Why is there no cure for dementia?

Dementia is caused by damage to the vascular infrastructure in the brain that has gradually built up there over many years. Vascular dementia occurs when the blood supply to part of the brain is cut off and a lack of oxygen causes the destruction of neurons. Also, the pumping mechanism for circulating cerebrospinal fluid (CSF) throughout the brain to cleanse it of toxins piggybacks on the pulsating expansion and contraction of healthy elastic arteries. 

When damaged arteries harden and lose elasticity, the pumping and circulation of CSF becomes compromised and no longer properly cleanses the brain of toxins which then destroy neurons to cause onset of Alzheimer’s disease. Neither type of dementia can be cured because it is impossible to repair the vascular damage.

Reference: John Dorey

What are the neural bases (causes) of mental diseases such as psychotic disorders (e.g. mania, schizophrenia), Parkinson's disease, and Alzheimer's disease?

They all have neurochemical bases (neurotransmitters).Yours is a very broad question, so I'll just address one I know best, Alzheimer's.

Alzheimer's is generally caused by problems with acetylcholine (ACh), a major neurotransmitter of the peripheral nervous system, parasympathetic nervous system, and gads of other systems in the body.

With Alzheimer's, cortical neurons and cholinergic neurons (ACh-releasing neurons) degenerate in major cholinergic pathways, particularly in the basal nucleus of Meynert, which projects to the entire neocortex, and the striatum (caudate nucleus and putamen), which contains ACh in its circuit neurons.

The disease is associated with a 60-90% loss of choline acetyltransferase (ChAT) in the cerebral cortex, which is the enzyme responsible for the production of ACh, due to the increasing absence of the aforementioned major cholinergic pathways.

Studies have also shown that on a histological-basis, Alz. is characterized by the presence of:

Neurofibrillary tangles (NFTs) in neurons, which are essentially degenerated neurofilaments that have preternatural clumps of the tauprotein,

Senile (or neuritic) plaques, which are degenerated nerve cell processes made of abnormal clusters of beta-amyloid protein chunks (which contribute to the relatively large aggregate of Hirano bodies in the hippocampus), and

The shrinkage of connections between neurons in the brain, which means there are few nerve cells and synapses.

As you can see, acetylcholine plays a huge role in Alzheimer's. However, it also has a huge role in myasthenia gravis and basic brain function.

Reference: Hannah Cho

Why don't brain cells regenerate?

Cells don’t often regenerate. In some animals, limbs regenerate, and some parts of the human body, such as the ends of the fingers, can regenerate. Such regeneration almost always results from the production of replacement cells.

Cells are replaced by production of stem cells and, most commonly, precursor cells that are derived from stem cells. Once a cell becomes specialized for a specific purpose, it generally loses the ability to divide. This loss is induced so that higher level processes can decide the lifetimes of various types of cells.

One exception to this lifetime rule is neurons, which are constructed of multiple compartments, allowing a compartment to die without dooming the whole cell. However, when a compartment dies, it is usually not replaced since there is no master plan which would guide its regeneration. The exception to this is that neurons in a neural sheathe (a nerve fiber), mostly peripheral system neurons, can extend a regenerated compartment within the sheathe and grow to the end of the sheathe, and may be lucky enough to reconnect there. There are no neural sheathes in the brain.

Another exception to the lifetime rule is cancer, where stem cells, precursor cells, and ordinary cells, can be modified by the cancer to allow mitosis. This fuels the characteristic runaway growth seen in cancer. It is also the reason most cell growth is limited to the smaller number of precursor cells rather than delegated to all cells, since the odds of a random mutation are less likely to be propagated.

Brain cells don’t regenerate because all their value is in their connections, so once they die (or a compartment dies), connection information is lost. This also contributes to the relative rarity of brain cancer.

It is reported (and likely) that precursor cells create new neurons in the hippocampus, and there is also strong evidence of new neurons in the cerebellum. This is not regeneration, but new growth. The hippocampus and cerebellum contain processes that exploit new neurons, and this creation seems to support both of their jobs of learning.

Reference: John Light

What areas of the brain are thought to be involved in depression?

