Currently, there is no cure for laminopathies and treatment is largely symptomatic and supportive. Physical therapy and/or corrective orthopedic surgery may be helpful for patients with muscular dystrophies. Cardiac problems that occur with some laminopathies may require a pacemaker. Treatment for neuropathies may include medication for seizures and spasticity.

The recent progress in uncovering the molecular mechanisms of toxic progerin formation in laminopathies leading to premature aging has opened up the potential for the development of targeted treatment. The farnesylation of prelamin A and its pathological form progerin is carried out by the enzyme farnesyl transferase. Farnesyl transferase inhibitors (FTIs) can be used effectively to reduce symptoms in two mouse model systems for progeria and to revert the abnormal nuclear morphology in progeroid cell cultures. Two oral FTIs, lonafarnib and tipifarnib, are already in use as anti-tumor medication in humans and may become avenues of treatment for children suffering from laminopathic progeria. Nitrogen-containing bisphosphate drugs used in the treatment of osteoporosis reduce farnesyldiphosphate production and thus prelamin A farnesylation. Testing of these drugs may prove them to be useful in treating progeria as well. The use of antisense oligonucleotides to inhibit progerin synthesis in affected cells is another avenue of current research into the development of anti-progerin drugs.

No treatment has yet proven effective. Most treatment options have focused on reducing complications (such as cardiovascular disease) with coronary artery bypass surgery and low-dose aspirin.

Growth hormone treatment has been attempted. The use of Morpholinos has also been attempted in mice and cell cultures in order to reduce progerin production. Antisense Morpholino oligonucleotides specifically directed against the mutated exon 11–exon 12 junction in the mutated pre-mRNAs were used.

A type of anticancer drug, the farnesyltransferase inhibitors (FTIs), has been proposed, but their use has been mostly limited to animal models. A Phase II clinical trial using the FTI lonafarnib began in May 2007. In studies on the cells another anti-cancer drug, rapamycin, caused removal of progerin from the nuclear membrane through autophagy. It has been proved that pravastatin and zoledronate are effective drugs when it comes to the blocking of farnesyl group production.

Farnesyltransferase inhibitors (FTIs) are drugs that inhibit the activity of an enzyme needed in order to make a link between progerin proteins and farnesyl groups. This link generates the permanent attachment of the progerin to the nuclear rim. In progeria, cellular damage can occur because that attachment takes place and the nucleus is not in a normal state. Lonafarnib is an FTI, which means it can avoid this link, so progerin can not remain attached to the nucleus rim and it now has a more normal state.

Studies of sirolimus, an mTOR Inhibitor, demonstrate that it can minimize the phenotypic effects of progeria fibroblasts. Other observed consequences of its use are: abolishment of nuclear blebbing, degradation of progerin in affected cells and reduction of insoluble progerin aggregates formation. These results have been observed only "in vitro" and are not the results of any clinical trial, although it is believed that the treatment might benefit HGPS patients.

The delivery of lonafarnib is not approved by the US Food and Drug Administration (FDA). Therefore, it can only be used in certain clinical trials. Until treatment with FTIs is thoroughly tested in progeria children in clinical trials, its effects on humans cannot be known, although its effects on mice seem to be positive. A 2012 clinical trial found that it improved weight gain and other symptoms of progeria.

At least one study suggests that gluten neuropathy can be effectively treated with a gluten-free diet. In the study, 35 patients with gluten neuropathy adhered to a gluten-free diet, where adherence was monitored serologically. After one year, the treatment group had improved significantly compared to the control group. The indicators of improvements were improvements of sural sensory action potential and subjective improvement of neuropathic symptoms. Subgroup analysis suggested that severe neuropathy might imply reduced capacity for recovery of the peripheral nerves or longer recovery.

Variably protease-sensitive prionopathy (VPSPr) (formerly known as Protease Sensitive Prionopathy) is a sporadic prion protein disease identified in 2008 and first described in 2010 by Zou W.Q. and coworkers from the United States National Prion Disease Pathology Surveillance Center.

VPSPr is very rare, occurring in just 2 or 3 out of every 100 million people. (Nine cases had been identified in the UK by 2013.) It has similarities to Creutzfeldt–Jakob disease, but clinical manifestations differ somewhat, and the abnormal prion protein (PrP) is less resistant to digestion by proteases; some variants are more sensitve to proteases than others, hence the name: variably protease-sensitive.

Patients present with psychiatric symptoms, speech deficits (aphasia and/or dysarthria), and cognitive impairment. Ataxia and parkinsonism can develop. Average age at onset is 70 years, and duration of survival is 24 months. About 40% of patients have a family history of dementia.

