Authors: Alka A. Subramanyam (alka.subramanyam@gmail.com), Shipra Singh (1Department of Psychiatry, Institute of Human Behaviour and Allied Sciences, Delhi, India), Nitin B. Raut (2Department of Psychiatry, Lady Hardinge Medical College, New Delhi, India)
Categories: Clinical Practice Guidelines
Source: Indian Journal of Psychiatry
Authors: Alka A. Subramanyam, Shipra Singh, Nitin B. Raut
Today, neuroscience has progressed to understand that dementia is actually a late diagnosis. Just as cholesterol plaques start in the vascular system as early as the first decade of life, so too brain degeneration may predate manifestation of frank symptoms by 2–3 decades. Therefore, it is important to understand if clinically there is a gray zone between apparent normal brain functioning and obvious brain decline. This gap is what mild cognitive impairment or mild neurocognitive disorder (Mild NCD) is.
A seminal discussion in 2003 led to acceptance of Mild NCD as a separate entity and the definition based on Petersen’s criteria. Subsequently, these were modified to Winblad criteria and those defined by NIA-AA (National Institute of Ageing and Alzheimer’s Association) as well as the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, DSM-5 (which spoke of Mild NCD). The common thread in all of these was subjective recognition of cognitive errors, objective decline in neuropsychological tests, and relatively intact ability to carry on with activities of daily living, the combination of which could lead to adequate distress and anxiety.[1]
Hence, systematic research of the same and the approach to assessment and care are really the need of the hour. In India, the research is even more limited, and hence, this guideline, which is a combination of the best advised practices, and those followed easily in the subcontinent, so it can be easy for the treating psychiatrist to approach and manage.
The development of the Clinical Practice Guidelines (CPG) for the assessment and management of Mild NCD was a rigorous and systematic effort led exclusively by a team of psychiatrists from leading institutions across India. The guidelines were crafted based on an extensive review of the latest scientific literature, including national and international guidelines such as those from the National Institute on Aging-Alzheimer’s Association (NIA-AA), the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), and the International Classification of Diseases (ICD-11).
This process was driven by the need to address the specific challenges and nuances of diagnosing and managing Mild NCD within the Indian population. The expert team engaged in multiple rounds of discussions and deliberations to ensure that the guidelines are evidence-based, clinically sound, and tailored to the Indian context. Following this, the draft was deliberated in an IPS workshop, incorporating the inputs of expert professionals throughout the country. The focus was on creating a comprehensive resource that reflects both the current scientific understanding of Mild NCD and the practical realities faced by psychiatrists in India. The resulting guidelines aim to standardize and enhance the quality of care provided to individuals with Mild NCD, ensuring that psychiatrists have a reliable and relevant framework for diagnosis and management. These guidelines may be modified by the clinicians as per the individual’s need and feasibility, as per the available facilities and setup.
When discussing about Mild NCD, it becomes imperative to understand what cognitive reserve is and how to assess it.
Cognitive reserve (CR) is nothing but the brain’s ability to cope with neuropathology/neurodegeneration by exploiting pre-existing cognitive processes and/or compensatory mechanisms, which is supposedly built through a number of factors over the years. It reflects the brain’s flexibility and efficiency in utilizing available resources to maintain cognitive function despite aging or disease [Figure 1].

Assessing cognitive reserve is crucial for understanding individual differences in susceptibility to cognitive decline and dementia. It helps in identifying those at higher risk and in tailoring interventions that can bolster cognitive reserve through lifestyle modifications and targeted cognitive training. Although there are no gold standard tests available, certain proxies are cumulatively reflective of CR [Table 1].
Some scales also have been formulated using one or more of the above proxies or domains but are not widely used and researched [Figure 2].
![Figure 2: Scales for assessment of CR[23]](IJPsy-67-21-g002.jpg)
The transition between normal aging and very early-stage dementia has been defined using various terms, such as Mild NCD, dementia prodrome, incipient dementia, and isolated memory impairment. Over the years, Mild NCD has become a widely used term and will be used here for the purpose of discussion. MILD NCD is positioned between normal aging and early dementia on the continuum, with overlapping stages at both ends of the MILD NCD [Figure 3], indicating that distinction between normal ageing and MILD NCD can be subtle and clinically challenging. However, Mild NCD has gradually been established as a distinct diagnosis, with specific criteria and intervention strategies.[4]