Increasingly sophisticated types of mind imaging - such as for example positron emission tomography (Dog), single-photon emission computed tomography (SPECT), and practical magnetic resonance imaging (fMRI) - enable a much nearer go through the working mind than was feasible before. An fMRI check out, for instance, can track modifications that happen when an area of the mind responds during numerous tasks. A Dog or SPECT check-out can map the mind by calculating the submission and denseness of neurotransmitter receptors using areas.

Usage of this technology offers led to a much better knowledge of which brain areas regulate mood and exactly how other functions, such as for example memory, could be affected by depressive disorders. Areas that have fun with a significant part in depression will be the amygdala, the thalamus, as well as the hippocampus.

Research demonstrates the hippocampus will be smaller in a few depressed people. For instance, in a single fMRI study released within the Journal of Neuroscience, researchers studied 24 ladies who had a brief history of depression. Normally, the hippocampus has been 9% to 13% smaller sized in depressed ladies compared with people who were not stressed out. The more rounds of depression a female had, small the hippocampus. Tension, which is important in depression, might be a key factor right here since experts think stress can control the manufacturing of fresh neurons (nerve tissues) within the hippocampus.

Researchers are discovering possible hyperlinks between sluggish manufacturing of fresh neurons within the hippocampus and reduced moods. A fascinating truth about antidepressants facilitates this concept. These medications instantly boost the focus of chemical substance messengers in the mind (neurotransmitters). Yet individuals typically don't commence to feel better for a number of weeks or more time. Experts have long wondered why, if depressive disorders were primarily the consequence of low degrees of neurotransmitters, individuals don't feel much better when degrees of neurotransmitters increase.

Reference: Grace Camerom

What are the best treatments for Multiple Sclerosis?

Multiple Sclerosis (MS) is a disabling disease in which brain and spinal cord (central nervous system) are potentially damaged.
Basically, the immune system attacks the protective sheath that covers nerve fibres and develops communication problems between your brain and the rest of the body.

Eventually, this causes physical, mental and sometimes, psychiatric problems that are concluded as the signs and symptoms of MS. Though, it also depends on the amount of nerve damage. Hence, the person loses the ability to walk independently.

Other symptoms are as follows:

1.      Weakness in one or more limbs

2.      Painful eye movement, partial or complete loss of vision - Vision problems

3.      Fatigue

4.      Dizziness

5.      Chronic pain

6.      Problems with speech or swallowing

Treatment

There is no particular cure for MS. The treatment mainly focuses on speedy recovery from attacks, slowing down the progression of MS and trying to lessen the impact of MS symptoms. In some cases, MS is quite mild that treatment isn’t possible.

Multiple Treatments

1.      Corticosteroids such as oral prednisone and intravenous methylprednisolone, are prescribed to relief the inflamed areas of the body and reduces swelling, itching, redness and other allergic diseases. Though one could suffer insomnia, fluctuation in blood pressure, and mood swings.

2.      Plasma exchange (plasmapheresis) In this procedure, the liquid part of the blood is removed and separated from your blood cells. These blood cells are then mixed with a protein solution, albumin and put back in the body. This treatment could make a positive impact if you are a sufferer just a few days back.

Ocrelizumab (Ocrevus) is the only FDA-approved disease-modifying therapy for primary-progressive MS. This antibiotic slowdowns the worsening condition of the patient, though doesn’t cure fully.

Other Treatments

1.      Physical Therapy: In this procedure, a physical therapist helps the patient in stretching exercises that should be done on daily basis. It aids in managing leg numbness or weakness.

2.      Muscle Relaxtants: As you may experience stiffness in your legs. In this case, you may be prescribed to have baclofen (Lioresal) and tizanidine (Zanaflex).

3.      Other Medications: You are also prescribed medicines that may reduce fatigue to some extent, for depression, pain, bowel control problems or sexual dysfunction, associated with MS.

Change in Life-style

Like every other disease, you must follow a good lifestyle in MS as well.

1.      You are advised to get proper rest.

2.      Regular exercise helps improve your strength, coordination, muscle tone. Swimming could be a good option as well.

