|Year : 2016 | Volume
| Issue : 1 | Page : 10-20
Mild cognitive decline: Concept, types, presentation, and management
Alka A Subramanyam, Shipra Singh
Department of Psychiatry, Topiwala National Medical College (TNMC) and BYL Nair Hospital, Mumbai, Maharashtra, India
|Date of Web Publication||6-May-2016|
Alka A Subramanyam
Department of Psychiatry, OPD-13, First Floor, OPD Building, Topiwala National Medical College (TNMC) and BYL Nair Hospital, Mumbai - 400 008, Maharashtra
Source of Support: None, Conflict of Interest: None
As advancements are being made in the medical field, the average life span is increasing and more complaints related to the elderly are coming into notice. Of these, mild cognitive decline (MCD) or mild cognitive impairment (MCI) is recently becoming an increasingly recognized entity that is often considered a precursor of dementia but is found to have other outcomes as well. It also has variations in presentations; it does not present only as memory complaint but also in the form of other cognitive or behavioral manifestations and has always been a point of controversy regarding the objectivity of the diagnosis. It is considered as the appropriate stage for intervention to prevent its progression to dementia and therefore, requires early identification for which various diagnostic modalities such as neuroimaging, neuropsychological tests, and biological markers are considered. Currently, there are no specific treatment guidelines for MCD. Drugs used in Alzheimer's disease (AD), lifestyle modifications, and other nonpharmacological approaches have shown some benefit in MCI but the results are variable; hence, the need for further research is warranted for effective preventive therapy. In this article, we will be discussing MCD as a clinical construct, evaluation of a person suspected of having MCD, and management of the same.
Keywords: Diagnosis, mild cognitive impairment (MCI), treatment
|How to cite this article:|
Subramanyam AA, Singh S. Mild cognitive decline: Concept, types, presentation, and management. J Geriatr Ment Health 2016;3:10-20
|How to cite this URL:|
Subramanyam AA, Singh S. Mild cognitive decline: Concept, types, presentation, and management. J Geriatr Ment Health [serial online] 2016 [cited 2021 Jan 16];3:10-20. Available from: https://www.jgmh.org/text.asp?2016/3/1/10/181910
| Introduction MCI as a clinical construct|| |
Mild cognitive decline (MCD) or mild cognitive impairment (MCI) refers to a transitional state between the cognition of normal aging and mild dementia. It is a clinical construct that describes individuals with mildly impaired performance on objective neuropsychological tests but relatively intact global cognition and daily functioning.  MCI has been validated as qualitatively different from both normal aging and dementia and has been a matter of debate regarding whether or not it is a risk factor for the development of dementia.  The overall prevalence of MCI in the general elderly population has a range of 2-20% and is lower in the amnestic subtype, i.e., 2-4% as compared to the broader group. , In one Indian study, the prevalence of MCI was found to be 14.89%. 
| History|| |
It was observed that some elderly became mildly forgetful who did not fit clearly either in "cognitively normal" or "demented."  Several terms emerged to describe this group such as "benign senescent forgetfulness" and "age-associated memory impairment" that were soon recognized as inadequate. Clinicians noted that dementia patients and their families retrospectively report cognitive deficits that started several years before evaluation. This in-between group, whose impairment is sometimes called "cognitive impairment not dementia,"  might be subdivided into individuals with memory loss that is age-related and those whose cognitive symptoms are the first clinical manifestations of dementia. The group initially thought to be in the prodromal stages of Alzheimer's disease (AD) is now said to have "mild cognitive impairment."  The term "vascular cognitive impairment" has been proposed to refer to the prodrome of vascular dementia.  A similar term, "subjective cognitive impairment (SCI)," came into existence where cognitive issues were reported by apparently normal-functioning elderly. Reisberg first described this entity in terms of the Global Deterioration Scale that measures cognitive and functional decline on a scale of 1 (cognitively normal) to 7 (severe dementia) with MCI defined as a Global Deterioration Scale (GDS) score of 3. , However, it was Peterson who first coined the term MCI that is now used worldwide. 
| Presentation and subtypes|| |
MCI identifies a spectrum of diseases that includes impairment in both memory and nonmemory cognitive domains. Peterson first gave the concept of MCI as having memory complaint, in the absence of other cognitive disorders or dementia or repercussions on daily life. However, this criterion has been under extensive debate that led to the formulation of various diagnostic guidelines. 
