There is no cure for GSS, nor is there any known treatment to slow the progression of the disease. However, therapies and medication are aimed at treating or slowing down the effects of the symptoms. Their goal is to try to improve the patient's quality of life as much as possible. Despite there being no cure for GSS, it is possible to undergo testing for the presence of the underlying genetic mutation. Testing for GSS involves a blood and DNA examination in order to attempt to detect the mutated gene at certain codons. If the genetic mutation is present, the patient will eventually be afflicted by GSS, and, due to the genetic nature of the disease, the offspring of the patient are predisposed to a higher risk of inheriting the mutation.

There is no cure or treatment for GSS. It can, however, be identified through genetic testing. GSS is the slowest to progress among human prion diseases. Duration of illness can range from 3 months to 13 years, with an average duration of 5 or 6 years.

An average clinical profile from published studies shows that the median onset age for HDLS patients is 44.3 years with a mean disease duration of 5.8 years and mean age of death at 53.2 years. As of 2012, there have been around 15 cases identified with at least 11 sporadic cases of HDLS. HDLS cases have been located in Germany, Norway, Sweden, and the United States, showing an international distribution focusing between Northern Europe and the United States.

Through the study of numerous kindred, it was found that the disease did not occur among just males or females, but rather was evenly distributed indicative of an autosomal rather than a sex-linked genetic disorder. It was also observed that the HDLS cases did not skip generations as it would occur with a recessive inheritance, and as such has been labeled autosomal dominant.

Exercise in middle age may reduce the risk of Parkinson's disease later in life. Caffeine also appears protective with a greater decrease in risk occurring with a larger intake of caffeinated beverages such as coffee. People who smoke cigarettes or use smokeless tobacco are less likely than non-smokers to develop PD, and the more they have used tobacco, the less likely they are to develop PD. It is not known what underlies this effect. Tobacco use may actually protect against PD, or it may be that an unknown factor both increases the risk of PD and causes an aversion to tobacco or makes it easier to quit using tobacco.

Antioxidants, such as vitamins C and E, have been proposed to protect against the disease, but results of studies have been contradictory and no positive effect has been proven. The results regarding fat and fatty acids have been contradictory, with various studies reporting protective effects, risk-increasing effects or no effects. There have been preliminary indications that the use of anti-inflammatory drugs and calcium channel blockers may be protective. A 2010 meta-analysis found that nonsteroidal anti-inflammatory drugs (apart from aspirin), have been associated with at least a 15 percent (higher in long-term and regular users) reduction of incidence of the development of Parkinson's disease.

Binswanger's disease has no cure and has been shown to be the most severe impairment of all of the vascular dementias. The best way to manage the vascular risk factors that contribute to poor perfusion in the brain is to treat the cause, such as chronic hypertension or diabetes. It has been shown that current Alzheimer’s medication, donepezil (trade name Aricept), may help Binswanger’s Disease patients as well . Donepezil increases the acetylcholine in the brain through a choline esterase inhibitor which deactivates the enzyme that breaks down acetylcholine. Alzheimer as well as Binswanger patients have low levels of acetylcholine and this helps to restore the normal levels of neurotransmitters in the brain. This drug may improve memory, awareness, and the ability to function. If no medical interception of the disease is performed then the disease will continue to worsen as the patient ages due to the continuing atrophy of the white matter from whatever was its original cause.

The Huntington's disease-like syndromes (often abbreviated as HD-like or "HDL" syndromes) are a family of inherited neurodegenerative diseases that closely resemble Huntington's disease (HD) in that they typically produce a combination of chorea, cognitive decline or dementia and behavioural or psychiatric problems.

Currently, there is no cure for FTD. Treatments are available to manage the behavioral symptoms. Disinhibition and compulsive behaviors can be controlled by selective serotonin reuptake inhibitors (SSRIs). Although Alzheimer's and FTD share certain symptoms, they cannot be treated with the same pharmacological agents because the cholinergic systems are not affected in FTD.

Because FTD often occurs in younger people (i.e. in their 40's or 50's), it can severely affect families. Patients often still have children living in the home. Financially, it can be devastating as the disease strikes at the time of life that often includes the top wage-earning years.

