Dementia is a syndrome characterized by difficulties with memory, language, problem solving, and other cognitive domains, which lead to functional impairment in the individual. In clinical practice, the nomenclature used to describe dementia is often defined by the DSM. The DSM-5 introduces the neurocognitive disorders category as a continuum of cognitive decline spanning from mild neurocognitive disorder, or preclinical dementia, to major neurocognitive disorder, or dementia. In doing so, this new nomenclature helps to facilitate the recognition and treatment of a neurocognitive impairment before its manifestation into a dementia syndrome. The DSM-5 defines major neurocognitive disorder as a significant cognitive decline from a previous level of performance in one or more cognitive domains, including complex attention, executive function, learning and memory, language, perceptual-motor, and social cognition. The cognitive deficits interfere with independence in everyday activities, do not occur exclusively in the context of a delirium, and are not better explained by another mental illness (1). Minor neurocognitive disorder is evidenced by a modest cognitive decline from a previous level of performance in one or more of the same aforementioned cognitive domains listed for major neurocognitive disorder. In mild neurocognitive disorder, the cognitive deficits do not interfere with capacity of independence in everyday activities (1). As the number of Americans ages 65 and older continues to increase, the cases of dementia will continue to grow. The population of Americans ages 65 and older is projected to grow from 43.1 million in 2012 to 83.7 million by 2050. The baby boomers are largely responsible for this growth; moreover, by 2030, all baby boomers will be older than age 65 (2, 3). The number of people ages 65 and older also continues to increase worldwide, from 617 million in 2015 to a projected 1.6 trillion by 2050 (4). The prevalence of dementia doubles every 5 years between ages 65 and 85, and it continues to increase after age 90 (5, 6). In 2010, it was estimated that 4.7 million individuals ages 65 and older had dementia caused by Alzheimer’s disease. Of these individuals, 0.7 million were between ages 65 and 74, and 2.3 million were between ages 75 and 84. By 2050, the number of individuals with dementia caused by Alzheimer’s disease is projected to be 13.8 million, with 7 million age 85 or older (7). Advanced age and sex, the two most prominent risk factors for dementia, are not modifiable. Gender has an influence on dementia risk when societal factors, such as differences in healthy lifestyle and opportunities for advanced educational attainment, come into play (8). Lifestyle factors such as smoking, excessive alcohol intake, and poor diet modulate susceptibility to dementia in both men and women. However, more women than men have dementia, with almost two-thirds of Americans with Alzheimer’s disease being women (9). Overall, little difference has been found between the sexes in incidence of dementia; however, by absolute numbers, more women than men have the disease because of differences in life expectancy (10). Racial-ethnic minority groups appear to make up a greater number of dementia cases. Studies in the United States showed incidence rates that were higher for African Americans and Latinos than for Whites; however, these differences disappeared after adjustment for education level or socioeconomic status (11, 12). This finding demonstrates that racial-ethnic differences are likely related to variations in medical conditions, such as higher incidence of cardiovascular disease and diabetes mellitus; health-related behaviors, such as perceptions of normal and abnormal aging and long-standing issues of trust between racial-ethnic minority groups and the medical establishment; and socioeconomic risk factors, such as access to adequate medical care, higher education, health literacy, and access to adequate nutrition. Genetic factors do not appear to play a role in the differences in prevalence or incidence among racial-ethnic minority groups (13). Because of the long duration of illness before death, dementia contributes significantly to the public health impact because much of that time is spent in a state of disability or dependence, especially in lieu of any currently available treatments to halt disease progression. Undeniably, this long duration of disability will have a far-reaching impact on national health care costs, including the increasing need for caregivers to shoulder the burden of care provided to older adults with dementia. In 2020, the total national cost of caring for people with dementia reached $305 billion. Individuals with dementia have twice as many hospital stays, more skilled nursing facility stays, and more home health care visits per year than older adults without dementia (9). In 2010, 83% of the help provided to older adults in the United States came from family members, friends, or other unpaid caregivers (14). In 2019, dementia caregivers provided an estimated 18.6 billion hours of unpaid assistance valued at $244 billion (9). The initial evaluation and diagnoses of dementia should include a thorough clinical assessment with a collateral history, if available; a neurological examination with assessment of mental status; selective labs to rule out metabolic and physiologic abnormalities; and structural brain imaging, preferably with magnetic resonance imaging (MRI) instead of computed tomography (CT) because these images generate