Several terms have been used in connection to cognitive decline before dementia, apart from MCI over time. Subjective cognitive impairment (SCI) is a self-perceived decline in cognitive abilities, particularly memory, without objective evidence from standardized cognitive tests. It represents the earliest symptomatic manifestation in the continuum from normal aging to dementia. Other terminologies which have been used are, for example, benign senescence forgetfulness, age-associated cognitive decline (AACD), age-associated memory impairment (AAMI), cognitive impairment no dementia (CIND), and very recently used Mild NCD in DSM-5 [Table 2].[5]
Along with changes in the nomenclature, simultaneous changes occurred in the understanding of Mild NCD, summarized in Table 3. In addition to symptoms and cognitive assessments, brain pathology was also deliberated. The protein theories of Mild NCD emphasize the significant role of abnormal protein accumulation and aggregation in the brain, which can lead to cognitive decline. Table 4 summarizes the key proteins involved, their roles in Mild NCD, and underlying mechanisms.
Mild NCD is heterogeneous in presentations, depending upon the affected cognitive domain. Due to this, it has also been classified on the basis of the cognitive domain affected. This classification relates to underlying etiology and pathology, clinical presentation, and outcomes. Figure 4 shows various subtypes and their probable outcome.[8] Today, we understand that this classification is more clinical and less etiopathological and probably too simplistic to understand Mild NCD. Nevertheless, it is important for the clinician to know.

The course of Mild NCD is variable. It may not always convert to dementia. Around 20–40% cases appear to improve over time on retesting. After diagnosis, the subtype may change on follow-up. A single domain particularly seems to be at risk of this shift. However, some have found that all Mild NCD subtypes either convert to dementia or retain their status. Rates of progression to dementia vary in the range of 20–40% (10–15% per year) with a few outliers at the lower and higher ends of the spectrum, around 80% cases in approximately 10 years, which keeps on increasing exponentially each year.[8]
Certain factors are associated with increased risk of progression to dementia which should be specifically looked for while assessment [Table 5].
Mild NCD may although affect one or more cognitive domains but does not interfere with a person’s capacity of independence in everyday activities and often gets overlooked, leading to delays in consultation, along with various other reasons [Table 6].
The need for diagnosis and intervention in Mild NCD is often questioned owing to the mild nature of its symptoms. Evidence suggests that Mild NCD may remain stable, return to neurologically intact conditions, or progress further to dementia. However, the risk of progressing to dementia compared to age-matched controls is higher, thus indicating the pathologic disease state of Mild NCD rather than normal aging. Mild NCD needs comprehensive assessment and timely interventions. Various reasons are listed in Table 7.
Any patient suspected of having Mild NCD should undergo detailed clinical evaluation and systematic investigations. A comprehensive history and physical examination [especially central nervous system (CNS) examination], focusing in detail on the status of cognitive functions, status of activities of daily living, medication use, neuropsychiatric evaluation, incorporating laboratory testing, and neuroimaging, are important components of this assessment [Figure 5].