Personality changes in individuals with FTD are involuntary. Managing the disease is unique to each individual, as different patients with FTD will display different symptoms, sometimes of rebellious nature.

Although cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes, and smoking, are associated with a higher risk of onset and course of AD, statins, which are cholesterol lowering drugs, have not been effective in preventing or improving the course of the disease.

Long-term usage of non-steroidal anti-inflammatory drugs (NSAIDs) is associated with a reduced likelihood of developing AD. Evidence also supports the notion that NSAIDs can reduce inflammation related to amyloid plaques. No prevention trial has been completed. They do not appear to be useful as a treatment. Hormone replacement therapy in menopause, although previously used, may increase the risk of dementia.

There is currently no effective treatment or cure for PSP, although some of the symptoms can respond to nonspecific measures. The average age at symptoms onset is 63 and survival from onset averages 7 years with a wide variance. Pneumonia is a frequent cause of death.

Repetitive transcranial magnetic stimulation temporarily improves levodopa-induced dyskinesias. Its usefulness in PD is an open research topic, Several nutrients have been proposed as possible treatments; however there is no evidence that vitamins or food additives improve symptoms. There is no evidence to substantiate that acupuncture and practice of Qigong, or T'ai chi, have any effect on the course of the disease or symptoms. Fava beans and velvet beans are natural sources of levodopa and are eaten by many people with PD; their intake is not free of risks as life-threatening adverse reactions have been described, such as the neuroleptic malignant syndrome.

There is no cure for Alzheimer's disease; available treatments offer relatively small symptomatic benefit but remain palliative in nature. Current treatments can be divided into pharmaceutical, psychosocial and caregiving.

Some hypotheses as to the cause of the disease include genetics, cycad seeds, and ingested beta-Methylamino-L-alanine (BMAA) from the consumption of fruit bats.

Riluzole has been found to modestly prolong survival by approximately two to three months. It may have a greater survival benefit for those with a bulbar onset. It is approved by the US Food and Drug Administration (FDA) and recommended by the National Institute for Health and Care Excellence (NICE) (England and Wales). Riluzole does not reverse damage already done to motor neurons but affects neurons by reducing their activity through blocking Na+ entrance into the neurons and thus blocking the release of the chemicals that causes the activity of the motor neurons. The reduction in activity prevents the ruining of the neuronal muscle and so the drug can act as a protective chemical. Studies have shown that the function of this drug is dependent on the amount taken at a given time. The higher the concentration, the better the drug will protect the neurons from ruin. The recommended dosage of Riluzole is 50 mg, twice a day for people with known ALS for more than 5 years.

There are a number of side effects caused by the drug including the feeling of weakness in muscles but this is normal due to the function of the drug. Studies have shown that people on the drug are not likely to stop responding to it or develop symptoms that might cause the activity of neurons to rise again, making Riluzole an effective drug for prolonging survival.

In 2015, edaravone was approved in Japan for treatment of ALS after studying how and whether it works on 137 people with ALS and has obtained orphan drug status in the EU and USA. On May 5, 2017, the FDA approved edaravone to extend the survival period of people with ALS. It costs about 145,000 USD per year in the US and 35,000 USD per year in Japan.

Other medications may be used to help reduce fatigue, ease muscle cramps, control spasticity, and reduce excess saliva and phlegm. Drugs also are available to help people with pain, such as non-steroidal and anti-inflammatory drugs and opioids, depression, sleep disturbances, dysphagia, and constipation. Baclofen and diazepam are often prescribed to control the spasticity caused by ALS, and trihexyphenidyl, amitriptyline or most commonly glycopyrrolate may be prescribed when people with ALS begin having trouble swallowing their saliva. There is no evidence that medications are effective at reducing muscle cramps experienced by people with ALS.

Frontotemporal lobar degeneration (FTLD) is a pathological process that occurs in frontotemporal dementia. It is characterized by atrophy in the frontal lobe and temporal lobe of the brain, with sparing of the parietal and occipital lobes.

Common proteinopathies that are found in FTLD include the accumulation of Tau proteins and TARDBPs. Mutations in the C9orf72 gene have been established as a major genetic contribution of FTLD, although defects in the GRN and MAPT genes are also associated with it.