a higher resolution image of cortical structures, enabling a more detailed assessment of atrophy (15). Collateral informants may include spouses, adult children, or other primary caretakers who can attest to the natural progression of symptoms and functional changes over the course of months or years. Having this additional information can be vitally important, especially if, because of degree of clinical severity, the patient is unable to give a thorough history or lacks insight into their impairments. Common labs important to a dementia workup include basic chemistries, a thyroid panel, a B12-folate test, and a vitamin D test. On the basis of the patient’s clinical history, additional tests may be warranted, including Treponemal pallidum antibody or venereal disease research laboratory, human immunodeficiency virus-ab, antinuclear antibody, erythrocyte sedimentation rate, and a heavy-metal screen. T1-weighted structural MRI is very useful in detecting focal loss of gray matter volume loss, otherwise indicated as atrophy, which is a common feature of neurodegenerative dementias (16). The emphasis of the clinical interview should be placed on establishing a thorough patient history backed by reliable collateral sources, when available, and creating a detailed timeline of clinical symptoms and functional decline. This timeline should include the rate of symptom onset (e.g., rapid vs. gradual) and the pace of symptom progression (e.g., decline over months vs. years) (15). For example, human prion diseases, such as Creutzfeldt-Jakob disease, typically progress quite rapidly, over weeks to months. In contrast, dementias caused by Alzheimer’s disease, diffuse Lewy body disease, and frontotemporal diseases progress much slower, over a period of years. As a result of the rapid or gradual cognitive decline, patients also lose the ability to perform complex instrumental activities of daily living (IADLs) and eventually basic activities of daily living (ADLs). For example, patients who have progressed to moderate and severe stages of dementia have marked impairments in cognitive function and have usually lost the ability to carry out most IADLs (17). At these stages, the accurate reporting of symptoms and functional decline will necessitate the use of reliable caretakers or family members. Accurately measuring functional loss is important because the nature and extent of functional losses associated with disease progression help determine the type and level of care needed, ranging from medication management in early stages to full-time care or institutionalization in later stages (18). A detailed mental status examination should assess several cognitive domains, including attention, memory, executive functioning, and visuospatial ability. Several instruments have been developed to help clinicians assess the presence and severity of cognitive impairment. Tools such as the 30-point Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA) are more commonly used and are helpful in assessing the presence and severity of dementia. The MoCA offers a broader assessment of cognitive domains and can be more sensitive than the MMSE for early detection of neurodegenerative diseases. Although commonly still used, the MMSE has a ceiling effect for higher functioning older adults and is poorly sensitivity for distinguishing mild cognitive impairment (MCI), which increases the likelihood that people in predementia stages will score within the normal range (≥24) (19–21). Full neuropsychological testing may be helpful in instances in which screening tests and clinical impression remain ambiguous. Alzheimer’s disease remains one of the leading causes of progressive dementia; moreover, as the number of Americans ages 65 and older continues to increase, the cases of Alzheimer’s disease and other dementias will also continue to grow. In 2020, an estimated 5.8 million Americans ages 65 and older were living with the disease; 80% were ages 75 or older (7). Out of the total U.S. population, one in 10 people (10%) ages 65 and older has Alzheimer’s disease; moreover, the percentage of people with Alzheimer’s disease increases with age: 3% of people ages 65–74, 17% of people ages 75–84, and 32% of people ages 85 and older (7, 9). It is also important to note that people younger than age 65 can also develop Alzheimer’s disease, but it is much less common. The Alzheimer’s disease continuum reflects the progression from brain changes that are not noticed by the affected person to brain changes that cause problems with memory and eventually physical disability. The continuum has three phases: preclinical Alzheimer’s disease, MCI due to Alzheimer’s disease, and dementia due to Alzheimer’s disease. Each of these phases is further broken down into mild, moderate, or severe stages that reflect the impact of the disease on an individual’s daily function. How long individuals spend in each part of the continuum varies and can be influenced by age, genetics, gender, and other factors (22). During the preclinical Alzheimer’s disease phase, individuals have the earliest signs of the disease, which are detectable with biomarkers; however, they have yet to develop symptoms such as memory loss or change in functionality. Biomarkers, the earliest measurable brain changes, include measures of beta-amyloid (Aβ) deposition and glucose metabolism in the brain. Positron emission tomography (PET) scans use an Aβ-specific ligand, known as Pittsburgh compound B, to detect levels of cerebral load in the brain. Analysis of cerebrospinal