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.

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.

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.

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.

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.

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.

No medications have been shown to prevent or cure dementia. Medications may be used to treat the behavioural and cognitive symptoms but have no effect on the underlying disease process.

Acetylcholinesterase inhibitors, such as donepezil, may be useful for Alzheimer disease and dementia in Parkinson's, DLB, or vascular dementia. The quality of the evidence however is poor and the benefit is small. No difference has been shown between the agents in this family. In a minority of people side effects include a slow heart rate and fainting.

As assessment for an underlying cause of the behavior is a needed before prescribing antipsychotic medication for symptoms of dementia. Antipsychotic drugs should be used to treat dementia only if non-drug therapies have not worked, and the person's actions threaten themselves or others. Aggressive behavior changes are sometimes the result of other solvable problems, that could make treatment with antipsychotics unnecessary. Because people with dementia can be aggressive, resistant to their treatment, and otherwise disruptive, sometimes antipsychotic drugs are considered as a therapy in response. These drugs have risky adverse effects, including increasing the patient's chance of stroke and death. Generally, stopping antipsychotics for people with dementia does not cause problems, even in those who have been on them a long time.

N-methyl-D-aspartate (NMDA) receptor blockers such as memantine may be of benefit but the evidence is less conclusive than for AChEIs. Due to their differing mechanisms of action memantine and acetylcholinesterase inhibitors can be used in combination however the benefit is slight.

While depression is frequently associated with dementia, selective serotonin reuptake inhibitors (SSRIs) do not appear to affect outcomes.

The use of medications to alleviate sleep disturbances that people with dementia often experience has not been well researched, even for medications that are commonly prescribed. In 2012 the American Geriatrics Society recommended that benzodiazepines such as diazepam, and non-benzodiazepine hypnotics, be avoided for people with dementia due to the risks of increased cognitive impairment and falls. Additionally, there is little evidence for the effectiveness of benzodiazepines in this population. There is no clear evidence that melatonin or ramelteon improves sleep for people with dementia due to Alzheimer's disease. There is limited evidence that a low dose of trazodone may improve sleep, however more research is needed.

There is no solid evidence that folate or vitamin B12 improves outcomes in those with cognitive problems. Statins also have no benefit in dementia. Medications for other health conditions may need to be managed differently for a person who also has a diagnosis of dementia. The MATCH-D criteria can help identify ways that a diagnosis of dementia changes medication management for other health conditions. It is unclear if there is a link between blood pressure medication and dementia. There is a possibility that people may experience an increase in cardiovascular-related events if these medications are withdrawn.

Specific and accepted scientific treatment for PCA has yet to be discovered; this may be due to the rarity and variations of the disease. At times PCA patients are treated with prescriptions originally created for treatment of AD such as, cholinesterase inhibitors, Donepezil, Rivastigmine and Galantamine, and Memantine. Antidepressant drugs have also provided some positive effects.

Patients may find success with non-prescription treatments such as psychological treatments. PCA patients may find assistance in meeting with an occupational therapist or sensory team for aid in adapting to the PCA symptoms, especially for visual changes. People with PCA and their caregivers are likely to have different needs to more typical cases of Alzheimer's disease, and may benefit from specialized support groups such as the PCA Support Group based at University College London, or other groups for young people with dementia. No study to date has been definitive to provide accepted conclusive analysis on treatment options.

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.

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.

Early-onset Alzheimer's disease, also called early-onset Alzheimer's, or early-onset AD, is Alzheimer's disease diagnosed before the age of 65. It is an uncommon form of Alzheimer's, accounting for only 5-10% of all Alzheimer's cases. Approximately 13% of the cases of early-onset Alzheimer's are familial Alzheimer's disease, where a genetic predisposition leads to the disease. The other incidences of early onset Alzheimer's, however, share the same traits as the 'late onset' form of Alzheimer's disease, and little is understood about how it starts.

Non-familial early onset Alzheimer's can develop in people who are in their thirties or forties, but that is extremely rare. The majority of people with early-onset Alzheimer's are in their fifties or early sixties.

Pick's disease is a term that can be used in two different ways. It has traditionally been used as a term for a group of neurodegenerative diseases with symptoms attributable to frontal and temporal lobe dysfunction. Common symptoms that are noticed early are personality and emotional changes, as well as deterioration of language. This condition is now more commonly called frontotemporal dementia by professionals, and the use of "Pick's disease" as a clinical diagnosis has fallen out of fashion. The second use of the term (and the one now used among professionals) is to mean a specific pathology that is one of the causes of frontotemporal lobar degeneration. These two uses have previously led to confusion among professionals and patients and so its use should be restricted to the specific pathological subtype described below. It is also known as Pick disease and PiD (not to be confused with pelvic inflammatory disease (PID) or Parkinson's disease (PD)). A defining characteristic of the disease is build-up of tau proteins in neurons, accumulating into silver-staining, spherical aggregations known as "Pick bodies".