Hereditary diffuse leukoencephalopathy with spheroids (HDLS) is a rare adult onset autosomal dominant disorder characterized by cerebral white matter degeneration with demyelination and axonal spheroids leading to progressive cognitive and motor dysfunction. Spheroids are axonal swellings with discontinuous or absence of myelin sheaths. It is believed that the disease arises from primary microglial dysfunction that leads to secondary disruption of axonal integrity, neuroaxonal damage, and focal axonal spheroids leading to demyelination. Spheroids in HDLS resemble to some extent those produced by shear stress in a closed head injury with damage to axons, causing them to swell due to blockage of axoplasmic transport. In addition to trauma, axonal spheroids can be found in aged brain, stroke, and in other degenerative diseases. In HDLS, it is uncertain whether demyelination occurs prior to the axonal spheroids or what triggers neurodegeneration after apparently normal brain and white matter development, although genetic deficits suggest that demyelination and axonal pathology may be secondary to microglial dysfunction. The clinical syndrome in patients with HDLS is not specific and it can be mistaken for Alzheimer's disease, frontotemporal dementia, atypical Parkinsonism, multiple sclerosis, or corticobasal degeneration.

Familial encephalopathy with neuroserpin inclusion bodies (FENIB) is a progressive disorder of the nervous system that is characterized by a loss of intellectual functioning (dementia) and seizures. At first, affected individuals may have difficulty sustaining attention and concentrating. Their judgment, insight, and memory become impaired as the condition progresses. Over time, they lose the ability to perform the activities of daily living, and most people with this condition eventually require comprehensive care.

The signs and symptoms of familial encephalopathy with neuroserpin inclusion bodies vary in their severity and age of onset. In severe cases, the condition causes seizures and episodes of sudden, involuntary muscle jerking or twitching (myoclonus) in addition to dementia. These signs can appear as early as a person's teens. Less severe cases are characterized by a progressive decline in intellectual functioning beginning in a person's forties or fifties.

Mutations in the "SERPINI1" gene cause familial encephalopathy with neuroserpin inclusion bodies. The "SERPINI1" gene provides instructions for making a protein called neuroserpin. This protein is found in nerve cells, where it plays a role in the development and function of the nervous system. Neuroserpin helps control the growth of nerve cells and their connections with one another, which suggests that this protein may be important for learning and memory. Mutations in the gene result in the production of an abnormally shaped, unstable version of neuroserpin. Abnormal neuroserpin proteins can attach to one another and form clumps (called neuroserpin inclusion bodies or Collins bodies) within nerve cells. These clumps disrupt the cells' normal functioning and ultimately lead to cell death. Progressive dementia results from this gradual loss of nerve cells in certain parts of the brain. Researchers believe that a buildup of related, potentially toxic substances in nerve cells may also contribute to the signs and symptoms of this condition.

This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In many cases, an affected person has a parent with the condition.

Pharmaceutical management, as with Parkinson's disease, involves striking a balance between treating the motor, emotive, and cognitive symptoms. Motor symptoms appear to respond somewhat to the medications used to treat Parkinson's disease (e.g. levodopa), while cognitive issues may improve with medications for Alzheimer's disease such as donepezil. Medications used in the treatment of ADHD (e.g. methylphenidate) might improve cognition or daytime sleepiness; however, medications for both Parkinson's disease and ADHD increase levels of the chemical dopamine in the brain, so increase the risk of hallucinations with those classes of pharmaceuticals.

Treatment of the movement and cognitive portions of the disease may worsen hallucinations and psychosis, while treatment of hallucinations and psychosis with antipsychotics may worsen parkinsonian or ADHD symptoms in DLB, such as tremor or rigidity and lack of concentration or impulse control. Physicians may find the use of cholinesterase inhibitors represents the treatment of choice for cognitive problems and donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl) may be recommended as a means to help with these problems and to slow or prevent the decline of cognitive function. DLB may be more responsive to donepezil than Alzheimer's disease. Memantine also may be useful. Levocarb may help with movement problems, but in some cases, as with dopamine agonists, may tend to aggravate psychosis in people with DLB. Clonazepam may help with rapid eye movement behavior disorder; table salt or antihypotensive medications may help with fainting and other problems associated with orthostatic hypotension. Botulinum toxin injections in the parotid glands may help with sialorrhea. Other medications, especially stimulants such as the ADHD drug methylphenidate (Ritalin) and modafinil, may improve daytime alertness, but as with the antiparkinsonian drug Levocarb, antihyperkinetics such as Ritalin increase the risk of psychosis. Experts advise extreme caution in the use of antipsychotic medication in people with DLB because of their sensitivity to these agents. When these medications must be used, atypical antipsychotics are preferred to typical antipsychotics; a very low dose should be tried initially and increased slowly, and patients should be carefully monitored for adverse reactions to the medications.