fluid (CSF) can detect drops in Aβ levels, indicating a reduced clearance of Aβ into the CSF and increased aggregation of the peptide into amyloid plaques in the brain (23). PET imaging with the 2-deoxy-2-fluoro-D-glucose (FDG) tracer measures the cerebral metabolism of glucose and has a specific topographic distribution pattern: bilateral reduction in FDG uptake in the temporal and parietal regions and especially in the cingulate cortex (23). It is important to note that not all individuals with evidence of Alzheimer’s disease–related brain changes go on to develop symptoms of MCI or dementia due to Alzheimer’s disease (24). Individuals with MCI due to Alzheimer’s disease have biomarker evidence of brain changes plus subtle changes in memory and thinking that do not interfere with overall daily function. These changes occur when the brain can no longer compensate for the damage and nerve cell death caused by Alzheimer’s disease. Eventually, these patients can progress to full Alzheimer’s dementia, with several studies indicating a range of conversion rates anywhere from 15% to nearly 40% within 2–5 years of initial MCI diagnosis (25–27). The 2018 study by Petersen et al. (25) demonstrated a cumulative dementia incidence of 14.9% over 2 years in individuals with MCI older than age 65. In some cases, MCI will revert to normal or remain stable over time. Patients diagnosed as having dementia due to Alzheimer’s disease have biomarker evidence of brain changes with very clear changes in memory, thinking, or behavior that affect an individual’s daily function. They can exhibit multiple symptoms that progress over years and reflect the degree of nerve cell damage in different parts of the brain. The rate at which dementia symptoms progress varies from person to person but is generally categorized in stages ranging from mild, moderate, to severe. In mild stages of Alzheimer’s disease, many people can function independently in many areas but typically require assistance with some activities to optimize safety and independence. In moderate stages of Alzheimer’s disease, which tend to last the longest, individuals may have trouble with communication and performing routine tasks, such as ADLs. Some may develop incontinence at times. Others may start to demonstrate personality and behavioral changes, which are often some of the first symptoms recognized by family members or caretakers that will prompt their desire for a clinical evaluation by a medical professional. In severe stages, individuals need help with ADLs 24 hours per day, 7 days per week, and the effects of Alzheimer’s disease on their general health become apparent. Damage to areas of the brain that control movement lead to patients being more at risk for falls and becoming bed bound, which makes them more vulnerable to blood clots, bed sores, infections, and even sepsis. Damage to the areas of the brain that control swallowing leads to increased risk of aspiration, which can cause aspiration pneumonia. Most people who develop dementia caused by Alzheimer’s disease do so at age 65 or older, which is often referred to as late onset. Several risk factors exist for late-onset Alzheimer’s disease, which is not thought to be related to any singular cause. Overall, age is the greatest risk factor for late-onset Alzheimer’s disease; moreover, the percentage of people with dementia caused by Alzheimer’s disease increases dramatically with age, as previously mentioned (7). Genetics is another risk factor, and researchers have found several genes that increase the risk of Alzheimer’s disease, with the apolipoprotein (APOE) e4 gene conferring the strongest impact on risk. Everyone inherits one of the three forms of the APOE gene from each parent, resulting in six possible pairs: e2-e2, e2-e3, e2-e4, e3-e3, e3-e4, and e4-e4. Having the e4 allele of APOE increases the risk of developing dementia in comparison with having the e3, but it does not guarantee that an individual will necessarily develop Alzheimer’s disease. Having the e2 form may decrease risk compared with having the e3 form. Those with just a single copy of the e4 allele have three times the risk of developing Alzheimer’s disease than those with two copies of the e3 form. Individuals who have two copies of the e4 allele are eight to 12 times more likely to develop Alzheimer’s disease (28–30). Finally, family history confers a risk on developing Alzheimer’s disease. Individuals who have a first-degree relative with Alzheimer’s disease are more likely to develop the disease, with an even higher risk for those who have more than one first-degree relative with the disease (28, 31). Of course, when diseases run in families, shared nongenetic factors such as access to healthy foods and habits related to physical activity may also play a role. Although age, genetics, and family history are considered nonmodifiable, certain risk factors can be changed or modified to reduce the risk of dementia. According to the 2019 published recommendations by the World Health Organization (32), cognitive impairment and dementia are associated with lifestyle-related risk factors, such as physical inactivity, tobacco use, unhealthy diets, and harmful use of alcohol. In addition, certain medical conditions, including hypertension, diabetes, hypercholesterolemia, obesity, and depression, also confer an increased risk of developing dementia. Other potentially modifiable risk factors include social isolation and cognitive inactivity. Less commonly, patients can develop dementia due to Alzheimer’s