Taking a comprehensive history in patients with Mild NCD is crucial for accurate diagnosis and management. The history may focus on clarifying the points as mentioned in Table 8.
The history should incorporate the following considerations in
Cognitive symptoms: Detailed history of cognitive symptoms needs to be elicited [Table 9]. Table 9Pointers in history of cognitive symptoms in suspected Mild NCD Defining the onset, duration, course, and progression of symptoms e.g., When was he/she last completely normal? Defining the nature of cognitive symptoms Memory Specific instances of forgetfulness (e.g., forgetting appointments, conversations, recent events).Frequency and duration of memory lapsesImpact on daily activities (e.g., losing items, repeating questions) Language Word-finding difficulties (e.g., trouble naming familiar objects or people).Problems with comprehension or following conversations.Changes in fluency or coherence in speech. Visuospatial Getting lost in familiar places.Difficulty judging distancesProblems with tasks requiring spatial orientation (e.g., driving, assembling objects). Attention and concentration Difficulty maintaining focus on tasks.Easily distracted or trouble following conversations.Impact on completing tasks or following instructions. Executive Problems with planning, organizing, and problem-solving.Difficulties in managing finances or medication.Inability to multitask or follow multi-step instructions.Ability to cook a mealHousehold appliance repairsUse of tools/appliances/instruments
Social cognitionDifficulty in understanding non-verbal signals, including facial expressions, body posture, and vocal tone.Reduced empathyAvoidance of social interactionsDifficulty in maintaining family or workplace relations
Situational TriggersTimes of day when symptoms are better or worse.Specific situations or conditions that exacerbate symptoms (e.g., stress, fatigue).
Compensatory StrategiesTechniques the patient uses to manage or mask symptoms (e.g., using reminders, relying on others, noting down things etc.).Effectiveness of these strategies.
The other important parameters to be assessed in history history (points b to k) are summarized in Table 10.
Table 10Specific parameters to be explored in each section of historyParametersSpecific points to be exploredb)Behavioral and psychological symptomsMood Changes: Presence of depression, anxiety, irritability, or apathy; and its impact on social interactions and relationships.Personality Changes: Noticeable changes in behaviour or personality (e.g., increased aggression, withdrawal, jocularity, disinhibition etc).Sleep Disturbances: Changes in sleep patterns (e.g., insomnia, excessive sleepiness).Psychotic Symptoms (if any): Presence of hallucinations or delusionsc)Impact on daily life OR Changes/reduced ability to performActivities of Daily Living (ADLs): Impact on basic activities (e.g., bathing, dressing, eating).Instrumental Activities of Daily Living (IADLs): more complex activities (e.g., managing finances, shopping, cooking, using technology)d)Past medical historyMedical history, with particular importance to prior neurologic (to exclude stroke, Parkinson’s disease, normal pressure hydrocephalus, or neuropathy) or psychiatric conditions.Complete information should be obtained to rule out potentially reversible causes of cognitive decline like depression, vitamin Folate/B12 deficiency, thyroid disorders, etc.e)History of ongoing medicationsReview of ongoing treatment with emphasis on Compliance to treatmentMedicines with CNS activity, over-the-counter drugs, illicit substances, supplements, and alternative forms of medicinesf)History of substance useAssessing chronicity and recent changes in the pattern of substance useg)Family HistoryPresence of family history of cognitive disorders, substance use, psychiatric illnesses, neurological illnesses, any illness with genetic predispositionh)Social HistoryPsychosocial history (family, friends, religious activities, hobbies, social involvement etc.)Living Alone, with family, assisted livingSupport Family, friends, caregiversDaily routine activities and hobbiesSocial and recreational activitiesEducational and occupational backgroundi)Diet to rule out any deficienciesj)Assess level of physical activity/exercisek)Extent of involvement in cognitively challenging tasks
Some of the relevant findings of neurological system examination are listed in Table 11.[9] In the briefest neurological examination, assessing extraocular movements and gait is crucial whenever feasible.
The mental state examination in a suspected case of cognitive impairment requires detailed evaluation of higher mental functions. This would include testing the cognitive domains already elaborated in the section of ‘History taking’. Some of the common tests and their usefulness are listed in Table 12.[910] The first six may be done by the sole practitioner in OPD as well.
Both DSM-5 and ICD-11 include mild cognitive impairment under the category of Mild NCD, with nearly similar diagnostic criteria.[1112] ICD-10 mentions the diagnosis of ‘Mild Cognitive Disorder’ (F06.7) under the head of ‘Other mental disorders due to brain damage and dysfunction and physical disease’[13] [Table 13].
Excessive focus on subjective symptoms could lead to missing the diagnosis, where the patient lacks insight and/or the family is in denial.Excessive focus on objective assessments may lead to missing the diagnosis in high functioning individuals, whose currently ‘normal’ performance might be a ‘decline from his/her baseline’.Assessment of the cognitive reserve of the individual (as has been explained earlier). Individuals with high cognitive reserve may not show symptoms of Mild NCD until they have a significant amount of brain pathology, which may delay the diagnosis of Mild NCD. Second, standard cognitive tests might not be sensitive enough to detect Mild NCD in such individuals.The neuropsychological assessment has a role in reaching to diagnosis. These tests, with performance compared against age-appropriate norms and educational and cultural backgrounds, are a critical part of the standard evaluation of NCDs, particularly that of Mild NCD.It is also interesting to note that none of the common definitions of Mild NCD includes advanced age as a criterion, in spite of the fact that most of the research in the domain occurs in the geriatric population and is presumed to be a disorder of old age.
When talking about making a diagnosis of mild NCD, it is crucial to consider the following common differential in relation to Mild NCD [Figure 6].[11]

