**3. Some comments about Alzheimer's disease**

Alzheimer's disease is a progressive nonreversible neurodegenerative disorder, characterized by cognitive decline including learning capacity, emotional and behavioral alterations, motor skills impairment, including dysfunction of the autonomic nervous system and desynchronization of circadian rhythms. According to Picard et al. [41], early-onset Alzheimer's disease (EOAD) and behavioral variant frontotemporal dementia (bvFTD) are the most common types of presenile neurodegenerative dementia (i.e., age at onset around 65 years old). Compared to the typical episodic memory dysfunction of late-onset AD, EOAD patients show a constellation of multidomain deficits at presentation, which can include not only memory, but also language, executive, visuospatial abnormalities, and behavioral disturbances like bvFTD cases [42].

the most promising state-of-the-art diagnostic tools for MCI. Their results provide evidence that features of connected language are associated with very early, subclinical memory loss in late-middle age. This study helped toward a better comprehension of early language dysfunc-

Recently, Shang et al. [30] investigated differences in plasma fatty acids, adiponectin, reptin, plasma markers of inflammation, serum amyloid A, plasma lipids, and low-density lipoprotein in patients with AD, MCI, vascular dementia, and ischemic stroke in comparison to normal controls. They found different levels in almost all patients, indicating that these diseases

The evaluation of inner retinal layers as a biomarker of MCI has brought more novel information about the possibility to predict cognitive decline, which can be used as prognostic information for patients who need to take financial and family decisions, advanced directives, afford care/residence decisions, etc. This reliable prognostic information and planification of the future will serve as significant societal benefit, taking into account the high societal cost of

The level of relationship between cognition and functional outcomes in the MCI population is affected mainly by cognitive domains and a little bit by age and educational level. Early identification of subtle functional disturbance in MCI and comprehension of its cognitive and noncognitive correlates are determinant in the diagnostic process because of its prediction for

A recent meta-analysis investigation showed that hearing impairment is associated with a

Recently, a group of Korean researches have confirmed that a dietary pattern based on sea-

Recent study made by Correa-Jaraba and colleagues confirmed that the event-related potential technique is useful for evaluating changes in brain electrical activity and increased amplitude of the P3a component is a novel neurocognitive marker for differentiating amnestic MCI [35]. On the other hand, it seems to be that telerehabilitation by videoconference can improve cognitive function in patients with MCI, but this procedure needs more investigation to confirm

Three months ago, some investigators documented the association between the presence of hallucinations, delusions, anxiety, depression, and abnormal motor behavior, with the risk of developing incident dementia*, independent of other known risk factors, including MCI in the future, a simple, low-cost strategy for screening population groups at dementia risk, particularly in environments with limited access to specialized services and very sophisticated resources* [37–40]*.*

Alzheimer's disease is a progressive nonreversible neurodegenerative disorder, characterized by cognitive decline including learning capacity, emotional and behavioral alterations, motor

food and vegetables in older Korean adults can reduce MCI remarkably [34].

tion associated with a cognitive decline.

196 Cognitive Disorders

have diverse pathological mechanisms.

cognitive disorder care all over the world [31].

higher risk of MCI and dementia in elderly people [33].

**3. Some comments about Alzheimer's disease**

dementia progression [32].

its feasibility [36].

Volumetric and cortical thickness studies have shown a prevalent involvement of posterior parietal regions in EOAD and of anterior fronto-insular-striatal areas in bvFTD [43, 44]. Some studies reported a greater white matter (WM) involvement in bvFTD compared to EOAD [45–50]. Filippi et al. and Zhou et al. [51, 52] found a divergent pattern of altered functional connectivity in the default mode network (DMN) and salience network comparing EOAD and bvFTD patients.

Some specialists from Alzheimer's Association consider that AD is the underlying cause of all types of dementia, and it is characterized by β-amyloid plaques, neurofibrillary tangles, and neurodegeneration in areas of the brain associated with cognition, such as the cortex and hippocampus. AD is also characterized by disturbances of the daily activities involving memory, speech and language, reasoning, planning, and other cognitive abilities [53].