Diagnosis is difficult. MRI, EEG, and tests for 14-3-3 protein and tau protein are usually not helpful, and no mutations have been observed in the coding region of the PrP gene.

There is no known cure at the moment but there are several things that can be done to relieve the symptoms. Moisturising products are very helpful to minimize the scaling/cracking, and anti-infective treatments are useful when appropriate because the skin is very susceptible to infection. Extra protein in the diet during childhood is also beneficial, to replace that which is lost through the previously mentioned "leaky" skin.

Steroid and retinoid products have been proven ineffective against Netherton syndrome, and may in fact make things worse for the affected individual.

Intravenous immunoglobulin has become established as the treatment of choice in Netherton's syndrome. This therapy reduces infection; enables improvement and even resolution of the skin and hair abnormalities, and dramatically improves quality of life of the patients; although exactly how it achieves this is not known. Given this; it is possible that the reason Netherton's usually is not very severe at or shortly after birth is due to a protective effect of maternal antibodies; which cross the placenta but wane by four to six months.

Anti-epileptic drugs are normally used to combat ADNFLE. These drugs are discussed in the main epilepsy article.

Not all affected patients seem to need a regular preventive plasma infusion therapy, especially as some reach longterm remission without it. Regular plasma infusions are necessary in patients with frequent relapses and in general situations with increased risk to develop an acute episode (as seen above) such as pregnancy. Plasma infusions are given usually every two to three weeks to prevent acute episodes of USS but are often individually adapted.

The therapy of an acute TTP episode has to be started as early as possible. The standard treatment is the daily replacement of the missing ADAMTS13 protease in form of plasma infusions or in more severe episodes by plasma exchange. In the latter the patients plasma is replaced by donated plasma. The most common sources of ADAMTS13 is platelet-poor fresh frozen plasma (FFP) or solvent-detergent plasma.

The benefit of plasma exchange compared to plasma infusions alone may result from the additional removal of ULVWF. In general both plasma therapies are well tolerated, several mostly minor complications may be observed. The number of infusion/exchange sessions needed to overcome a TTP episode are variable but usually take less than a week in USS. The intensive plasma-therapy is generally stopped when platelet count increases to normal levels and is stable over several days.

Reversion of lipodystrophy does not occur after withdrawal of protease inhibitors.

GHRH analogs such as tesamorelin can be used to treat HIV-associated lipodystrophy.

A slow virus is a virus, or a viruslike agent, etiologically associated with a disease, having a long incubation period of months to years and then a gradual onset of symptoms which progress slowly but irreversibly and terminate in a severe compromised state or, more commonly, death.

A slow virus disease is a disease that, after an extended period of latency, follows a slow, progressive course spanning months to years, frequently involving the central nervous system and ultimately leading to death. Examples include the Visna-Maedi virus, in the genus Lentivirus (family Retroviridae), that causes encephalitis and chronic pneumonitis in sheep, and subacute sclerosing panencephalitis which is apparently caused by the measles virus, as well as Paget's Disease of Bone (Osteitis Deformans) which is associated with paramyxoviridae, especially RSV and Rubeola (Measles).

As there is no known cure, few people with progeria exceed 13 years of age. At least 90% of patients die from complications of atherosclerosis, such as heart attack or stroke.

Mental development is not adversely affected; in fact, intelligence tends to be average to above average. With respect to the features of aging that progeria appears to manifest, the development of symptoms is comparable to aging at a rate eight to ten times faster than normal. With respect to features of aging that progeria does not exhibit, patients show no neurodegeneration or cancer predisposition. They also do not develop conditions that are commonly associated with aging, such as cataracts (caused by UV exposure) and osteoarthritis.

Although there may not be any successful treatments for progeria itself, there are treatments for the problems it causes, such as arthritic, respiratory, and cardiovascular problems. Sufferers of progeria have normal reproductive development and there are known cases of women with progeria who had delivered healthy offspring.

Gluten-sensitive idiopathic neuropathies are apparently sporadic neuropathy of unknown cause in the absence of an alternative cause and where there is serological evidence of gluten sensitivity.

Treatment of lung disease may include bronchodilators, inhaled steroids, and when infections occur antibiotics. Intravenous infusions of the A1AT protein or in severe disease lung transplantation may also be recommended. In those with severe liver disease liver transplantation may be an option. Avoiding smoking and vaccination for influenza, pneumococcus, and hepatitis is also recommended.

Neither the combination of antivirals and interferons (ribavirin + interferon alfa-2a or interferon alfa-2b) nor corticosteroids improved outcomes.