1. National Institute on Ageing and Alzheimer's Association (2010) revised the criteria of MCI as: 1) concern regarding change in cognition, 2) impairment in one or more cognitive domains, 3) preservation of independence in functional abilities, and 4) not demented. 
2. "Diagnostic and Statistical Manual of Mental Disorders" (DSM)-5 includes MCI under the category of mild neurocognitive disorders. 
3. MCI is classified into two subtypes: Amnestic and nonamnestic, based on the involvement of memory and single domain or multiple domain, based on involvement of the number of cognitive domains affected. Amnestic MCI is a clinically significant memory impairment that does not meet the criteria for dementia. It has been stated that mini-mental state examination (MMSE) scores of less than 26 in uneducated individuals and less than 28 in educated individuals warrant assessment for MCI.
Typically, patients and their families are aware of the increasing forgetfulness. However, other cognitive capacities are relatively preserved and functional activities are intact, except for some mild inefficiency. Nonamnestic MCI is characterized by a subtle decline in functions not related to memory, affecting attention, language, problem-solving, word-finding, or visuospatial skills. 
The criteria for subtypes were operationalized using the results of neuropsychological testing in a study  as: (1) MCI amnestic type: Participants with isolated progressive or static memory deficits (delayed recall verbal memory, nonverbal memory, or both) who had a score on a standardized test that was 1.5 standard deviation (SD) below the mean compared with individuals of the same age and level of education (other tests were healthy) and (2) MCI multiple cognitive deficits type: Participants with a progressive or static deterioration in at least one cognitive domain (not including memory) or one abnormal test (1.5 SD below the mean adjusted for age and education) in at least two other domains but who had not crossed the threshold for dementia.
4. In studying the prodromal phase of dementia, another group was observed, known as "mild behavioral impairment" (MBI) that presented only with behavioral symptoms and yet progressed toward dementia. Thus, Taragano et al. proposed another classification: 1) MCI with neuropsychiatric symptoms, 2) MCI without neuropsychiatric symptoms, 3) MBI with cognitive symptoms, and 4) MBI without cognitive symptoms. 
5. Based on etiopathology, it can be neurodegenerative (pre-Alzheimer's, Lewy body, frontotemporal) or vascular. The nonamnestic type is probably less common than the amnestic type and may be the forerunner of non-Alzheimer's Disease in the text such as frontotemporal or dementia with Lewy bodies.  To understand this simplistically, [Figure 1] may be of help.
| Neuropsychiatric manifestations|| |
MCI frequently presents with neuropsychiatric symptoms. The most comprehensive studies of behavioral manifestations have been documented as at least one neuropsychiatric symptom in 35-75% of MCI patients, which was probably why Terragano et al. thought of MBI as a separate entity.  Depression, apathy, and anxiety are consistently among the most common behavioral abnormalities in MCI despite different study designs, behavioral instruments, or MCI diagnostic criteria used. 
Of the neuropsychiatric manifestations of MCI, depression is the most widely studied. In the Cardiovascular Health Study Cognition Study, prevalence of depression was 20% in MCI.  However, figures varied from 11%  to 45%  in various studies. Depression has also been extensively studied as a risk factor for further cognitive decline. ,,,,
Apathy is the most prevalent neuropsychiatric symptom in AD.  It commonly starts during the MCI stage and progressively increases as AD progresses,  and is related to worsening on tests of memory and executive control.
The results for prevalence of anxiety in MCI are varied. , Psychotic symptoms such as delusions and hallucinations were reported to be less than 5%. , However, an association between lower MMSE scores and the onset of psychotic symptoms was reported in one study. Subjects with misidentification symptoms tended to have longer disease duration and lower MMSE scores.  The rates of disinhibition ranged from 3% to 10% and of agitation from 4% to 18% that is not significantly different from those observed in the normal elderly. , Varied results are found for euphoria, aberrant motor behavior, and irritability in MCI. ,
| Stability of diagnosis and outcome|| |
MCI 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. Single domain particularly seems to be at risk of this shift. ,,, However, some have found that all MCI subtypes either convert to dementia or retain their MCI status. ,
MCI may have different outcomes. Multidomain amnestic MCI appear to be at the greatest risk of dementia. , Amnestic MCI has the highest risk for conversion to Alzheimer's dementia, , whereas multidomain presentation to vascular dementia. ,, Nonamnestic subtype with multiple domain involvement more likely converts to non-AD,  with single domain at particular risk of progressing to fronto-temporal dementia. 