The Framingham Study, which followed up 2611 cognitively intact participants (1550 women and 1061 men) on many for 20 years, indicated that risk factor for AD in 65-year-old woman was almost twice that of men [1] because it seems to be that life expectancy is longer in ladies. Other epidemiologic investigations also confirmed that neurodegeneration develops more rapidly in females who are often diagnosed earlier than males [54, 55]. And they are often diagnosed earlier in the course of illness than men. In many cases, inflammation is another risk factor for AD that dysregulated neuroinflammatory reaction is another possible AD etiology, which is more pronounced in females [56, 57].

Some research suggests the important of sex differences in microglia development and in response to fluctuating gonadal steroids during the life and there are more microglia in female than males [58]. Females have been shown to have more microglia than males [1].

Apart from the previous statements, some authors suggest that particular aspects of music perception such as pitch pattern analysis may open a channel on the processing of information streams in major dementia syndromes. Therefore, the potential selectivity of musical deficits for particular dementia syndromes and particular dimensions of processing warrants further systematic investigation [59].

Between classical thiamine deficiency and Alzheimer's disease (AD), many similarities exist and in both are associated reductions in brain glucose metabolism with cognitive deficits. Vitamin B1-dependent enzymes are critical components of glucose metabolism that are reduced in the brains of AD patients and by thiamine deficiency, and their decline could account for the reduction in glucose metabolism [59]. Nevertheless, many other conditions not related with AD can cause dementia as well, and it should be taken into account in the process of diagnosis and management. As the reader can see below, apart from AD, other types of dementia and their etiology are also listed.

In the past decade, we applied the term "mild cognitive impairment (MCI) due to AD" to refer to the symptomatic predementia phase of AD; in other words, patients with cognitive decline whose primary underlying pathophysiologic was AD but no evidence of a remarkable impairment in social or occupational activities; currently, we separate those patients in two groups.

Now, the pathological criteria for AD require the presence of Aβ deposition in plaques and tau deposition in neurofibrillary tangles. The absence of biomarkers of Aβ deposition strongly

Updated Information on Some Cognitive Disorders http://dx.doi.org/10.5772/intechopen.81826 199

The definitive absence of evidence of either Aβ deposition strongly suggests that the MCI syndrome is not due to AD. This marker analyses the lower Aβ42 levels on CSF [68] and the evidence of Aβ deposition, using a variety of specific ligands in PET scan [69] and the increased

AD and atrophy in entorhinal cortex (ERC), the hippocampus, and its subfields Cornu Ammonis 1(CA1) and subiculum are simultaneous, and these abnormalities can predict conversion from MCI to clinical AD. It has been documented that in the early stages of AD, some changes at the stratum radiatum, lacunosum, and molecular involving ERC and CA1 can be

Lewy body dementia and other types of cognitive disorder are not included in this revision

Parkinson's disease (PD) is an idiopathic type of parkinsonism, which progresses gradually in spite of the medical or surgical treatment implemented and it is characterized by bradykinesia, tremor at rest, gait disturbance, postural problems, rigidity, dysarthria, dysfunction of the judgment, reasoning, memory, depression, anxiety, insomnia, and cognitive decline due to loss of midbrain dopaminergic neurons in the pars compacta of the substantia nigra and consequent loss of dopamine input to the caudate nucleus and putamen (striatum), and it is more prevalent in men, whereas rigidity, difficulties pertaining to daytime sleepiness, dribbling saliva, interest in sex, and problems having sex are more common among men with PD [71]. Dementia affected almost 50% of our patients with PD within the first decade after diagnosis is made, but the intensity of their manifestations varied considerably among them. Prospective investigations reveal patient differences in the progression of cognitive deficits and in risk

*Identifying patients at risk of dementia and those at the earliest stages of cognitive involvement is* 

**1.** As new disease-modifying treatments in Parkinson's are emerging, early intervention to

**3.** Finding the earliest features of cognitive involvement may provide insights into underlying mechanisms of disease progression, ultimately leading to identification of novel thera-

The concept of MCI is introduced in the 1980s, and it is characterized mild cognitive deficits that did not qualify to a diagnosis of dementia in patients with AD, and more recently, it was

**2.** Earlier detection of cognitive involvement offers the hope of prognostic information.

slow or prevent Parkinson's dementia is becoming a realistic prospect.

accumulation of tau or phosphorylated tau in the CSF is another biomarker [68].