The diagnosis of Mild NCD is based on the diagnostic criteria. However, there are a number of underlying factors or causes which may be causative or contributory to the condition. This has been taken into cognizance by the specifier ‘Another Medical Condition’ of the Mild Neurocognitive Disorder in DSM-5.[11] Similar to dementia, Mild NCD too has many reversible causes, which, although less commonly, show good prognosis with optimum treatment of underlying conditions. Thus, such potentially reversible causes should be thoroughly investigated. Some of the common ones are listed in Figure 7, along with the mode of assessment.[141516] However, it is essential to elicit symptoms and signs as well, while clinical assessment, which would provide clues to the etiology and accordingly the investigations, may be conducted. For example, metabolic causes generally have some or the other clinical manifestation, which can be identified. Atrial fibrillation may cause small, undetectable embolic events, similar to small strokes or transient ischemic attacks, leading to Mild NCD and ultimately vascular cognitive impairment.

Neuroimaging has not been routinely recommended in diagnosis of Mild NCD but may be helpful in evaluating the overall brain structure, in addition to serving the following Identifying underlying causative conditions like brain tumors, normal pressure hydrocephalus, vascular malformation, and strokes.Serving as a potential biomarker for progression to Alzheimer’s dementia (AD). However, there is lack of consensus of different guidelines on this.
Advances in both structural and functional neuroimaging have been providing valuable insights into the structural, functional, and biochemical alterations in the brain, enabling the physicians to make the diagnosis of Mild NCD and in predicting its progression to dementia more accurately. Commonly observed neuroimaging findings are summarized in Figure 8.[1718]

Recently, newer methodologies for existing techniques have been introduced to improve clinical value of methods that process obtained data. In relation to MRI, various morphometry methods are being used for data processing, for example, voxel-based, pattern-based, tensor-based, and deformation-based. In Alzheimer’s dementia, the earliest changes occur in the medial temporal lobe, specifically in the entorhinal cortex, perirhinal cortex, and hippocampus. Since neuronal damage in the hippocampus leads to a decrease in its volume, volumetric MRI scan of the hippocampus is a commonly accepted method for assessing AD pathology, suggests the anatomic validity of the underlying disease process, and is an early indication for AD.
Additionally, diffusion tensor imaging (DTI) studies have demonstrated a relationship between white matter integrity and disease severity. Optical coherence tomography links pathological changes in the retina to Alzheimer’s dementia.[17]
Several CSF biomarkers have been identified in AD.[1920] The three CSF biomarkers—total tau, phospho-tau, and Aβ42—are highly effective in diagnosing early-stage Alzheimer’s disease and predicting its progression in patients with MILD NCD. Testing for these markers can be valuable if accessible.
Genetic studies may provide potential biomarkers. Genetic testing has not been considered or recommended in any of the recent guidelines. The important features concerning genetic studies are summarized in Figure 9.[11] Figure 9Importance and indications of genetic testing in Mild NCD Patients requiring genetic studies should be imparted genetic counseling beforehand
Application of appropriate cognitive tests, applicable to patient’s age, education, and cultural background, is another crucial part for evaluation of patients with Mild NCD. The DSM-5 does not require specific neuropsychological tests, but these tests can help assess changes in six key areas of attention, executive function, memory, language, perceptual-motor skills, and social cognition. However, no such assessment incorporates all these domains. The performance typically lies within 2 standard deviation (SD) range (between 3^rd^ and 16^th^ percentiles). Some of the commonly used tests along with their properties are listed in Table 14.[10212223]
In addition to above, clinicians should also collect information on cognitive functioning from caregivers/informants using standardized assessment tools such as the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) and the Dementia Severity Rating Scale (DSRS). Other tests used are Memory Impairment Screen, Quick Screen for Mild Cognitive Impairment, CDT- Sunderland, and CERAD.
Assessment of functional status is also important to differentiate Mild NCD from dementia. Several scales/tools are [1024]
Lawton-Brody Instrumental Activities of Daily Living: Subtle deficits in instrumental activities of daily living (IADL) are noticed in Mild NCD.Functional Activities Questionnaire (FAQ): Assess functional status, using information from an informant. A score of 6 or higher has over 85% accuracy in distinguishing mild cognitive impairment from dementia.Performance Assessment of Self-Care Skills (PASS) test: It is a valid and reliable instrument which measures occupational performance in daily life activities.
The psychological and behavioral symptoms of Mild NCD and the subsequent caregiver distress may be assessed using Neuropsychiatric inventory (NPI) and (NPI-Q), a short questionnaire form of the NPI, and for depression by Geriatric Depression Scale (GDS).[2526]
Figure 10 presents an algorithm to approach a person with suspected Mild NCD.