Rates of progression from MCI 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. Data from Mayo Alzheimer's Disease Research Center demonstrated a conversion to AD in 80% cases in approximately 10 years  that keeps on increasing exponentially each year.
| Risk factors for progression of mci|| |
Progression of MCI may be determined by the following factors: ,
- Older age.
- Fewer years of education.
- Multidomain amnestic MCI.
- High fat diet.
- Medical comorbidities: Metabolic syndrome, chronic inflammatory diseases, vascular disease, thyroid disorders, and elevated homocysteine levels.
- Excessive alcohol intake.
- Stressful lifestyle.
- Untreated depression.
- Presence of apolipoprotein E (ApoE) E4 allele.
- Magnetic resonance imaging (MRI), with volumetric measurements of the hippocampus at or below the 25th percentile for matched age and sex.
[TAG:2]EVALUATION OF A PATIENT SUSPECTED OF MCI [/TAG:2]
Any patient suspected of having MCI should undergo detailed clinical and investigatory evaluations. A thorough history and physical examination focusing on the status of cognitive functions, status of activities of daily routine, medications, neuropsychiatric evaluation, and laboratory testing are important components of this assessment.
1. HISTORY TAKING
- Details about the onset, duration, nature, and progression of cognitive symptoms.
- Functional status: Information from family members, wherever available, is essential, especially in knowing the previous level of functioning, both personal as well as instrumental, in order to differentiate MCI from dementia. Subtle deficits in instrumental activities of daily living (IADL) are noticed in MCI. IADL requiring higher neuropsychological functioning seem to be most severely affected in patients with MCI.  The Functional Activities Questionnaire is used for assessing these, using data from an informant. Score of 6 or more has >85% accuracy in differentiating MCI from dementia. 
- Information to rule out potentially reversible causes of MCI (depression, vitamin B 12 /folate deficiency, thyroid diseases, and medication). 
- Presence of neurological or psychiatric symptoms (to rule out Parkinson's disease, normal pressure hydrocephalus, stroke, or neuropathy). 
- History of substance use disorders, family history of cognitive disorders, and psychosocial history.
- Thorough Neurological and Psychiatric Evaluation: A complete psychiatric evaluation and neurological examination including orthostatic hypotension, extraocular movements, vision, hearing, speech, focal weakness, ability to stand from a chair, and gait are useful for identifying potential contributors to cognitive decline including stroke, Parkinson disease, normal-pressure hydrocephalus, or neuropathy due to toxins or vitamin deficiency. 
- Depression associated with cognitive impairment in the elderly can be assessed using Geriatric Depression Scale (GDS), on which a score of 6 or more suggests depression. 
a. Laboratory Testing: Testing complete blood count, electrolytes, glucose, calcium, thyroid function, vitamin B 12 , and folate is recommended to identify potentially reversible forms of MCI including infection, renal failure, hypomagnesaemia or hypermagnesemia, hyperglycemia, hypocalcaemia or hypercalcemia, hypothyroidism or hyperthyroidism, and vitamin B 12 or folate deficiency. Laboratory testing for liver function, syphilis, and human immunodeficiency virus (HIV) may reveal rarer causes.  About 9% of the causes of dementia seem to be reversible.  While studies have suggested that levels of biomarkers in the cerebrospinal fluid (e.g., Aί 42 and tau protein) may help identify patients with MCI who are more likely to progress to AD,  routine lumbar puncture is not generally recommended for clinical evaluation. 
i. Structural: The National Institute of Aging-Alzheimer's Association (NIA-AA) diagnostic guidelines do not recommend routine neuroimaging in the assessment of MCI but suggest that it may help in determining MCI etiology and prognosis.  Structural MRI may be useful for identifying MCI and those at greater risk for progression from MCI to dementia. ,
Decreased size of the hippocampus on volumetric measures is suggestive of MCI and correlated with the likelihood of progression to dementia.  MRI in nonamnestic MCI revealed a significant reduction in the dorsolateral and dorsomedial prefrontal cortices and reduction in volume of caudate nucleus; meanwhile, in amnestic MCI, atrophy in bilateral posterior temporoparietal cortices, medial temporal cortices, posterior cingulate gyrus, and right inferior parietal cortex were noted. However, the lack of standardization and validation for these measures limit their usefulness in clinical practice,  and they are not currently recommended for informing prognosis. Nevertheless, they may rule out other potential causes for cognitive decline such as subdural hematoma, stroke, normal pressure hydrocephalus (NPH), or tumor, if suggested by history and physical or laboratory studies. 