disease before age 65, sometimes as early as age 30. This manifestation is called early-onset Alzheimer’s disease, which occurs in less than 1% of Alzheimer’s disease cases and develops from mutations to any three specific genes (33). Mutations in the genes for amyloid precursor protein, presenilin 1 protein, or presenilin 2 protein virtually guarantee the development of Alzheimer’s disease during a normal life span. Amyloid precursor protein and presenilin 1 mutations are associated with complete penetrance, whereas mutations in presenilin 2 are associated with a 95% penetrance (34). Each of the Alzheimer’s disease genes plays a role in the production, trafficking, and clearance of Aβ, where its deposition into amyloid plaques, along with neurofibrillary tangles, plays a major role in the pathologic process of Alzheimer’s disease. As previously described, the identification and use of biomarkers for Alzheimer’s disease allow for early disease detection. In addition, biomarkers have become a powerful tool in clinical practice and research by improving diagnoses, increasing clinical trials, and helping to accelerate the development of new therapies (9, 23). None of the current pharmacologic treatments available today prevent the progression of neurodegeneration that causes Alzheimer’s disease. Acetylcholinesterase inhibitors (AChEIs) and N-methyl-D-Aspartate antagonists are the only drugs approved by the U.S. Food and Drug Administration (FDA) for the treatment of Alzheimer’s disease; however, no consensus has been reached that either drug even modestly delays progression (35). The drugs included within these two groups are rivastigmine, galantamine, donepezil, memantine, and memantine combined with donepezil. The modest benefits of these drugs have to be balanced against the potential adverse effects, including gastrointestinal intolerance, bradycardia, and gastrointestinal bleeding, to name a few. Since the discovery that Alzheimer’s disease may begin 20 years or more before symptom onset, a significant window has emerged allowing for future therapies to intervene earlier along the continuum. As of March 13, 2020, the IgG1 monoclonal antibody BIIB037 (aducanumab) is being used in a phase 3b open-label trial among participants with Alzheimer’s disease, who participated in previous aducanumab studies (including PRIME, ENGAGE, and EMERGE), as a potential new treatment for Alzheimer’s disease (36). The previous phase 3 efficacy trial with aducanumab, EMERGE, demonstrated that it had met its primary endpoint. Patients on the highest dose, 10 mg/kg, had significant reduction in decline on the Clinical Dementia Rating Scale-Sum of Boxes, a tool that the FDA uses as a single primary efficacy endpoint and to assess disease progression (37, 38). The current phase 3b trial is projected to run through September 2023. FTD is a heterogenous spectrum of neurodegenerative disorders with diverse clinical presentations, genetic attributes, and neuropathological characteristics (39). They are linked by the selective degeneration of the frontal and temporal lobes. In the past considered to be a rare disease, FTD has been shown to be more frequent than previously thought, with an estimated lifetime risk of one in 742 by recent epidemiological studies and updated clinical criteria (39, 40). FTD has been established as the second most common cause of dementia for people younger than age 65, with a prevalence that approximates that of Alzheimer’s disease (40–42). However, the overall prevalence increases beyond age 65, with a rate doubling that of those ages 40–64 (40, 42). Clinically, FTD is characterized by behavioral abnormalities, language impairment, and deficits of executive function. In accordance, the current revised diagnostic criteria list two different clinical forms: behavioral variant of FTD (bvFTD) and primary progressive aphasia (PPA; the two most common forms include the semantic variant of PPA [svPPA] and the agrammatic variant of PPA [avPPA]). Frequently thought of as a tauopathy, or a neurodegenerative disease involving aggregation of tau protein in the brain, the heterogeneity in both the clinical presentations and the neuropathological hallmarks of FTD subtypes are all primarily related to neuronal protein tau or transactive response DNA-binding protein 43 (TDP-43) depositions. Considered the most common clinical form of FTD, bvFTD is predominately characterized by personality changes, apathy, disinhibited or compulsive behaviors, executive dysfunction, as well as stereotypic speech and motor behaviors (15, 43). According to the new consensus criteria for the diagnosis of bvFTD, the degree of diagnostic certainty can be ranked as possible, probable, or definite. To reach a diagnosis of possible bvFTD, three of six core criteria must be met. To reach a diagnosis of probable bvFTD, patients have to first meet possible criteria and also show changes in frontal or temporal regions on neuroimaging. When pathologic or genetic confirmation has been made, the bvFTD diagnosis is considered definite (43, 44). Social cognition is core to the syndrome and refers to the ability to recognize emotion in others, mentalizing about other people’s state of mind (i.e., theory of mind), empathy, knowledge of social norms, moral reasoning, reward sensitivity, evaluating relevance of incoming social and emotional information, and flexibly using this information to behave appropriately within social contexts (41). Dysfunction in social cognition is a key feature in bvFTD, with changes indicating