Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, June 2, 2015

Detrimental role of prolonged sleep deprivation on adult neurogenesis

One more thing you'll have to make sure your doctor is taking care of for you. You want lots of neurogenesis. What exactly is your doctors' protocol to accomplish that? No protocol? Then call the hospital president and ask why they are employing incompetent doctors.
Excuses like 'All strokes are different, all stroke recoveries are different' ARE NOT ALLOWED.
http://journal.frontiersin.org/article/10.3389/fncel.2015.00140/full?
Carina Fernandes1,2, Nuno Barbosa F. Rocha3, Susana Rocha4, Andrea Herrera-Solís5, José Salas-Pacheco6, Fabio García-García7, Eric Murillo-Rodríguez8, Ti-Fei Yuan9, Sergio Machado10,11 and Oscar Arias-Carrión5*
  • 1Faculty of Medicine, University of Porto, Porto, Portugal
  • 2Laboratory of Neuropsychophysiology, Faculty of Psychology and Education Sciences, University of Porto, Porto, Portugal
  • 3School of Health Technologies, Polytechnic Institute of Porto, Porto, Portugal
  • 4School of Accounting and Administration of Porto, Polytechnic Institute of Porto, Porto, Portugal
  • 5Unidad de Trastornos del Movimiento y Sueño, Hospital General Dr. Manuel Gea González/Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
  • 6Instituto de Investigación Científica, Universidad Juárez del Estado de Durango, Durango, Mexico
  • 7Departamento de Biomedicina, Instituto de Ciencias de la Salud, Universidad Veracruzana, Xalapa, Mexico
  • 8División Ciencias de la Salud, Laboratorio de Neurociencias Moleculares e Integrativas, Escuela de Medicina, Universidad Anáhuac Mayab, Mérida, México
  • 9School of Psychology, Nanjing Normal University, Nanjing, China
  • 10Panic and Respiration, Institute of Psychiatry of Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
  • 11Physical Activity Neuroscience, Physical Activity Sciences Postgraduate Program, Salgado de Oliveira University, Niterói, Brazil
Adult mammalian brains continuously generate new neurons, a phenomenon called adult neurogenesis. Both environmental stimuli and endogenous factors are important regulators of adult neurogenesis. Sleep has an important role in normal brain physiology and its disturbance causes very stressful conditions, which disrupt normal brain physiology. Recently, an influence of sleep in adult neurogenesis has been established, mainly based on sleep deprivation studies. This review provides an overview on how rhythms and sleep cycles regulate hippocampal and subventricular zone neurogenesis, discussing some potential underlying mechanisms. In addition, our review highlights some interacting points between sleep and adult neurogenesis in brain function, such as learning, memory, and mood states, and provides some insights on the effects of antidepressants and hypnotic drugs on adult neurogenesis.

Introduction

Thousands of new neurons are daily added to the adult brain of different species, including humans (Yuan et al., 2014), and this constant lifelong generation implies significant structural changes (Eriksson et al., 1998; Curtis et al., 2007). Neurogenesis is involved in numerous brain processes but its association with sleep deprivation was only recently addressed. Previous research has focused on how generation and development of new neurons are affected by sleep loss. Short periods of sleep deprivation do not significantly alter the basal rate of cell proliferation, whereas long periods result in a decrease of cell proliferation and survival in the hippocampus (Mirescu et al., 2006). In this review, we will discuss the possible effects of sleep deprivation on the natural course of neurogenesis, and address the potential connections between sleep and neurogenesis that may influence other cognitive and neuropsychobiological functions, such as learning, memory, and mood disorders.

Adult Neurogenesis

Neurogenesis includes the generation, proliferation, fate specification and integration of new functional neurons in the existing neural circuits from undifferentiated progenitor cells. Traditionally, it was believed that neurogenesis mainly occurred during the embryonic stages of the central nervous system (CNS), ending permanently at puberty (Ming and Song, 2005; Meerlo et al., 2009).
New findings, based on techniques such as [3H]-thymidine autoradiography (Sidman et al., 1959) and 5-bromo-2-deoxyuridine (BrdU; Nowakowski et al., 1989), which mark cells in S phase of mitosis, electronic microscopy (Kaplan, 1977, 1981, 1984, 1985) and combining retroviral-based lineage tracing with electrophysiological methods (Sanes et al., 1986; Price et al., 1987) revealed the continuous adult neurogenesis and synaptic integration. Newborn neurons were found in certain CNS regions of birds (Goldman and Nottebohm, 1983), rats (van Praag et al., 1999), monkeys (Kornack and Rakic, 1999), and humans (Eriksson et al., 1998; Curtis et al., 2007), throughout life.
Neurogenesis occurs in specific areas of the CNS, namely in the subventricular zone (SVZ), lining the wall of the lateral ventricles, and in the subgranular zone (SGZ) of the hippocampal dentate gyrus (Alvarez-Buylla and Lim, 2004). The neurogenic behavior of these areas appears to be determined by signals of endothelial cells and astrocytes (Alvarez-Buylla and Lim, 2004).
Similarly, a cohort of glucogenic and neurogenic signals (Lim et al., 2000) regulates the underlying molecular mechanisms of neuronal differentiation, fate specification (Ming and Song, 2005; Arias-Carrión et al., 2007; Yuan and Arias-Carrion, 2011; Höglinger et al., 2014) and migration of new generated cells (Hu et al., 1996; Conover et al., 2000; Murase and Horwitz, 2002; Bolteus and Bordey, 2004). Newly formed neurons in the SVZ reach the olfactory bulb, by the rostral migratory stream (Saghatelyan et al., 2004), forming granule and periglomerular neurons. These neurons establish dendro-dendritic synapses with tufted cells (Abrous et al., 2005), beginning a maturation process by receiving GABAergic and glutamatergic synaptic inputs (Belluzzi et al., 2003). When maturate, the granule neurons secrete GABA, while periglomerular neurons secrete GABA and dopamine (Wang et al., 2000; Arias-Carrión et al., 2007). In the dentate gyrus, newborn neurons reach the anterior layer of the granule cells (Hastings and Gould, 1999), maintaining their neuronal maturation and synaptogenesis over several months (van Praag et al., 2002). It is believed that these neurons receive initially GABAergic and later glutamatergic inputs (Ming and Song, 2005). Once mature, most of these neurons secrete glutamate, while a small population releases GABA (Wang et al., 2000).
Adult neurogenesis is modulated by intrinsic and extrinsic factors (Table 1), being possible that several modulating factors remain unknown (Kempermann, 2002).

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