Question

how does Alzheimer's affect the central nervous system?

Explain the role of neurotransmitters in both the muscular and nervous system.

Explain how muscle contraction is achieved as described by the sliding filament theory

Answer 1

In Alzheimer’s disease, however, damage is widespread, as many neurons stop functioning, lose connections with other neurons, and die. Alzheimer’s disrupts processes vital to neurons and their networks, including communication, metabolism, and repair.

At first, Alzheimer’s disease typically destroys neurons and their connections in parts of the brain involved in memory, including the entorhinal cortex and hippocampus. It later affects areas in the cerebral cortex responsible for language, reasoning, and social behavior. Eventually, many other areas of the brain are damaged. Over time, a person with Alzheimer’s gradually loses his or her ability to live and function independently. Ultimately, the disease is fatal.

Many molecular and cellular changes take place in the brain of a person with Alzheimer’s disease. These changes can be observed in brain tissue under the microscope after death. Investigations are underway to determine which changes may cause Alzheimer’s and which may be a result of the disease.

Amyloid Plaques

The beta-amyloid protein involved in Alzheimer’s comes in several different molecular forms that collect between neurons. It is formed from the breakdown of a larger protein, called amyloid precursor protein. One form, beta-amyloid 42, is thought to be especially toxic. In the Alzheimer’s brain, abnormal levels of this naturally occurring protein clump together to form plaques that collect between neurons and disrupt cell function. Research is ongoing to better understand how, and at what stage of the disease, the various forms of beta-amyloid influence Alzheimer’s.

Neurofibrillary Tangles

Neurofibrillary tangles are abnormal accumulations of a protein called tau that collect inside neurons. Healthy neurons, in part, are supported internally by structures called microtubules, which help guide nutrients and molecules from the cell body to the axon and dendrites. In healthy neurons, tau normally binds to and stabilizes microtubules. In Alzheimer’s disease, however, abnormal chemical changes cause tau to detach from microtubules and stick to other tau molecules, forming threads that eventually join to form tangles inside neurons. These tangles block the neuron’s transport system, which harms the synaptic communication between neurons.

Emerging evidence suggests that Alzheimer’s-related brain changes may result from a complex interplay among abnormal tau and beta-amyloid proteins and several other factors. It appears that abnormal tau accumulates in specific brain regions involved in memory. Beta-amyloid clumps into plaques between neurons. As the level of beta-amyloid reaches a tipping point, there is a rapid spread of tau throughout the brain.

2)ROLE OF NEUROTRANSMITTER IN NERVOUS SYSTEM

Neurons do not touch each other (except in the case of an electrical synapse through a gap junction); instead, neurons interact at contact points called synapses: a junction within two nerve cells, consisting of a miniature gap within which impulses are carried by a neurotransmitter. A neuron transports its information by way of a nerve impulse called an action potential. When an action potential arrives at the synapse's presynaptic terminal button, it may stimulate the release of neurotransmitters. These neurotransmitters are released into the synaptic cleft to bind onto the receptors of the postsynaptic membrane and influence another cell, either in an inhibitory or excitatory way. The next neuron may be connected to many more neurons, and if the total of excitatory influences minus inhibitory influences is great enough, it will also "fire". That is to say, it will create a new action potential at its axon hillock, releasing neurotransmitters and passing on the information to yet another neighboring neuron.

• Glutamate is used at the great majority of fast excitatory synapses in the brain and spinal cord. It is also used at most synapses that are "modifiable", i.e. capable of increasing or decreasing in strength. Modifiable synapses are thought to be the main memory-storage elements in the brain. Excessive glutamate release can overstimulate the brain and lead to excitotoxicity causing cell death resulting in seizures or strokes.Excitotoxicity has been implicated in certain chronic diseases including ischemic stroke, epilepsy, amyotrophic lateral sclerosis, Alzheimer's disease, Huntington disease, and Parkinson's disease.
• GABA is used at the great majority of fast inhibitory synapses in virtually every part of the brain. Many sedative/tranquilizing drugs act by enhancing the effects of GABA. Correspondingly, glycine is the inhibitory transmitter in the spinal cord.
• Acetylcholine was the first neurotransmitter discovered in the peripheral and central nervous systems. It activates skeletal muscles in the somatic nervous system and may either excite or inhibit internal organs in the autonomic system.It is distinguished as the transmitter at the neuromuscular junction connecting motor nerves to muscles. The paralytic arrow-poison curare acts by blocking transmission at these synapses. Acetylcholine also operates in many regions of the brain, but using different types of receptors, including nicotinic and muscarinic receptors.

ROLE OF NEUROTRANSMITTER IN MUSCLE

neurotransmitter are present in the neuromuscular junction of the muscle

when an action potential is reached the neuromuscular junction through a motor neuron.in thhe terminal of the pre synaptic neuron axon their will influx of calcium ion into the axonal terminal.this will activate the synaptic vesicle containing excitatory or inhibitory neuron. this vesicle move towards the pre synaptic membrane and the neurotransmiter are released in to the synapticc cleft.this neurotransnitter bind with the receptors on the post synaptic membrane.it will produce an action potential in the muscle. this further causes teh muscl contraction

3) The sliding filament theory explains the mechanism of muscle contraction based on muscle proteins that slide past each other to generate movement. According to the sliding filament theory, the myosin (thick) filaments of muscle fibers slide past the actin (thin) filaments during muscle contraction, while the two groups of filaments remain at relatively constant length.

1. the backbone of a muscle fibre is actin filaments which extend from Z line up to one end of H zone, where they are attached to an elastic component which they named S filament;
2. myosin filaments extend from one end of the A band through the H zone up to the other end of the A band;
3. myosin filaments remain in relatively constant length during muscle stretch or contraction;
4. if myosin filaments contract beyond the length of the A band, their ends fold up to form contraction bands;
5. myosin and actin filaments lie side-by-side in the A band and in the absence of ATP they do not form cross-linkages;
6. during stretching, only the I bands and H zone increase in length, while A bands remain the same;
7. during contraction, actin filaments move into the A bands and the H zone is filled up, the I bands shorten, the Z line comes in contact with the A bands; and
8. the possible driving force of contraction is the actin-myosin linkages which depend on ATP hydrolysis by the myosin.