a progressive disintegration of the neural circuits involved in social cognition, emotion regulation, motivation, and decision making (45–47). Apathy is very common and manifests as inertia, reduced motivation, lack of interest in previous hobbies, and decreased social interest leading to progressive social withdrawal. Disinhibition often coexists with apathy, leading to impulsive actions such as excessive spending, sexually inappropriate remarks, and other socially tactless behaviors. Repetitive or stereotypic behaviors might present with perseveration and tendency to repeat phrases, stories, or jokes. Excessive hoarding leading to a state of squalor, new-onset pathological gambling, or (even more rarely) hyper-religiosity can be presenting features (48). Hyperorality, typically seen as increased food consumption with predominate sweet cravings, is another defining feature reflecting early involvement in the hypothalamus (41). Mental rigidity is also common, and patients can have difficulty adapting to new situations or routines. Onset is often difficult to determine because of limited or absent insight on the part of the patient. Therefore, the history of a caregiver is essential during the interview process because prominent changes in social comportment, appropriateness, and apathy are often reported (48). Early in the disease process, patients with bvFTD can perform well on formal neuropsychological tests despite the presence of significant personality and behavioral changes (48). Later, the neuropsychological profile is characterized by deficits in executive function. Prior studies have emphasized a relative sparing of episodic memory and visuospatial skills on neuropsychological testing (44). However, more recent evidence from a synthesis of neuropsychological studies, in light of neuroimaging and neuropathological findings, demonstrates involvement of structures known to be crucial for episodic memory (43, 49). It was initially presumed that episodic memory difficulties in bvFTD reflected degeneration of prefrontal cortical regions; however, it is becoming increasingly clear that anterior and medial temporal regions, including the hippocampi, are heavily involved (50, 51). Psychotic symptoms in FTD, previously considered rare, occur more frequently than previously thought (52). Currently, psychotic symptoms are increasingly recognized as a presenting or early feature of FTD (53). More recent studies have demonstrated a linkage between patients with FTD and a hexanucleotide repeat expansion in the chromosome 9 open reading frame 72 (C9ORF72) gene; C9ORF72 is often specifically associated with bvFTD and motor neuron disease (54, 55). The prevalence of the mutation in FTD varies depending on the population studied and ranges from 5% to 35% (56). Prominent features among most patients with this mutation are highly abnormal behaviors of a psychotic nature. Many patients presenting with florid psychosis are initially classified by their psychiatrist as having primary psychotic disorders, such as paranoid schizophrenia (54). Delusions are more frequently present than hallucinations and are mainly persecutory or paranoid in nature; however, erotomania, somatic delusions, and Cotard’s syndrome can also occur (53, 55). PPA is the second major form of FTD that affects language skills, speaking, writing, and comprehension. Neuroimaging shows asymmetric atrophy of the anterior temporal lobe among affected individuals, usually the left side is more involved than the right side (43). The two most common forms of PPA are svPPA and avPPA. The progressive breakdown of semantic memory, which stores knowledge about objects and words, is a characterization of svPPA. Speech remains fluent with normal grammar, but it increasingly contains meaningless content, prominent anomia, and impaired word comprehension (43). Individuals lose the ability to understand or formulate words in a spoken sentence. Over time, patients develop impaired recognition and worsening behavioral symptoms, as seen in bvFTD. In avPPA, a person’s speech is very hesitant, labored, or ungrammatical. Speech distortion is due to the breakdown in motor planning, or speech apraxia, causing impairment of rhythm and the normal stress patterns of speech (43). Word comprehension is normal, but sentence comprehension is impaired because of problems with grammatical structure. Word repetition is also often impaired because of errors in articulation (57). Frontotemporal dementia can be caused by a highly heritable group of neurodegenerative disorders, with nearly 30% of patients having a strong family history (58). Autosomal dominant transmission accounts for the majority of heritability, with mutations in the C9ORF72, progranulin, and microtubule-associated protein tau genes. However, other genes are associated with rare FTD cases, such as valosin-containing protein mutations, charged multivesicular body protein 2B, fused in sarcoma (FUS) protein, TDP-43, sequestosome 1 protein, TANK-binding kinase 1 protein, and ubiquilin 2 protein (39). C9ORF72 seems to be the most common worldwide cause of genetic FTD, followed by progranulin and then microtubule-associated protein tau genes (58). In each of the gene groups with amyotrophic lateral sclerosis, bvFTD is most common; among C9ORF72 carriers, bvFTD is also common. Frontotemporal pathology in FTD is characterized by severe focal atrophy of frontal and temporal regions, subcortical gliosis, and neuronal loss (43). Neuroimaging studies, such as MRI and FDG-PET, can show gray matter