When rhesus macaques were given interferon-α2b and ribavirin and exposed to MERS, they developed less pneumonia than control animals. Five critically ill people with MERS in Saudi Arabia with ARDS and on ventilators were given interferon-α2b and ribavirin but all ended up dying of the disease. The treatment was started late in their disease (a mean of 19 days after hospital admission) and they had already failed trials of steroids so it remains to be seen whether it may have benefit earlier in the course of disease. Another proposed therapy is inhibition of viral protease or kinase enzymes. Researchers are investigating a number of ways to combat the outbreak of Middle East respiratory syndrome coronavirus, including using interferon, chloroquine, chlorpromazine, loperamide, and lopinavir, as well as other agents such as mycophenolic acid and camostat.

People with lung disease due to A1AD may receive intravenous infusions of alpha-1 antitrypsin, derived from donated human plasma. This augmentation therapy is thought to arrest the course of the disease and halt any further damage to the lungs. Long-term studies of the effectiveness of A1AT replacement therapy are not available. It is currently recommended that patients begin augmentation therapy only after the onset of emphysema symptoms.

As of 2015 there are four IV augmentation therapy manufacturers in the United States, Canada, and several European countries. Intravenous (IV) therapies are the standard mode of augmentation therapy delivery. Researchers are exploring inhaled therapies. IV augmentation therapies are manufactured by the following companies and have been shown to be clinically identical to one another in terms of dosage and efficacy.

Augmentation therapy is not appropriate for people with liver disease; treatment of A1AD-related liver damage focuses on alleviating the symptoms of the disease. In severe cases, liver transplantation may be necessary.

A wide variety of treatment modalities are currently recommended including Immunosuppressive agents, intravenous immunoglobulins (IVIG), and antiviral agents although the effectiveness of these treatments are not well established and no specific treatment is available.

Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are a group of progressive, invariably fatal, conditions that affect the brain (encephalopathies) and nervous system of many animals, including humans. According to the most widespread hypothesis, they are transmitted by prions, though some other data suggest an involvement of a "Spiroplasma" infection. Mental and physical abilities deteriorate and myriad tiny holes appear in the cortex causing it to appear like a sponge (hence spongiform) when brain tissue obtained at autopsy is examined under a microscope. The disorders cause impairment of brain function, including memory changes, personality changes and problems with movement that worsen chronically.

Prion diseases of humans include Creutzfeldt–Jakob disease—which has four main forms, the sporadic (sCJD), the hereditary/familiar (fCJD), the iatrogenic (iCJD) and the variant form (vCJD)—Gerstmann–Sträussler–Scheinker syndrome, fatal familial insomnia, kuru, and the recently discovered variably protease-sensitive prionopathy. These conditions form a spectrum of diseases with overlapping signs and symptoms. TSEs in non-human mammals include scrapie in sheep, bovine spongiform encephalopathy (BSE)—popularly known as 'mad cow's disease'—in cattle and chronic wasting disease (CWD) in deer and elk. The variant form of Creutzfeldt–Jakob disease is caused by exposure to bovine spongiform encephalopathy prions.

Unlike other kinds of infectious disease, which are spread by agents with a DNA or RNA genome (such as virus or bacteria), the infectious agent in TSEs is believed to be a prion, thus being composed solely of protein material. Misshapen prion proteins carry the disease between individuals and cause deterioration of the brain. TSEs are unique diseases in that their aetiology may be genetic, sporadic, or infectious via ingestion of infected foodstuffs and via iatrogenic means (e.g., blood transfusion). Most TSEs are sporadic and occur in an animal with no prion protein mutation. Inherited TSE occurs in animals carrying a rare mutant prion allele, which expresses prion proteins that contort by themselves into the disease-causing conformation. Transmission occurs when healthy animals consume tainted tissues from others with the disease. In the 1980s and 1990s, bovine spongiform encephalopathy (BSE) spread in cattle in an epidemic fashion. This occurred because cattle were fed the processed remains of other cattle, a practice now banned in many countries. In turn, consumption (by humans) of bovine-derived foodstuff which contained prion-contaminated tissues resulted in an outbreak of the variant form of Creutzfeldt–Jakob disease in the 1990s and 2000s.

Prions cannot be transmitted through the air or through touching or most other forms of casual contact. However, they may be transmitted through contact with infected tissue, body fluids, or contaminated medical instruments. Normal sterilization procedures such as boiling or irradiating materials fail to render prions non-infective.

No specific treatment exists for Pendred syndrome. Speech and language support and hearing aids are important. Cochlear implants may be needed if the hearing loss drops to severe to profound levels and can improve language skills. If thyroid hormone levels are decreased, thyroid hormone supplements may be required. Patients are advised to take precautions against head injury.