ii. Functional and amyloid imaging: Fludeoxyglucose (FDG) positron emission tomography (PET) can detect regions of hypometabolism in the brain that may be suggestive of MCI such as hypoperfusion in bilateral temporoparietal cortices and posterior cingulate cortices, with relative sparing of sensorimotor and occipital cortices. , Most recently, PET imaging of the extent of Aί plaques in the brain is being done with radiotracer florbetapir  and it has been useful in identifying individuals with AD or at high risk for developing the same.  Assessment with 18-FDG Pittsburgh Compound B (PiB) PET was found sensitive in differentiating amnestic and nonamnestic MCI. It shows a good correlation with cognitive measures in patients with MCI, with a sensitivity of 92% and specificity of 89% to predict conversion to AD. A recent review, however, suggested that there is no sufficient evidence yet that will improve health outcomes in cases of suspected MCI. Hence, its use is limited to research purposes. 
c. Neuropathology: Most patients with amnestic MCI demonstrate the deposition of tau proteins in neurofibrillary tangles in the medial temporal lobe and neuronal plaques due to deposition of beta amyloid. Cerebral spinal fluid (CSF) studies have revealed low Aβ42 and elevated tau or phosphorylated tau in cases of Alzheimer's dementia as compared to age-matched cognitively healthy controls. These biomarkers, thus, seem to be useful in a multistep approach in the diagnosis and intervention of MCI or dementia. But this hypothesis still remains questionable as certain studies have reported variable results and there has been no therapeutic breakthrough yet. 
Ongoing research is also targeted toward the process of inflammation and oxidative stress such as cytokines and isoprostanes, using a variety of markers. However, it would be too early to predict the significance of these markers in clinical practice.
d. Genetic testing: The presence of mutations in A4 precursor protein (APP) and PS1 and PS2 genes are likely predictors of the conversion of MCI to early Alzheimer's dementia. In addition, there is increased risk for the development of dementia in an individual with MCI, in the presence of apolipoprotein (Apo) E4 allele. On the other hand, E2 allele is associated with decreased risk.  In an Indian study, frequencies for ApoE2, ApoE3, and ApoE4 alleles were found to be 0.25, 0.35, and 0.4 in Alzheimer's patients and their first-degree relatives. ApoE4 was present in 71% of the patients with Alzheimer's and their relatives that was 2.7 times higher than the controls. However, the cost and availability of the testing have limited its use in the Indian context. 
4. NEUROPSYCHOLOGICAL TESTING
Assessment of cognition in the elderly can be a challenging task. There are a variety of tests that can be used for the assessment of MCI; however, tests such as MMSE, clinical dementia rating (CDR) scale, repetition, fluency, and digit span are the ones that are handy, easy, and quick to administer and can be readily used by the clinicians. The commonly used tests are as follows:
a. Brief cognitive tests:
A comprehensive set of tests is applied when there is suspicion of having MCI. Though there are no clear-cut guidelines, the following tests are commonly used for screening:
- MMSE: It is probably the most widely used test for bedside memory testing. It has sensitivity and specificity of 70% with a cutoff score of 26. The scores of 26 (in noneducated individuals) and 28 (in educated individuals) warrant further assessment, follow up and surveillance for MCI.  Addition of a recall after a longer delay improves the sensitivity and specificity to >80%. 
- Montreal Cognitive Assessment (MoCA): This was developed specifically for the detection of MCI and takes approximately 10 min to administer.  It has a high sensitivity as well as specificity. , Its assesses orientation, attention, immediate and delayed recall, executive function and language, etc. 
- DemTect: This evaluates immediate and delayed recall of word list, number transcoding, verbal fluency and reverse digit span. It has sensitivity of 80% and specificity of 92% in differentiating MCI from normal controls. 
- Clinical Dementia Rating (CDR) Scale: It considers six domains - memory, orientation, judgment and problem solving, community affairs, home and hobbies, and personal care. Score of 0.5 on this scale is of diagnostic importance for MCI, according to Peterson's modified criteria. American Academy of Neurology (AAN) accepts this score as equivalent to the presence of MCI.  It has a high inter-rater reliability and appears to be a reliable and valid tool for assessing and staging dementia.
- Global deterioration scale: A score of 3 is considered to be indicative of MCI. 