atrophy and hypometabolism at least 10 years before symptom onset (58). Initially, pathological diagnosis was based on atrophy and neuronal and glial cell inclusions of hyperphosphorylated tau protein; however, more than 50% of patients with FTD proved to be tau negative but ubiquitin positive (59). Most FTD-ubiquitin inclusions are composed of TDP-43. The remaining 5% are tau and TDP-43 negative with inclusions of FUS protein, referred to as FTD-FUS (59). Because of its heterogeneity, the diagnostic process in FTD can be fraught with difficulty; moreover, having a correct diagnosis is essential to the future of clinical trials for disease-modifying treatments. Great efforts have been made over the last 2 decades to identify biomarkers sensitive to FTD, with a predominant focus on fluid biomaterial and neuroimaging. FTD studies have primarily focused on structural changes assessing gray matter atrophy and hypometabolism, which have been fairly consistent and validated diagnostic biomarkers between studies. However, white matter changes are probably more sensitive for the earliest changes in FTD than gray matter changes (60). Studies within the last 5–10 years have examined white matter integrity using diffusion tensor imaging. This technique measures the microstructural integrity of white matter by determining the rate of diffusion in different directions; the changes in different diffusion tensor imaging metrics are thought to reflect different pathological changes in microstructure. In FTD, white matter diffusivity has been found to precede gray matter atrophy and with a more widespread distribution in the brain. Four potential areas of application have been identified: differentiating between individuals with FTD, individuals with other types of dementia, and individuals without dementia; differentiating between subtypes of FTD; disease monitoring; and detection of early changes before disease onset (60). A combination of fluid biomarkers in the CSF are likely to yield more information than single markers. For example, phosphorylated TDP-43 constitutes one of the major pathological subtypes of FTD; moreover, neurofilaments are a major constituent of the neuroaxonal cytoskeleton and play an important role in axonal transport and in the synapse (61). Neurofilament light chain blood and CSF levels are 2.5–11 higher among patients with FTD than among control groups and are thought to reflect axonal damage (62–66). No treatments are available that will change the course of FTD, so the focus of medical therapy is on symptomatic relief using pharmacological and nonpharmacologic methods. Nonpharmacologic interventions should focus on patient safety and well-being. Discussions with family should include management of financial accounts and credit cards, driving safety, and environmental factors to ensure physical safety. Exercise and physical therapy can be helpful for patients with motor problems. Among patients with hyperorality, special attention to diet should be made by caretakers to avoid excessive weight gain. No FDA-approved pharmacologic interventions exist for any of the FTD subtypes. Anticholinesterase inhibitors are not recommended because no evidence supports a deficit of acetylcholine in this disease (67). Studies in bvFTD have shown serotonergic network disruption, with decreased serotonin levels and 5-HT1A and 5-HT2A receptors in frontotemporal regions and neuronal loss in the raphe nuclei (68, 69). Evidence suggests that selective serotonin reuptake inhibitors (SSRIs) are effective in helping with various symptoms of FTD, including disinhibition, impulsivity, repetitive behaviors, and eating disorders (69–71). Evidence also exists for dopaminergic disruption, with low levels of dopamine metabolites and severely reduced presynaptic dopamine transporters in the putamen and caudate of patients with FTD (70, 72). Some patients with bvFTD will require the use of antipsychotics for the treatment of severe neurobehavioral symptoms; however, they are usually reserved if no success was achieved with nonpharmacologic interventions or SSRIs. These patients tend to be more sensitive to extrapyramidal side effects because of diminished dopaminergic function; therefore, agents with less D2 receptor antagonism, such as quetiapine, are preferred (73). Parkinson’s disease (PD) and Lewy body disease (LBD) are both neurodegenerative diseases caused by filamentous aggregates of misfolded alpha-synuclein protein, which form the eosinophilic intracytoplasmic inclusions known as Lewy bodies in the brain (74). Alpha-synuclein is normally present in synapses and encoded by chromosome 4 (75). Although its function is not fully understood, it seems to play a role in vesicle production. Staining for alpha-synuclein is now used routinely for identifying Lewy bodies and Lewy neurites (76). As with most neurodegenerative disorders, no disease-modifying drugs exist, limiting treatment options to symptomatic relief and palliative measures. Parkinson’s disease dementia (PDD) and LBD affect cognition, behavior, movement, and autonomic function. In both dementias, the accumulation of misfolded alpha-synuclein protein in the form of Lewy bodies and Lewy neuritis leads to the loss of dopaminergic and cholinergic cells, often with a variable degree of coexisting Alzheimer’s disease pathology. Both have overlapping clinical features. However, the main difference is in the sequence of symptoms. In PDD, motor symptoms precede dementia or develop within 12 months of dementia. In LBD, motor symptoms