Binswanger's disease, also known as subcortical leukoencephalopathy, is a form of small vessel vascular dementia caused by damage to the white brain matter. White matter atrophy can be caused by many circumstances including chronic hypertension as well as old age. This disease is characterized by loss of memory and intellectual function and by changes in mood. These changes encompass what are known as executive functions of the brain. It usually presents between 54 and 66 years of age, and the first symptoms are usually mental deterioration or stroke.

It was described by Otto Binswanger in 1894, and Alois Alzheimer first used the phrase "Binswanger's disease" in 1902. However, Olszewski is credited with much of the modern-day investigation of this disease which began in 1962.

The symptoms of the disease as a distinct nosologic entity were first identified by Emil Kraepelin, and the characteristic neuropathology was first observed by Alois Alzheimer in 1906. In this sense, the disease was co-discovered by Kraepelin and Alzheimer, who worked in Kraepelin's laboratory. Because of the overwhelming importance Kraepelin attached to finding the neuropathological basis of psychiatric disorders, Kraepelin made the decision that the disease would bear Alzheimer's name.

There is no known cure for PSP and management is primarily supportive. PSP cases are often split into two subgroups, PSP-Richardson, the classic type, and PSP-Parkinsonism, where a short-term response to levodopa can be obtained. Dyskinesia is an occasional but rare complication of treatment. Amantadine is also sometimes helpful. After a few years the Parkinsonian variant tends to take on Richardson features. Other variants have been described. Botox can be used to treat neck dystonia and blephrospasm, but this can aggravate dysphagia.

Two studies have suggested that rivastigmine may help with cognitive aspects, but the authors of both studies have suggested a larger sampling be used. There is some evidence that the hypnotic zolpidem may improve motor function and eye movements, but only from small-scale studies.

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.

Neurodegeneration is the progressive loss of structure or function of neurons, including death of neurons. Many neurodegenerative diseases – including amyotrophic lateral sclerosis, Parkinson's, Alzheimer's, and Huntington's – occur as a result of neurodegenerative processes. Such diseases are incurable, resulting in progressive degeneration and/or death of neuron cells. As research progresses, many similarities appear that relate these diseases to one another on a sub-cellular level. Discovering these similarities offers hope for therapeutic advances that could ameliorate many diseases simultaneously. There are many parallels between different neurodegenerative disorders including atypical protein assemblies as well as induced cell death. Neurodegeneration can be found in many different levels of neuronal circuitry ranging from molecular to systemic.

The process of neurodegeneration is not well understood, so the diseases that stem from it have, as yet, no cures. In the search for effective treatments (as opposed to palliative care), investigators employ animal models of disease to test potential therapeutic agents. Model organisms provide an inexpensive and relatively quick means to perform two main functions: target identification and target validation. Together, these help show the value of any specific therapeutic strategies and drugs when attempting to ameliorate disease severity. An example is the drug Dimebon (Medivation). This drug is in phase III clinical trials for use in Alzheimer's disease, and also recently finished phase II clinical trials for use in Huntington's disease. In March 2010, the results of a clinical trial phase III were released; the investigational Alzheimer's disease drug Dimebon failed in the pivotal CONNECTION trial of patients with mild-to-moderate disease. With CONCERT, the remaining Pfizer and Medivation Phase III trial for Dimebon (latrepirdine) in Alzheimer's disease failed in 2012, effectively ending the development in this indication.

In another experiment using a rat model of Alzheimer's disease, it was demonstrated that systemic administration of hypothalamic proline-rich peptide (PRP)-1 offers neuroprotective effects and can prevent neurodegeneration in hippocampus amyloid-beta 25–35. This suggests that there could be therapeutic value to PRP-1.

Protein degradation offers therapeutic options both in preventing the synthesis and degradation of irregular proteins. There is also interest in upregulating autophagy to help clear protein aggregates implicated in neurodegeneration. Both of these options involve very complex pathways that we are only beginning to understand.

The goal of immunotherapy is to enhance aspects of the immune system. Both active and passive vaccinations have been proposed for Alzheimer's disease and other conditions, however more research must be done to prove safety and efficacy in humans.

Studies have shown that PCA may be a variant of Alzheimer's disease (AD), with an emphasis on visual deficits. Although in primarily different, but sometimes overlapping, brain regions, both involve progressive neural degeneration, as shown by the loss of neurons and synapses, and the presence of neurofibrillary tangles and senile plaques in affected brain regions; this eventually leads to dementia in both diseases. PCA patients have more cortical damage and gray matter (cell body) loss in posterior regions, especially in the occipital, parietal, and temporal lobes, whereas Alzheimer’s patients typically experience more damage in the prefrontal cortex and hippocampus. PCA tends to impair working memory and anterograde memory, while leaving episodic memory intact, whereas AD patients typically have damaged episodic memory, suggesting some differences still lie in the primary areas of cortical damage.