3.      Its symptoms could make you short-tempered. You should avoid exposure to sun, heat and use cooling devices such as cooling scarves, etc.

4.      Follow a regular balanced diet low in saturated fats and high in omega-3 fatty acids.

 Reference: Komal Khera

What are some activities that can lower the advancement of Alzheimer's or dementia?

HIGHEST PROBABILITY FOR CAUSES OF ALZHEIMER’S AND PARKINSON’S DISEASE

1. ANTIDEPRESSANTS, ANTIMUSCARINIC, ANTIHISTAMINE USE

2. LACK OF EXERCISE

3. DEPRESSION

4. NEGATIVE THOUGHTS ON AGING

5. EXPOSURE TO LEAD

6. HIGH BLOOD PRESSURE

7. EXPOSURE TO INSECTICIDES

8. HEAD TRAUMA/ UNCONSCIOUS FOR MORE THAN 24 HOURS

9. DIABETES

10. LONELINESS

11. SLEEP DEPRIVATION/APNEA

12. FAMILY HISTORY/GENETICS (APOLIPOPROTEIN GENE)

13. DOWN’S SYNDROME

14. CARDIOVASCULAR DISEASE/STROKE

15. ROSACEA/AUTOIMMUNE DISORDERS

16. ALCOHOL ABUSE

HOW TO IDENTIFY ONSET OF ALZHEIMER’S DISEASE

1. Worsened ability to take in and remember new information, for example:

§ "Repetitive questions or conversations

§ Misplacing personal belongings

§ Forgetting events or appointments

§ Getting lost on a familiar route."

2. Impairments to reasoning, complex tasking, exercising judgment:

§ "Poor understanding of safety risks

§ Inability to manage finances

§ Poor decision-making ability

§ Inability to plan complex or sequential activities."

3. Impaired visuospatial abilities (but not, for example, due to eye sight problems):

§ "Inability to recognize faces or common objects or to find objects in direct view

§ Inability to operate simple implements, or orient clothing to the body."

4. Impaired speaking, reading and writing:

§ "Difficulty thinking of familiar words while speaking, hesitations

§ Speech, spelling, and writing errors."

5. Changes in personality and behaviour, for example:

§ Out-of-character mood changes, including agitation; less interest, motivation or initiative; apathy; social withdrawal

§ Loss of empathy

§ Compulsive, obsessive or socially unacceptable behaviour.

Once the number and severity of these example symptoms confirm dementia, the best certainty that they are because of Alzheimer's disease is given by:

§ A gradual onset "over months to years" rather than hours or days (the case with some other problems)

§ A marked worsening of the individual person's normal level of cognition in particular areas.11

The most common presentation marking Alzheimer's dementia is where symptoms of memory loss are the most prominent, especially in learning and recalling new information. But the initial presentation can also be one of mainly language problems, in which case the greatest symptom is struggling to find the right words

Reference: Samuel Shepherd

Parkinson's disease is caused by the loss of dopamine production. Are there other diseases that affect different neurotransmitters similarly?

I would be cautious with saying that Parkinson’s disease (PD) is caused by the loss of dopamine production. The pathogenesis of PD is rather complex and not yet quite understood. But let’s say the majority of the symptoms in PD can be attributed to the degeneration of dopaminergic neurons in substantia nigra (SNpc).

There are quite a few diseases with disturbances in neurotransmitter production. Here are some examples:

Huntington’s disease is characterized by the degeneration of neurons predominantly in another part of the basal ganglia - the striatum, where neurons producing gamma-Aminobutyric acid (GABA) are preferentially affected. GABA is an inhibitory neurotransmitter, and reduction in its content results in uncontrolled movement, known as chorea.

Reduction in GABA-mediated inhibition also plays a role in epilepsy.

Acetylcholine (ACh) is a neurotransmitter implicated in learning and memory processing, and cholinergic neurons (among others) are severely affected by Alzheimer’s disease. 

 Perhaps most famously, reduction in serotonin signalling is a factor in major depression, evidenced best by the effectiveness of serotonin reuptake inhibitors in treatment of depression.

Reference: Minja Belić