either occur simultaneously or follow dementia. The two disorders represent two entities on a continuum, with many similarities but some differences (77). LBD is currently considered the second most common type of neurodegenerative disorder leading to dementia among older people, accounting for 10%–15% of cases at autopsy (78). However, DLB is often underrecognized and underdiagnosed because of difficulties differentiating DLB from Alzheimer’s disease. As a result, the true prevalence and incidence rates of DLB in the community are difficult to estimate (79). Lewy bodies are the primary lesions found in degenerating neurons of the limbic system, brainstem (substantia nigra, locus coeruleus), and neocortex of patients with DLB. As previously mentioned, Lewy bodies consist of abnormal eosinophilic intracytoplasmic filamentous aggregates of misfolded alpha-synuclein protein. These abnormal neurofilaments have been found to also contain tau and ubiquitin (74). However, patients with DLB may also have amyloid deposition because of the high occurrence of mixed Alzheimer’s disease and PD pathology found postmortem (79). This finding is supported by evidence that alpha-synuclein stimulates the fibrillation of Aβ and tau proteins (80). Some structural changes are similar to those seen among patients with Alzheimer’s disease, with wide cerebral atrophy being a feature of both Alzheimer’s disease and DLB (81). However, unlike Alzheimer’s disease, the medial temporal lobe is relatively spared in DLB (82). Most patients with DLB show a loss of pigmented, dopaminergic neurons in the substantia nigra, similar to what is seen in PD (83). However, the main pathological changes in DLB affect the neocortex and limbic system. On the basis of current international neuropathological staging systems, it is impossible to distinguish DLB from PDD, which shares similar clinical, neurochemical, and morphological characteristics with DLB. However, imaging and postmortem studies suggest that patients with DLB exhibit elevated limbic and striatal Alzheimer’s disease–related pathologies as well as a lesser degree of dopaminergic cell loss compared with patients with PDD (84–86). In 2017, the DLB Consortium published its revised recommendations for the clinical and pathologic diagnosis of DLB in its fourth consensus report, updating its previous report that was used widely for the last decade (87). Probable DLB is diagnosed if two or more core clinical features of DLB are present with or without the presence of indicative biomarkers, or if only one core clinical feature is present with one or more indicative biomarkers. Possible DLB is diagnosed if one core clinical feature is present with no indicative biomarker evidence, or if one or more indicative biomarkers are present with no core clinical features. Essential to the diagnosis of DLB is dementia, a progressive cognitive decline sufficient to interfere with function or daily activities. Prominent or persistent memory impairment may not occur in the early stages but is evident with progression. However, disproportionate deficits on tests for attention, executive function, and visuospatial ability may be prominent and occur early. Dementia screens such as the MMSE and the MoCA are useful to characterize global impairment in DLB; however, neuropsychological assessment should include tests covering the full range of cognitive domains affected. Tests of processing speed and divided-alternating attention are measures of attention and executive function that can help to differentiate DLB from Alzheimer’s disease and normal aging. Examples include the Stroop tasks, trail-making tasks, phonemic fluency, and computerized tasks of reaction time. Tasks of figure copy can help to detect spatial and perceptual deficits that often occur early in DLB. Examples include block design or puzzle tasks, spatial matching, and perceptual discrimination. The core clinical features of DLB include fluctuating cognition, recurrent complex visual hallucinations, rapid eye movement (REM) sleep behavior disorder, and parkinsonism. Fluctuating cognition, visual hallucinations, and REM sleep behavior disorder tend to occur early and can persist throughout the course of DLB. The supportive clinical features include severe sensitivity to antipsychotic agents, postural instability, repeated falls, syncope, severe autonomic dysfunction, hypersomnia, hyposmia, hallucinations, delusions, apathy, anxiety, and depression. According to the 2017 consensus report of the DLB Consortium, direct biomarker evidence of Lewy body pathology is not yet available for clinical diagnosis; however, several useful indirect methods exist (87). Indicative biomarkers include reduced dopamine transporter uptake in the basal ganglia by single photon emission computed tomography (SPECT) or PET imaging; reduced uptake on metaiodobenzylguanidine myocardial scintigraphy, which quantifies postganglionic sympathetic cardiac innervation and is reduced in LBD; and polysomnography confirmation of REM sleep without atonia, which is highly predictive of Lewy-related pathology. Supportive biomarkers are consistent with DLB and help the diagnostic evaluation even though they lack clear diagnostic specificity. These biomarkers include relative preservation of medial temporal lobe structures on CT or MRI scans, generalized low uptake on SPECT-PET perfusion-metabolism scans, reduced occipital activity and the posterior cingulate island sign on FDG-PET imaging, and prominent posterior slow-wave electroencephalography activity with