The clinical presentation of prion diseases will vary from patient to patient. However, some general characteristics of prion diseases are listed below.

Anti-tumour necrosis factor α antagonists (e.g. infliximab)

Dietary restriction of a particular suspected or proven antigen may be involved in the management of OFG, such as cinnamon or benzoate-free diets.

In GRA, the hypersecretion of aldosterone and the accompanying hypertension are remedied when ACTH secretion is suppressed by administering glucocorticoids.

Dexamethasone, spironolactone and eplerenone have been used in treatment.

Laminopathies ("" + "") are a group of rare genetic disorders caused by mutations in genes encoding proteins of the nuclear lamina. They are included in the more generic term "nuclear envelopathies" that was coined in 2000 for diseases associated with defects of the nuclear envelope. Since the first reports of laminopathies in the late 1990s, increased research efforts have started to uncover the vital role of nuclear envelope proteins in cell and tissue integrity in animals.

The degenerative tissue damage caused by human prion diseases (CJD, GSS, and kuru) is characterised by four features: spongiform change, neuronal loss, astrocytosis, and amyloid plaque formation. These features are shared with prion diseases in animals, and the recognition of these similarities prompted the first attempts to transmit a human prion disease (kuru) to a primate in 1966, followed by CJD in 1968 and GSS in 1981. These neuropathological features have formed the basis of the histological diagnosis of human prion diseases for many years, although it was recognized that these changes are enormously variable both from case to case and within the central nervous system in individual cases.

The clinical signs in humans vary, but commonly include personality changes, psychiatric problems such as depression, lack of coordination, and/or an unsteady gait (ataxia). Patients also may experience involuntary jerking movements called myoclonus, unusual sensations, insomnia, confusion, or memory problems. In the later stages of the disease, patients have severe mental impairment (dementia) and lose the ability to move or speak.

Early neuropathological reports on human prion diseases suffered from a confusion of nomenclature, in which the significance of the diagnostic feature of spongiform change was occasionally overlooked. The subsequent demonstration that human prion diseases were transmissible reinforced the importance of spongiform change as a diagnostic feature, reflected in the use of the term "spongiform encephalopathy" for this group of disorders.

Prions appear to be most infectious when in direct contact with affected tissues. For example, Creutzfeldt–Jakob disease has been transmitted to patients taking injections of growth hormone harvested from human pituitary glands, from cadaver dura allografts and from instruments used for brain surgery (Brown, 2000) (prions can survive the "autoclave" sterilization process used for most surgical instruments). It is also believed that dietary consumption of affected animals can cause prions to accumulate slowly, especially when cannibalism or similar practices allow the proteins to accumulate over more than one generation. An example is kuru, which reached epidemic proportions in the mid-20th century in the Fore people of Papua New Guinea, who used to consume their dead as a funerary ritual. Laws in developed countries now ban the use of rendered ruminant proteins in ruminant feed as a precaution against the spread of prion infection in cattle and other ruminants.

There exist evidence that prion diseases may be transmissible by the airborne route.

Note that not all encephalopathies are caused by prions, as in the cases of PML (caused by the JC virus), CADASIL (caused by abnormal NOTCH3 protein activity), and Krabbe disease (caused by a deficiency of the enzyme galactosylceramidase). Progressive Spongiform Leukoencephalopathy (PSL)—which is a spongiform encephalopathy—is also probably not caused by a prion, although the adulterant that causes it among heroin smokers has not yet been identified. This, combined with the highly variable nature of prion disease pathology, is why a prion disease cannot be diagnosed based solely on a patient's symptoms.

Recent research suggests that sulfur amino acids have a protective effect against the toxicity of ODAP.

Eating the chickling pea with grain having high concentrations of sulphur-based amino acids reduces the risk of lathyrism if grain is available. Food preparation is also an important factor. Toxic amino acids are readily soluble in water and can be leached. Bacterial (lactic acid) and fungal (tempeh) fermentation is useful to reduce ODAP content. Moist heat (boiling, steaming) denatures protease inhibitors which otherwise add to the toxic effect of raw grasspea through depletion of protective sulfur amino acids. During times of drought and famine, water for steeping and fuel for boiling is frequently also in short supply. Poor people sometimes know how to reduce the chance of developing lathyrism but face a choice between risking lathyrism or starvation.

The underlying cause for excessive consumption of grasspea is a lack of alternative food sources. This is a consequence of poverty and political conflict. The prevention of lathyrism is therefore a socio-economic challenge.