- Neuropsychological tests: These are helpful but not definitive for the diagnosis of MCI. Various cognitive domains can be tested and tests used include tests for recall (Hopkins verbal learning test, Wechsler's memory delayed recall), verbal category and semantic fluency, attention (digit span forward and backward), processing speed (trail making test A), visuoconstructional function (clock drawing test and Rey-Osterrieth complex figure test), and executive functioning (trail making test B and symbol digit substitution).
b. A typical battery assessing these domains is more sensitive than routine office tests and can provide a thorough profile of deficits, differentiating between amnestic from nonamnestic and single domain from multiple domain MCI. 
- Neuropsychiatric inventory (NPI) and short questionnaire form of the NPI (NPI-Q): The presence of psychiatric symptoms and caregiver distress can be assessed. 
- Addenbrooke's cognitive assessment: It assesses five domains - orientation/attention, memory, verbal fluency, language and visuospatial. At the cutoff of 82, the likelihood of dementia is 100:1. It has high sensitivity of 0.94 and specificity of 1, and correlates well with CDR.
- AD assessment scale - cognitive subscale (ADAS-Cog): It assesses 11 domains in cognition, along with 10 clinician-rated items for psychosis, depression, agitation, etc. Its results can range from MCI to severe impairment, and is a good tool for longitudinal assessment; however, it takes a long time to administer.
- Informant questionnaire on cognitive decline in the elderly (IQCODE) addresses the objective reporting by the caretaker on the day-to-day behavior of the person. It requires a very well-informed caregiver for the same. 
A simple approach to a patient with MCI for clinicians is outlined in [Figure 2].
| Management of mci|| |
There have been no specific recommendations for the treatment of MCI but the management can be divided into pharmacological and nonpharmacological (that are mostly the preventive factors for MCI) for the sake of simplicity.
1. PHARMACOLOGICAL: Although no drug is approved for treating MCI, the following have been the focus of interest:
- Acetylcholinesterase Inhibitors: The Alzheimer's Disease Cooperative Study favored donepezil at 1 year but not at 3 years follow-up. Its effect was greater in Apoù4-positive individuals that seemed to be an important predictor for progression.  Based on these studies, the screening of patients with amnestic MCI for ApoE4 allele is recommended and only if ApoE4 allele is present the patients should be given AChEIs. ,,
- Memantine: Memantine has not been reported to benefit patients with MCI. 
- Piribedil: It is a dopamine receptor agonist, having acetylcholine release in the hippocampus and the frontal cortex as a putative mechanism of action. Pirbidel improved cognition over 3 months on the primary outcome in placebo-controlled study by Nagraj et al. in National Institute of Mental Health and Neurosciences (NIMHANS). 
- Nicotine: Brain nicotinic receptors are important for cognitive function. Nicotine patches improved attention, but not global functioning, over 6 months. 
- Cyclooxygenase (COX)-2 inhibitors: Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce brain neurotoxic inflammatory responses and so was assumed to improve cognition. Rofecoxib increased incident cases of Alzheimers dementia in the study and has a fair evidence against its use.  Trifusal (COX-1 and COX-2 inhibitors) had no effect on cognition but was associated with a reduced risk of conversion to AD. 
- Gingko biloba: The proposed mechanisms of action include increasing brain the blood supply, modifying neurotransmitter systems, and reducing oxygen-free radical density.  But the results of its use have been inconsistent. ,
- Vitamin B: Higher homocysteine plasma concentrations are associated with cognitive impairment, the levels of which are decreased by B vitamins. Immediate memory did not improve;  however, attention and executive functioning had varying results. 
- Antioxidants such as vitamin E, vitamin C, and curcumin (from turmeric) are hypothesized to reduce oxidative stress and ageing, yet work in this field is largely in the incipient stages. 
- Omega-3 polyunsaturated fatty acids (PUFAs): With PUFAs, cognition, in terms of verbal fluency and depressive symptoms improved at 6 months follow-up. ,
- Antiamyloid therapies: Secretase inhibitors reduce amyloid production by inhibiting the secretase activity. Similarly, fibrillogenesis inhibitors (alzhmed and cliniquinol) are also under research, along with the vaccines that would prevent amyloid plaque formation. 
- Neurotonics: The use of piracetam has not met with any evidence. 
- Estrogens: These have been found to actually increase the risk for MCI and AD. ,
- Others: Huannao Yicong responded on a cognition and social functioning measure but the result was not significant. CDP choline, calcium channel blocker nimodipine and testosterone supplementation seem partially effective. 