periodic fluctuations in the pre-alpha-theta range. Cognitive impairment is the most common nonmotor feature of PD (88). Although subtle cognitive deficits may be detected in the early stages of PD, overt cognitive deficits usually manifest in the later stages as the age advances (77). The point prevalence of PDD is estimated to be up to 30%, but longitudinal data demonstrate dementia prevalence rates as high as 80% at more advanced stages of PD; these data support the theory that dementia is an inevitable manifestation of the disease (89–91). Old age at the time of disease onset or at the time of evaluation is the most established risk factor for PDD. Older patients and those with severe disease are 12 times more likely to develop dementia compared with younger patients with mild disease (92). Low baseline cognitive scores, early development of confusion or hallucinations on dopaminergic medications, postural imbalance, and excessive daytime sleepiness have also been associated with increased risk of dementia (77). Similar to DLB, the cognitive profile of PDD is a dysexecutive syndrome with early and prominent impairment of attention and visuospatial functions, moderately impaired episodic memory, and relatively preserved core language function. Similar to DLB, a range of neuropsychiatric symptoms can be displayed in PDD; the most common symptoms include hallucinations, apathy, depression, and insomnia. Visual hallucinations, similar to those displayed in DLB, are well-formed and vivid, often with preserved insight and little emotional content (77). Delusions are also common. Autonomic disturbances such as urinary incontinence as well as orthostatic and postprandial hypotension are frequent in PDD. As previously discussed, PDD is characterized by a variable combination of synucleinopathy (Lewy body degeneration), cellular loss in subcortical nuclei, and Alzheimer’s disease pathology (Aβ plaques and tau protein forming neurofibrillary tangles). Degeneration of subcortical nuclei results in various neurochemical abnormalities, including cholinergic, dopaminergic, serotonergic, and noradrenergic deficits, of which cholinergic loss is the most prominent. Loss of cholinergic neurons in the nucleus basalis of Meynert (nbM) is greater than that displayed in Alzheimer’s disease, and Lewy bodies are more frequently found in the nbM (77). As in all of the neurodegenerative disorders discussed previously, no cure exists for dementia caused by either PD or LBD. Symptomatic treatment remains the focus of medical interventions. Patients with PDD or DLB have significant cholinergic deficits; therefore, AChEIs such as donepezil or rivastigmine represent the logical choice for pharmacological treatment of dementia in both cases. Donepezil is the most widely used AChEI in the treatment for dementia, and it selectively inhibits acetylcholinesterase (AChE). Rivastigmine is unique in that it has both AChE and butylcholinesterase inhibitory activity. In 2012, the FDA approved rivastigmine for mild to moderate dementia associated with PD on the basis of the 2004 study by Emre et al. (93), a large, randomized, double-blind, placebo-controlled study of rivastigmine lasting 24 weeks among 541 patients with mild to moderate dementia that developed at least 2 years after receiving a clinical diagnosis of PD. Patients treated with rivastigmine had a mean improvement of 2.1 points on the 70-point Alzheimer’s Disease Assessment Scale, with a baseline score of 23.8, compared with a 0.7-point worsening in the placebo group, with a baseline score of 24.3 (p<0.001). The study also demonstrated clinically meaningful improvements in the scores for the Alzheimer’s Disease Cooperative Study-Clinician’s Global Impression of Change; improvements were observed in 19.8% of patients in the rivastigmine group and 14.5% of those in the placebo group, and clinically meaningful worsening was observed in 13.0% and 23.1%, respectively (mean score at 24 weeks=3.8 and 4.3, respectively; p=0.007). When the psychotic symptoms of DLB and PDD become more distressful or threatening, the use of low doses of second-generation antipsychotics with low D2 potency, such as quetiapine, should be considered to minimize motor side effects. Pimavanserin, a novel antipsychotic drug that is a selective 5-HT2A receptor inverse agonist, was recently approved by the FDA for the treatment of psychosis in PD (94). It has negligible effects on dopamine and histamine receptors; therefore, it avoids the motor and sedative side effects common with other antipsychotics. However, risks are still associated with pimavanserin, especially the prolongation of the QT interval. Like other antipsychotics, risk of death is increased with pimavanserin among elderly patients with dementia. Dementia is a significant contributor to the U.S. burden of disease, and it is projected to significantly increase over the next few decades as the U.S. population continues to grow. In this review, I apprised some of the more common dementia syndromes from among dozens of different diseases. The clinician’s ability to understand and diagnose distinct types of neurodegenerative disorders on the basis of core clinical and biological features is essential for the success of future research trials and therapeutic interventions. Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston The author reports no financial relationships with commercial interests. References 1. Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 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