Managing MILD NCD is challenging due to variability in symptoms, difficulty in distinguishing it from normal aging or dementia, and lack of universally effective treatments. Effective management focuses on early detection, regular monitoring, and implementing strategies to maintain cognitive function and delay progression to dementia [Figure 11]. Treatment setting is usually outpatient and management relies heavily on nonpharmacological measures due to lack of approved medication and heterogeneity in presentation. This has, to some extent, contributed to the spread of numerous myths regarding its management [Table 15].

Management goals for Mild NCD largely include forming a collaborative care approach, aiming for MILD NCD reversal whenever possible, effectively managing comorbidities, promoting overall health, promoting independence, preparing for disease progression, and maintaining continuous monitoring [Table 16], helping patients and caregivers to restructure their activities and environment to achieve independence, as is developing a trusting therapeutic relationship to facilitate the management process.[27]
The predisposing factors for Mild NCD as highlighted earlier are a potential point for intervention to reduce the risk of developing Mild NCD at a later stage. The common ones along with possible intervention strategies are listed in Table 17.
As discussed in the assessment section, numerous treatable factors can contribute to or even cause Mild NCD. Unfortunately, these factors are often ignored and underrated, even though some are easily manageable and can significantly improve cognition. Treatment of underlying causes is the principle, discussed in Table 18.
Lecanemab (Leqembi), an IgG1 monoclonal antibody, received accelerated Food and Drug Administration (FDA) approval for treating Mild NCD and early AD in 2023. In phase III trials, it significantly reduced brain amyloid levels slowing cognitive decline by 27% compared to placebo.
Mechanism of Reduce cerebral amyloid deposition, thereby reducing cognitive declineRoute of 10 mg/kg IV administered once every 2 weeksSafety Risk of treatment-induced Amyloid-Related Imaging Abnormalities (ARIAs), particularly in individuals with a homozygous ApoE ε4 genotype. Other serious side effects include brain edema (ARIA-E) and microhemorrhages (ARIA-H). Symptoms can include confusion, dizziness, headache, and visual disturbances and close monitoring is warranted.Indications: Mild NCD due to AD and early ADNot recommended for patients with MRI evidence of non-AD dementia and should be used cautiously in ApoE-ε4 carriers due to the risk of ARIAs.Considerations around cost, serious adverse effects, need of strict monitoring, and lack of long-term safety data need to be addressed to ensure the wide application.[2930]
Currently, there are no other pharmacological agents approved by the FDA for treatment of Mild NCD. Table 19 lists medications useful in management of dementia, tried in NCD, without much effect.[16] Overall, while various pharmacologic and supplement interventions have been tested, none have shown significant benefits in delaying the progression of Mild NCD to dementia. Consequently, the focus has shifted to nonpharmacological approaches.
Furthermore, management of neuropsychiatric symptoms should be done by nonpharmacological measures; however, when warranted, symptomatic management using appropriate psychotropics as approved in the elderly population may be prescribed for symptoms like depression, anxiety, sleep disturbance, and apathy.[162427]
There is emerging evidence of utility of noninvasive brain stimulation methods like rTMS (repetitive transcranial magnetic stimulation) and tDCS (transcranial direct current stimulation) in Mild NCD. More robust research with standardized methodology is needed to assess the impact of the same on Mild NCD.[31]
Cognitive Remediation for Mild NCD aims to improve cognitive function and enhance quality of life. Early and targeted interventions are essential as they can lead to symptomatic improvements, reduce neuropsychiatric symptoms, and ultimately improve outcomes for individuals with Mild NCD. This can be classified into cognitive training (CT), cognitive rehabilitation (CR), and cognitive stimulation (CS). Each approach has distinct goals, methods, and types of activities [Table 20].
These interventions are well researched and found to have lasting positive effects on the cognitive functioning of healthy elder individuals. These three approaches involve varying tasks and exercises targeting the specific cognitive domain or skill, thereby affecting the overall functioning, These may be carried out individually or in group settings, at specialized settings or at home, facilitated by a trained therapist or family member with support of a therapist [Table 21].[3233343536]
It is seen that lifestyle modification can greatly help reducing the risk of worsening of cognitive decline and to promote cognitive health in elderly individuals. Table 22 below provides with a few recommendations for the same. The Nun Study highlighted the protective role cognitive reserve and healthy lifestyle choices have in reducing cognitive decline. The findings of the study revealed that higher linguistic ability earlier in life, regular mental and physical activity, and maintaining cardiovascular health significantly reduced the risk of cognitive impairment and dementia despite the presence of Alzheimer’s pathology.[37] In a similar study, the 10/66 Dementia Research Group indicated that regular intake of fish, rich in omega-3 fatty acids, is associated with a reduced risk of cognitive impairment and dementia, emphasizing the neuroprotective and anti-inflammatory benefits of omega-3 fatty acids,[38] reiterating the importance of dietary practices in maintaining cognitive health.
Common myths pertaining to management of Mild NCD
Based on detailed assessment, a personalized management plan should be developed in collaboration with the patient and family members, which includes relevant cognitive and lifestyle interventions, along with specific goals, plans, and treatment settings.Provide resources and support to help the patient and family implement the interventions. Schedule regular follow-up appointments to track progress and make necessary adjustments to the plan.By tailoring a management plan to the distinct needs of the patient and involving family members in the process, it is possible to create a supportive environment that promotes cognitive health and improve quality of life for individuals with Mild NCD.This personalized approach ensures that the interventions are practical, achievable, and aligned with the patient’s lifestyle and preferences.
Caregiver interventions play a crucial role in managing Mild NCD and supporting both patients and their caregivers. These interventions can significantly improve the quality of life, reduce caregiver burden, and enhance caregiving capabilities. Some key types of caregiver interventions[40] are listed in Figure 12.