Due to hypersensitivity to neuroleptics, preventing DLB patients from taking these medications is important. People with DLB are at risk for neuroleptic malignant syndrome, a life-threatening illness, because of their sensitivity to these medications, especially the older typical antipsychotics, such as haloperidol. Other medications, including medications for urinary incontinence and the antihistamine medication diphenhydramine (Benadryl), also may worsen confusion.

Several international organizations serve the needs of patients with PSP and their families and support research. The Foundation for PSP, CBD and Related Brain Diseases is based in the US and the PSP Association is based in the UK. The PSP-France association is based in Paris. With the help of the CurePSP Association based in the United States, in 2014/15 Canada will have its own CUREPSP organization.

No cure for dementia with Lewy bodies is known. Treatment may offer symptomatic benefit, but remains palliative in nature. Current treatment modalities are divided into pharmaceutical and caregiving.

Management of ALS attempts to relieve symptoms and extend life expectancy. This supportive care is best provided by multidisciplinary teams of healthcare professionals working with the person and their caregivers to keep them as mobile and comfortable as possible.

Symptoms of frontotemporal dementia progress at a rapid, steady rate. Patients suffering from the disease can survive between 2–15 years. Eventually patients will need 24-hour care for daily function.

CSF leaks are a known cause of reversible frontotemporal dementia.

HDL1 is an unusual, autosomal dominant familial prion disease. Only described in one family, it is caused by an eight-octapeptide repeat insertion in the "PRNP" gene. More broadly, inherited prion diseases in general can mimic HD.

A complete recovery following immunotherapy and tumor removal. Untreated cases died within few months of onset. Some patients have a poor outcome despite sustained immunosuppression, but that is often related to tumor progression or associated with the presence of Abs directed against intracellular Ags such as GAD Abs or amphyphysin Abs, which can reflect the involvement of an additional cytotoxic T-cell mechanism in the progression of the disease.

Lytico-bodig disease, sometimes spelled Lytigo-bodig, is the name of a disease in the language of Chamorro. It is referred to by neuroscientists as amyotrophic lateral sclerosis-parkinsonism-dementia (ALS-PDC), a term coined by Asao Hirano and colleagues in 1961. It is a neurodegenerative disease of uncertain etiology that exists in the United States territory of Guam.

The disease resembles Amyotrophic Lateral Sclerosis (ALS), Parkinson's disease, and Alzheimer's. First reports of the disease surfaced in three death certificates on Guam in 1904. These death certificates made some mention of paralysis. The frequency of cases grew amongst the Chamorro people on Guam until it was the leading cause of adult death between 1945 and 1956. The incidence rate was 200 per 100,000 per year and it was 100 times more prevalent than in the rest of the world.

Neurologist Oliver Sacks detailed this disease in his book "The Island of the Colorblind"

. Sacks and Paul Alan Cox subsequently wrote that a local species of flying fox, which is now extinct due to overhunting, had been feeding on cycads and concentrating β-methylamino--alanine (BMAA), a known neurotoxin, in its body fat. The hypothesis suggests that consumption of the fruit bat by the Chamorro exposed them to BMAA, contributing to or causing their condition. Decline in consumption of the bats has been linked to a decline in the incidence of the disease.

A number of factors can decrease the risk of dementia. A group of efforts is believed to be able to prevent a third of cases and include early education, treating high blood pressure, preventing obesity, preventing hearing loss, treating depression, being active, preventing diabetes, not smoking, and preventing social isolation.

Among otherwise healthy older people, computerized cognitive training may improve memory. However it is not known if it prevents dementia. Short term exercise has limited evidence. In those with normal mental function evidence for medications is poor. The same applies to supplements.