The computerized LASSI-BC Test versus the Standard LASSI-L Paper-and-Pencil Version in Community-Based-Samples

Proactive Semantic Interference (PSI) and failure to recover from PSI (frPSI), are novel constructs assessed by the LASSI-L. These measures are sensitive to cognitive changes in early Mild Cognitive Impairment (MCI) and preclinical AD determined by Aβ load using PET. The goal of this study was to compare a new computerized version of the LASSI-L (LASSI-Brief Computerized) to the standard paper-and-pencil version of the test. In this study, we examined 110 cognitively unimpaired (CU) older adults and 79 with amnestic MCI (aMCI) who were administered the paper-and-pencil form of the LASSI-L. Their performance was compared with 62 CU older adults and 52 aMCI participants examined using the LASSI-BC. After adjustment for covariates (degree of initial learning, sex, education, and language of evaluation) both the standard and computerized versions distinguished between aMCI and CU participants. The performance of CU and aMCI groups using either form was relatively commensurate. Importantly, an optimal combination of Cued B2 recall and Cued B1 intrusions on the LASSI-BC yielded an area under the ROC curve of .927, a sensitivity of 92.3% and specificity of 88.1%, relative to an area under the ROC curve of .815, a sensitivity of 72.5%, and a specificity of 79.1% obtained for the paper-and-pencil LASSI-L. Overall, the LASSI-BC was comparable, and in some ways, superior to the paper-and-pencil LASSI-L. Advantages of the LASSI-BC include a more standardized administration, suitability for remote assessment, and an automated scoring mechanism that can be verified by a built-in audio recording of responses.

Donepezil rescues the medial septum cholinergic neurons via nicotinic ACh receptor stimulation in olfactory bulbectomized mice

Olfactory bulbectomy (OBX) causes cognitive dysfunction by degeneration of cholinergic neurons in the medial septum. Here, we define an involvement of nicotinic acetylcholine receptor (nAChR) in neuroprotective effect of donepezil in the septum neurons of OBX mice. Neuroprotective effects on the medial septal cholinergic neurons were assessed after chronic donepezil administration in OBX mice. We also measured Akt and ERK phosphorylation to define the neuroprotective mechanism of donepezil. We found that treatment with donepezil (1 - 3 mg/kg) for 15 consecutive days completely rescued cholinergic neurons in the OBX mice with concomitant improved memory. Reduction of both protein kinase B (Akt) and extracellular signal-regulated kinase (ERK) phosphorylation were restored by chronic donepezil administration (1 - 3 mg/kg) in OBX mouse medial septum. Both phosphorylated Akt and ERK immunoreactivities were localized in cell bodies of choline acetyltransferase (ChAT)-positive cholinergic cells in the medial septum. Enhancement of Akt and ERK phosphorylation seen following donepezil administration was totally blocked by pre-administration of mecamylamine (10 μM), a nicotinic acetylcholine receptor antagonist. Donepezil increases phosphorylation of Akt and ERK via nAChR stimulation in the medial septum cholinergic neurons. The Akt and ERK stimulation by donepezil is associated with its ability of neuroprotection in the medial septum and memory improvement.

Paradoxical prosopagnosia in semantic dementia

Objective: To study episodic and semantic memory for faces and other non-verbal information in semantic dementia (SD). Background: Semantic memory impaired in the rare diagnosis of SD by definition, including knowledge about well- known persons and their appearance. Episodic memory is held to be better preserved. Methods: Two computerized face recognition tests were administered, one measuring episodic memory (Male Faces) and one semantic memory (Political Faces) in addition to a comprehensive test battery. A computerised test of non-verbal semantic memory for national symbols (Euro Flags) was also administered druring the retention interval of the Male Faces test. Results: The SD participants were severely impaired in the episodic face recognition test. In contrast, their performance was in the normal range in Euro Flags and Political Faces, based on knowledge of national political figures. Conclusion: The results are discussed in terms of preserved dynamic memory and severely impaired memory for static facial information in semantic dementia. Research proposals regarding further studies of this paradoxical prosopagnosia in semantic dementia are presented in order to clarify issues regarding static versus dynamic aspects of face memory.