Over time, however, atrophy in PCA patients may spread to regions commonly damaged in AD patients, leading to common AD symptoms such as deficits in memory, language, learning, and cognition. Although PCA has an earlier onset, many PCA patients have also been diagnosed with Alzheimer’s, suggesting that the degeneration has simply migrated anteriorly to other cortical brain regions.

There is no standard definition of PCA and no established diagnostic criteria, so it is not possible to know how many people have the condition. Some studies have found that about 5 percent of people diagnosed with Alzheimer’s disease have PCA. However, because PCA often goes unrecognized, the true percentage may be as high as 15 percent. Researchers and physicians are working to establish a standard definition and diagnostic criteria for PCA.

PCA may also be correlated with the diseases of Lewy body, Creutzfeldt–Jakob disease, Bálint's syndrome, and Gerstmann syndrome. In addition, PCA may result in part from mutations in the presenilin 1 gene (PSEN1).

Tauopathy belongs to a class of neurodegenerative diseases associated with the pathological aggregation of tau protein in neurofibrillary or gliofibrillary tangles in the human brain. Tangles are formed by hyperphosphorylation of a microtubule-associated protein known as tau, causing it to aggregate in an insoluble form. (These aggregations of hyperphosphorylated tau protein are also referred to as paired helical filaments). The precise mechanism of tangle formation is not completely understood, and it is still controversial as to whether tangles are a primary causative factor in the disease or play a more peripheral role. Primary tauopathies, i.e., conditions in which neurofibrillary tangles (NFT) are predominantly observed, include:

- Primary age-related tauopathy (PART)/Neurofibrillary tangle-predominant senile dementia, with NFTs similar to AD, but without plaques.

- Chronic traumatic encephalopathy, including dementia pugilistica

- Progressive supranuclear palsy

- Corticobasal degeneration

- Frontotemporal dementia and parkinsonism linked to chromosome 17

- Lytico-Bodig disease (Parkinson-dementia complex of Guam)

- Ganglioglioma and gangliocytoma

- Meningioangiomatosis

- Postencephalitic parkinsonism

- Subacute sclerosing panencephalitis

- As well as lead encephalopathy, tuberous sclerosis, Hallervorden-Spatz disease, and lipofuscinosis

Neurofibrillary tangles were first described by Alois Alzheimer in one of his patients suffering from Alzheimer's disease (AD), which is considered a secondary tauopathy. AD is also classified as an amyloidosis because of the presence of senile plaques.

The degree of NFT involvement in AD is defined by Braak stages. Braak stages I and II are used when NFT involvement is confined mainly to the transentorhinal region of the brain, stages III and IV when there's also involvement of limbic regions such as the hippocampus, and V and VI when there's extensive neocortical involvement. This should not be confused with the degree of senile plaque involvement, which progresses differently.

In both Pick's disease and corticobasal degeneration, tau proteins are deposited as inclusion bodies within swollen or "ballooned" neurons.

Argyrophilic grain disease (AGD), another type of dementia, is marked by an abundance of argyrophilic grains and coiled bodies upon microscopic examination of brain tissue. Some consider it to be a type of Alzheimer's disease. It may co-exist with other tauopathies such as progressive supranuclear palsy and corticobasal degeneration, and also Pick's disease.

Huntington's disease (HD): a neurodegenerative disease caused by a CAG tripled expansion in the Huntington gene is the most recently described tauopathy (Fernandez-Nogales et al. Nat Med 2014). JJ Lucas and co-workers demonstrate that, in brains with HD, tau levels are increased and the 4R/3R balance is altered. In addition, the Lucas study shows intranuclear insoluble deposits of tau; these "Lucas' rods" were also found in brains with Alzheimer's disease.

Tauopathies are often overlapped with synucleinopathies, possibly due to interaction between the synuclein and tau proteins.

The non-Alzheimer's tauopathies are sometimes grouped together as "Pick's complex" due to their association with frontotemporal dementia, or frontotemporal lobar degeneration.

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.

The symptoms of Pick's disease include difficulty in language and thinking, efforts to dissociate from family, behavioral changes, unwarranted anxiety, irrational fears, CBD (Compulsive buying disorder, or oniomania), impaired regulation of social conduct (e.g., breaches of etiquette, vulgar language, tactlessness, , misperception), passivity, low motivation (aboulia), inertia, over-activity, pacing and wandering. It is a characteristic of Pick’s disease that dysfunctional, argumentative, or hostile social conduct is initially exhibited towards family members and not initially exhibited in a workplace or neutral environment. The changes in personality allow doctors to distinguish between Pick's disease and Alzheimer's disease. Pick's disease is one of the causes of the clinical syndrome of frontotemporal lobar degeneration which has three subtypes. Pick's disease pathology is associated more with the frontotemporal dementia and progressive nonfluent aphasia subtypes than the semantic dementia subtype.

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.