**4. Some information about Parkinson's disease**

factors for developing PD dementia (PDD) [72].

*important for three important reasons:*

also introduced for patients with PD [5].

peutic targets [73].

suggests that AD is not the cause of MCI.

observed [70].

due to limitation of space.

Typically, amnestic MCI is the type of prodromal stage of dementia due to AD, but other phenotypes can also mimic to this kind of dementia, such as posterior cortical atrophy (also known as the visual variant), logopenic aphasia, or a frontal lobe-dysexecutive presentation of AD. Therefore, as a general agreement, not all MCI is early AD. The Key Symposium characterization of MCI helps to differentiate between the amnestic form of MCI and the nonamnestic one. These clinical syndromes appeared to be aligned with causes in a differential fashion and may have variable outcomes [60]. The Alzheimer's Disease Neuroimaging Initiative (ADNI) criteria are useful in prediction of amnestic MCI progression to AD, including medial temporal lobe atrophy and hypometabolism in MRI and FDG-PET, respectively [10, 61, 62].

Recently, some researchers reported that plasma total tau and pTau181 levels were higher in AD dementia patients than those in cognitively unimpaired. Plasma pTau181 was more strongly associated with both Aβ and tau PET. Plasma pTau181 was a more sensitive and specific predictor of elevated brain Aβ than total tau and better than the combination of age and apolipoprotein E, and they concluded that plasma pTau181 may have utility as a biomarker of AD pathophysiology and as a noninvasive screener for elevated brain Aβ [63].

Few weeks ago, some authors have found that [18F]AV-1451 uptake showed the strongest regional correlation with hypometabolism. Correlations between [18F]AV-1451 uptake and both hypometabolism and cortical thickness were stronger in participants with greater cortical tau severity. In addition, age, tau asymmetry, and clinical diagnosis influenced the strength of the correlation between [18F]AV-1451 uptake and cortical thickness. Therefore, all these findings support a close relationship between tau and hypometabolism in Alzheimer's disease but show that correlations between neuroimaging modalities vary across participants [64].

Some investigations have confirmed that people with MCI and a positive amyloid PET scan are more liable to progress rapidly and, again, ADNI data confirmed this. Nevertheless, it is well known that carriers of the apolipoprotein E4 (*APOE4*) genotype are more susceptible to progress rapidly; however, in clinical practice, *APOE* testing did not contribute remarkable to the diagnostic assessment [65].

The study done by Hansson and colleagues relieved more information with regard to these data and corroborates the suspicion that those individuals, particularly with amnestic MCI presenting low CSF levels of Aβ42 and elevated total tau and phosphorylated tau, are at the higher risk for progressing faster than those patients with the same clinical phenotype but normal biomarkers on the CSF [66, 67].

All people presenting a mild cognitive impairment in our series did not present an early Alzheimer's disease later.

The criteria for MCI due to AD developed by the National Institute on Aging and the Alzheimer's Association essentially adopted the Key Symposium criteria and explained more explicit some of the diagnostic features. These criteria also considered biomarkers for underlying AD's pathophysiology trying to define the underlying cause and, hence, predict outcome.

Now, the pathological criteria for AD require the presence of Aβ deposition in plaques and tau deposition in neurofibrillary tangles. The absence of biomarkers of Aβ deposition strongly suggests that AD is not the cause of MCI.

The definitive absence of evidence of either Aβ deposition strongly suggests that the MCI syndrome is not due to AD. This marker analyses the lower Aβ42 levels on CSF [68] and the evidence of Aβ deposition, using a variety of specific ligands in PET scan [69] and the increased accumulation of tau or phosphorylated tau in the CSF is another biomarker [68].

AD and atrophy in entorhinal cortex (ERC), the hippocampus, and its subfields Cornu Ammonis 1(CA1) and subiculum are simultaneous, and these abnormalities can predict conversion from MCI to clinical AD. It has been documented that in the early stages of AD, some changes at the stratum radiatum, lacunosum, and molecular involving ERC and CA1 can be observed [70].

Lewy body dementia and other types of cognitive disorder are not included in this revision due to limitation of space.
