Answer: Made mostly of collagen, bone is living, growing tissue. Collagen is a protein that provides a soft framework, and calcium phosphate is a mineral that adds strength and hardens the framework. This combination of collagen and calcium makes bone strong and flexible enough to withstand stress.
Answer:
After a disturbance such as a fire or flood has occurred, an area can get reestablished by the process of secondary succession. Secondary succession can be described as an ecological succession in which life begins to form again in area which has been eradicated due to disturbances. Firstly, the pioneer species, such as small grasses or shrubs, will start to form on this land. Them with the passage of time the pioneer species will be replaced by the intermediate species such as different plants and trees. animals will start to occur more on this land. Finally, a complex community will arise to support life.
Answer: Option A and D.
Soups chemical synaptic transmission.
Sparks direct electrical transmission.
Explanation:
Intercellular communication refers to the communication and interaction that exists between two cells in the body. It could be hormonal or synaptic transmission.
Synapse is the site where electric nerve impulses are transmitted between two nerve impulses.
There are two synapse possibilities which are electrical and chemical.
The Sparks and soups mean that the scientific discovery over the transmission of nerve impulses as to whether they are electrical impulses (Sparks) or chemical impulses(soup).
Chemical synaptic transmission means there is no physical touch in the space chemical are released and move to the neighbouring cells.
Electrical transmission means neuron physically touch and give way for flow of impulses between cells.
The required answer is Neurogenesis increases.
Neurogenesis:
- Alzheimer's disease and other tauopathies have been linked to impaired adult hippocampal neurogenesis, which may be a factor in these diseases' learning and memory deficits. We examined adult neurogenesis in the hippocampal dentate gyrus of wild-type mice, Tg30 mice expressing an FTDP-17 mutant tau, and the same Tg30 mice deficient for mouse tau (Tg30/tauKO) in order to determine the impact of tau pathology, a frequent key-lesion in these diseases, on adult hippocampal neurogenesis. Unbiased stereological techniques were used to measure the density of the granular layer, the number of granule cells, and the number of neuronal precursors expressing the immature markers DCX or 3R-tau in the dentate gyrus (DG). It was also examined how neurogenic markers co-localized with human mutant tau.
- The volume of the granular layer and the number of granule cells were significantly reduced in mutant tau Tg30 mice, but not in Tg30/tauKO animals. The number of cells expressing the proliferation marker Ki-67 and the number of neuronal precursors displaying the immaturity markers DCX or 3R-tau (the latter only expressed in wild-type and Tg30 mice) in the neurogenic sub granular zone of the DG were decreased in Tg30 but not in Tg30/tauKOmice.
- In comparison to Tg30 mice, Tg30/tauKO mice had reduced levels of soluble human phosphate and phosphate-positive cell density in the DG. In Tg30 and Tg30/tauKO mice, the human mutant tau was expressed in adult granule cells but not in Sox2 positive neural stem cells, DCX positive neuronal progenitors, or immature newborn neurons. These findings show that adult hippocampus neurogenesis is impaired in tau FTDP-17 mutant mice due to a reduction in proliferation that affects the pool of neural progenitors.
- These mutant tau animals did not express mutant tau in precursor cells, indicating that this neurogenic defect is not cell-autonomous. As this decreased adult neurogenesis was restored by reducing tau expression in Tg30/tauKO mice, it is interesting to note that expression of endogenous wild-type tau in mature granule cells was required to see this harmful effect of human mutant tau. These findings imply that human tauopathies also reduce adult hippocampal neurogenesis through the development of tau pathology in dentate gyrus granule cells by inhibiting proliferation of neural progenitors, and that reducing tau expression may be a way to reverse this impairment.
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