there are no USFDA-approved medications for the treatment of mild cognitive impairment. Moreover, as of January 2018, there is no high-quality evidence that supports the efficacy of any pharmaceutical drugs or dietary supplements for improving cognitive symptoms in individuals with mild cognitive impairment. A moderate amount of high-quality evidence supports the efficacy of regular physical exercise for improving cognitive symptoms in individuals with MCI. The clinical trials that established the efficacy of exercise therapy for MCI involved twice weekly exercise over a period of six months. A small amount of high-quality evidence supports the efficacy of cognitive training for improving some measures of cognitive function in individuals with mild cognitive impairment. Due to the heterogeneity among studies which assessed the effect of cognitive training in individuals with MCI, there are no particular cognitive training interventions that have been found to provide greater symptomatic benefits for MCI relative to other forms of cognitive training.

The American Academy of Neurology's (AAN) clinical practice guideline on mild cognitive impairment from January 2018 stated that clinicians "should" identify modifiable risk factors in individuals with MCI, assess functional impairments, provide treatment for any behavioral or neuropsychiatric symptoms, and monitor the individual's cognitive status over time. It also stated that medications which cause cognitive impairment "should" be discontinued or avoided if possible. Due to the lack of evidence supporting the efficacy of cholinesterase inhibitors in individuals with MCI, the AAN guideline stated that clinicians who choose to prescribe them for the treatment of MCI "must" inform patients about the lack of evidence supporting this therapy. The guideline also indicated that clinicians "should" recommend that individuals with MCI engage in regular physical exercise for cognitive symptomatic benefits; clinicians "may" also recommend cognitive training, which appears to provide some symptomatic benefit in certain cognitive measures.

As MCI may represent a prodromal state to clinical Alzheimer's disease, treatments proposed for Alzheimer's disease, such as antioxidants and cholinesterase inhibitors, could potentially be useful; however, there is no evidence to support the efficacy of cholinesterase inhibitors for the treatment of mild cognitive impairment. Two drugs used to treat Alzheimer's disease have been assessed for their ability to treat MCI or prevent progression to full Alzheimer's disease. Rivastigmine failed to stop or slow progression to Alzheimer's disease or to improve cognitive function for individuals with mild cognitive impairment; donepezil showed only minor, short-term benefits and was associated with significant side effects.

In a two-year randomized trial of 168 people with MCI given either high-dose vitamins or placebo, vitamins cut the rate of brain shrinkage by up to half. The vitamins were the three B vitamins folic acid, vitamin B6, and vitamin B12, which inhibit production of the amino acid homocysteine. High blood levels of homocysteine are associated with increased risk of cognitive decline, dementia, and cardiovascular disease. A single study from 2012 showed a possible connection between macronutrient intake and development of MCI. It is also suggested that a dietary pattern with relatively high caloric intake from carbohydrates and low caloric intake from fat and proteins may increase the risk of MCI or dementia in elderly persons

Experimental non-pharmacological treatments for MCI include transcranial magnetic stimulation and transcranial direct current stimulation; the efficacy of these interventions for the treatment of MCI has not yet been established.

MCI does not usually interfere with daily life, but around 50 percent of people diagnosed with it go on to develop the far more severe Alzheimer's disease within five years. However, some instances of MCI may simply remain stable over time or even remit.

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.

Except for the treatable types listed above, there is no cure. Cholinesterase inhibitors are often used early in the disorder course; however, benefit is generally small. Cognitive and behavioral interventions may be appropriate. There is some evidence that educating and providing support for the person with dementia, as well as caregivers and family members, improves outcomes. Exercise programs are beneficial with respect to activities of daily living and potentially improve dementia.

The body's inflammatory response to surgery likely plays an important role, at least in elderly patients. Various research initiatives during recent years have evaluated whether actions taken before, during and after surgery can lessen the possible deleterious effects of inflammation. For example, anti-inflammatory agents can be given before surgery. During surgery, inflammation can be modulated by temperature control, use of regional rather than general anesthesia or the use of beta blockers. After surgery, optimal pain management and infection control is important. Several studies have shown variable-significance positive effects when a multidisciplinary, multifactorial approach to elderly patient is followed during pre, peri and post-operative care.

Animal studies indicate that volatile anaesthestics may augment the pathological processes of Alzheimer's Disease by affecting amyloid-beta processing. However, in young healthy mice, the volatile anesthetic isoflurane can also produce long-lasting memory impairment. This adverse effect is preventable by pre-administering the GABA(A)α5 inverse agonist L-655,708.

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 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.

POCD is common after cardiac surgery, and recent studies have now verified that POCD also exists after major non-cardiac surgery, although at a lower incidence. The risk of POCD increases with age, and the type of surgery is also important because there is a very low incidence associated with minor surgery. POCD is common in adult patients of all ages at hospital discharge after major noncardiac surgery, but only the elderly (aged 60 years or older) are at significant risk for long-term cognitive problems. Patients with POCD are at an increased risk of death in the first year after surgery. Research interest has increased since early 2000, especially as more elderly patients are able to undergo successful minor and major surgeries.

POCD has been studied through various institutions since the inception of the IPOCDS-I study centred in Eindhoven, Netherlands and Copenhagen, Denmark. This study found no causal relationship between cerebral hypoxia and low blood pressure and POCD. Age, duration of anaesthesia, introperative complications, and postoperative infections were found to be associated with POCD.

- POCD is just as likely to occur after operations under regional anesthesia as under general anesthesia.

- More likely after major operations than minor operations.

- More likely after heart operations than other types of surgery.

- More likely in aged than in younger patients.

- More likely in older patients with high alcohol intake/abuse.

- People with higher preoperative ASA physical status scores are more likely to develop POCD.

- People with lower educational level are more likely to develop POCD than those with a higher educational level.

- People with prior history of a stroke, even though there is complete functional recovery, are more likely to develop POCD.

- More likely in the elderly with pre-existing declining mental functions, termed mild cognitive impairment (MCI). MCI is a transitional zone between normal mental function and evident Alzheimer's disease or other forms of dementia. It is insidious, and seldom recognized, except in retrospect after affected persons are evidently demented.

- Delirium and severe worsening of mental function is very likely in those with clinically evident Alzheimer's disease or other forms of dementia, as well as those with a history of delirium after previous operations.

There have been assertions of a possible link between TGA and the use of statins (a class of drug used in treating cholesterol).

En bloc memory loss which is total, permanent, and irrecoverable can occur as an alcoholic "black out," usually lasting longer than an hour and up to 2–5 days.

Marijuana intoxication, Halogenated hydroxyquinolines such as Clioquinol, PDE inhibitors such as sildenafil, Digitalis and scopolamine intoxication, and general anaesthesia have been reported with TGA.

Transient global amnesia (TGA) is a neurological disorder whose key defining characteristic is a temporary but almost total disruption of short-term memory with a range of problems accessing older memories. A person in a state of TGA exhibits no other signs of impaired cognitive functioning but recalls only the last few moments of consciousness, as well as deeply encoded facts of the individual's past, such as their own name.