- Drugs on trial for MCI include vasoactive intestinal peptide (AL-208), a selective metabotropic glutamate receptor antagonist (C-105), a novel L-type calcium channel blocker (MEM- 1003), a phosphodiesterase inhibitor (MEM-1414), a gamma-aminobutyric acid B receptor antagonist (SGS-742), and a selective serotonin receptor (5HT6) antagonist (SGS-518). 
Intervention in MCI remains a matter of debate owing to its varied course. Though till date there are no particular guidelines for treating MCI, the amnestic type is widely viewed as being an optimal stage to intervene with preventative therapies due to its greater risk of progressing to dementia. Studies have typically aimed to identify treatments that can stabilize symptoms or delay the onset of dementia. Recognition of MCI itself is in the early stage. Thus, further research is required with clinical trials that are designed to select more homogeneous samples at entry with optimal treatment durations and more sensitive cognitive and global outcome measures that reflect subtle impairments in complex activities.
2. NONPHARMACOLOGICAL: Although the outcome of MCI is still a matter of debate, efforts are made to prevent progression of the disorder and much emphasis is given for its prevention at the first place. The following are some nonpharmacological measures that have been discussed, which have a role in preventing MCI and reducing the risk of its progression.
- Treatment of vascular and other comorbidities such as hypertension, diabetes, atrial fibrillation, obesity, vitamin deficiency, hypothyroidism, depression, and sleep disturbances. ,
- Abstention from heavy alcohol, smoking, and other substances of abuse. ,
- Establishment of a fixed and disciplined routine.
- Diet: A Mediterranean diet (with high intake of cereals, fruits, fish, legumes, and vegetables) reduces risk of cardiovascular disease, increases concentration of plasma neutrophins, limits proinflammatory cascades, thereby helping in preventing cognitive decline.  Second dietary factor that has been implicated is curcumin (a pharmacologically active ingredient in the Indian spice "haldi") that was a probable contributory factor mentioned for the lower prevalence of MCI in India than in developed countries. 
- Socialization with people, apart from one's immediate family members, e.g., friends, being part of a senior citizen's group, etc. 
- Spiritual activity of some form is also of importance in maintaining cognition. 
- Physical exercise/activity: It has favorable effects on neuronal survivability and function, neuroinflammation, vascularization, neuroendocrine response to stress, and brain amyloid burden. , Inconsistent results of improvement in fluency, memory, and trail-making were found. , It has been claimed that any frequency of moderate exercise reduced odds of having MCI. 
- Computer-assisted cognitive training: It involves teaching individuals empirically-supported strategies and skills in order to optimize current cognitive functioning and independence in daily life. Its effect was seen on objective and subjective measures of memory, quality of life, and mood. 
- Cognitive stimulation: It involves activities designed to increase cognitive and social functioning in a nonspecific manner (e.g., reading, board games, group discussions). Engagement in such activities is associated with a decreased risk of cognitive decline, amnestic MCI  and AD. ,
- Family psychological intervention: Kinsella et al. found prospective memory improvement up to 4 months later in a trial that was not placebo-controlled. 
REGULAR FOLLOW-UP: Given the uncertainty of prognosis in this population, it has been recommended that MCI patients should be seen every 6-12 months for follow-up. This would consist of repeat cognitive screening, functional inquiry, and careful history taking (including family collateral) to assess for conversion to dementia.  It is also important to educate patients and families about the kinds of warning signs that would suggest the possibility of progression and warrant the need for follow-up. Neuropsychological testing should be repeated every 1-2 years or when conversion is suspected.
| Conclusion and future directions|| |
The hopelessness that a treating geriatric specialist feels while treating a patient with dementia and the realization that it may be too late to intervene at the dementia stage has given MCI an increasing importance as a recognized clinical entity. Older adults fear cognitive decline and many prefer getting evaluated that can have its own financial, social, and emotional bearings.
But owing to its potential importance for early identification and intervention in those at risk for the development of dementia, the concept of MCI has received considerable research attention. It seems that in the near future, we would get a better insight into the illness, its standard clinical criteria, and diagnostic modalities. In addition, options for newer targeted drugs and therapies would be possible that might give hope to many and would cause cognitive decline to be seen as somewhat modifiable instead of an unchangeable reality.
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Conflicts of interest
There are no conflicts of interest.
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