and other brain trauma. 

Moreover,bioactive lipids maybe considered dual messengers they modulate cell functions as messengers and they become part of the response of the nervous tissue to injury, broadly referred to as the inflammatory response. This response occurs in ischemia-reperfusion damage associated with stroke, various forms of neurotrauma, infectious diseases and neurodegenerative diseases such as Alzheimer s disease. Inflammation in the nervous system differs from that in other tissues. If the blood-brain barrier is broken, blood-borne inflammatory cells (e.g. polymorphonuclear leukocytes, monocytes, macrophages) invade the intercellular space and glial cells are activated, particularly microglia, which play a prominent role in the inflammatory response. These responses may... 

Metals in Brain and Their Role in Various Neurodegenerative Diseases... 

An inevitable consequence of ageing is an elevation of brain iron in specific brain regions, e.g. in the putamen, motor cortex, pre-frontal cortex, sensory cortex and thalamus, localized within H- and L-ferritin and neuromelanin with no apparent adverse effect. However, ill-placed excessive amounts of iron in specific brain cellular constituents, such as mitochondria or in specific regions brain, e.g. in the substantia nigra and lateral globus pallidus, will lead to neurodegenerative diseases (Friedreich s ataxia and Parkinson s disease (PD), respectively). We discuss here a few of the examples of the involvement of iron in neurodegenerative diseases. From more on iron metabolism see Crichton, 2001. 

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