The following should be included in any follow-up visit for those with Mild NCD:
A validated cognitive instrument that is consistently repeatedA comparative structured history from informantA comparative structured functional capacity assessment. Details in Table 23. Table 23Follow-up assessments in Mild NCD[1441]Follow-Up IntervalComponents6–12 Month Follow-Up• Health professional assessment • Reassessment of cognitive functions • Formal Informant Report • Comprehensive Functional AssessmentEarlier Review Triggers• Concerns raised by the patient or family • Recent hospital admission • Multi-domain amnestic mild cognitive impairment (Mild NCD) • Presence of neurological signs • Mood or behavioral symptoms • Unexpected changes
A number of ethical considerations when dealing with individuals with Mild NCD may arise, especially in context of clinical trials and other research settings. The clinician may also face issues pertaining to assessment, disclosing diagnosis and management of such individuals. Table 24 summarizes the key points and possible ways to [42434445]
Capacity refers to the ability of an individual to understand the benefits and risks of available options, make an informed decision, and communicate that decision independently. Mild NCD represents an intermediate or transitional stage between normal aging and more severe of cognitive impairment and thus raises concerns about the capacity of these individuals to make informed decisions and manage their routine affairs. One such concern was participation in research and clinical decision making, which was addressed in the previous section. Others are tabulated below [Table 25].[4647]
An overview of the assessment and management of Mild NCD is depicted in Figure 13.

Comprehensive assessment and management of Mild NCD is essential to prevent its progression and to enhance the quality of life of the individuals. Early and precise diagnosis, utilizing clinical assessment, laboratory tests, and neuropsychological testing, allows for timely intervention. Integrating multidisciplinary approaches, including cognitive training, pharmacological treatments, and lifestyle modifications, can effectively address both cognitive and neuropsychiatric symptoms associated with Mild NCD.
Furthermore, recognizing and managing Mild NCD-related behavioral symptoms is essential in reducing caregiver burden and improving overall patient outcomes. Regular follow-up assessments are crucial to monitor disease progression and adjust treatment plans accordingly. Continuous research and validation of biomarkers, tests, and interventions are necessary to improve diagnostic accuracy and treatment efficacy. By adhering to these clinical practice guidelines, clinicians can ensure a comprehensive, structured, and effective approach to the assessment and management of Mild NCD, with Table 26 serving as a ready reference for practitioners.
There are no conflicts of interest.