Certain new aspects of etiology and pathogenesis of Alzheimer’s disease

The research focuses on the possibility of early detection of AD-specific vascular and atrophic brain changes in families which have a tendency to inherit the disease. The research includedthree families with AD inheritance. All patientsunderwent: cognitive function assessment(MMSE),determination of dementia severity(CDR) and AD stages (TDR), computed tomography (CT), magnetic resonance imaging (MRI), scintigraphy of the brain (SG), rheoencephalography (REG), and cerebral multigated angiography (MUGA). All patients with different AD stages, as well as their descendants, have specific atrophic changes in the temporal lobes of the brain. The degree of these changes increases as AD becomes more severe and ranges from 4% - 8% (TDR-0) to 33% - 62% (TDR-3) of the total mass of a healthy person’s temporal lobes. Simultaneously, thepatients examined have changes of microcirculation manifested by reduction of the capillarybed in the temporal and frontalparietal regions,the development of multiple arteriovenousshunts in the same areas, early venous dumping, anomalous expansion of venoustrunks that receive blood from the arterialvenous shunts, venous stasis on the frontoparietal boundary. Similar changes are found among AD patients’ descendants aged 8 - 11, the only difference being in the degree of temporal lobes atrophy which is 4.7%. This proves that microcirculatory disorders are primary and atrophic changes of the temporal lobes are secondary in AD development. The data obtained indicate that the examination of AD patients’ relatives should begin well before the possible manifestations of the disease, even in childhood. It will allow to reveal the possibility of inheritance and the signs of the disease at the earliest possible stage and to begin its treatment in time.

Two Cases of Severe Dementia Showing Dramatic Improvement after Denture Placement

Severe dementia, including Alzheimer’s disease, is intractable and progressive. The purpose of this study was to document the improvement observed in two cases of severe dementia after denture placement. The subjects, two women in their 70s with severe dementia, were diagnosed with Alzheimer’s disease by the medical doctors in charge of their cases. In the first case, the subject’s symptoms included severe disorientation, impaired communication, and a tendency to wander. Two weeks after a lower complete denture placement, she was able to greet others. Five weeks later, she was able to communicate and precisely read an analog clock. Her condition continued to improve for at least 3 months. In the second case, the subject’s mouth was always open. She was bedridden in a vegetative state and hardly moved, talked, or laughed;it was impossible to communicate with her. Only a few seconds after an upper complete denture placement, she started to talk, albeit unintelligibly. Two weeks after a lower complete denture placement, she could communicate normally, laugh, and walk without help. Although the underlying mechanism has not yet been clarified, the author hypothesizes that positive signals from the oral area are transferred to the brain as positive stimulation via the trigeminal nerve, the largest cranial nerve.

The Drug Development Based on Pathogenetic Research in Alzheimer’s Disease

Neuropathologically, Alzheimer’s disease is characterized by the presence of extracellular deposits of amyloid-β peptides, intracellular neurofibrillary tangles and atrophy of the basal forebrain cholinergic neurons. The research of pathogenesis of Alzheimer’s disease inspirits potential clinical drugs for treatment. To block the progression of the disease, drugs under development have to interfere with the pathogenic steps responsible for the clinical symptoms, including cholinergic deficit, calcium dysregulation, inflammation and oxidative damage, and the deposition of amyloid- β plaques and of neurofibrillary tangles. In this review, the pertinent literature about drugs targeted on relieving symptoms above is reviewed. We aim to discuss possible research priorities in the future.

Feasibility Study of Neurofeedback Therapy for Alzheimer’s Disease

Objective: This study aims to evaluate the feasibility and effectiveness of neurofeedback therapy based on brain-computer interface (BCI) games in enhancing cognitive functions and reducing disruptive behaviors in patients with Alzheimer’s disease (AD). Methods: Forty-six AD patients aged 49 - 76 years were recruited for the study. Neurofeedback regulation was conducted using a BCI game designed to modulate EEG rhythms. Cognitive function was assessed using MMSE, MoCA, and ADAS-cog scales before and after a 10-day training period. EEG measurements were taken to evaluate changes in brain activity complexity. Statistical analyses were performed using SPSS25.0 software to compare pre- and post-training scores. Results: Post-intervention results showed significant improvement in the cognitive function of AD patients. The total scores of MMSE, MoCA, and ADAS-cog scales increased significantly (P < 0.01). Notable improvements were observed in memory, language, and attention domains. EEG complexity in the left frontal area also showed a significant increase (P < 0.05). Additionally, the disruptive behaviors of patients were significantly reduced, improving their overall quality of life. Conclusions: Neurofeedback therapy based on BCI games is a promising intervention for enhancing cognitive functions and reducing disruptive behaviors in AD patients. This innovative approach demonstrates significant potential for clinical application, providing a non-invasive method to improve patient outcomes. Further studies with larger sample sizes and long-term follow-ups are recommended to validate these findings and explore the specific effects of NFB training on different cognitive impairment levels.

Psychophysiological Effects of Sideritis and Bacopa Extract and Three Combinations Thereof—A Quantitative EEG Study in Subjects Suffering from Mild Cognitive Impairment (MCI)

Mild cognitive impairment (MCI) is regarded as a transitional stage during the development of Alzheimer’s disease. Diagnosis of MCI can be obtained by the questionnaire “DemTect” in German speaking countries. Quantitative assessment has been successfully performed using psychometric testing concomitantly with quantitative EEG recording. The present investigation aimed at the possible treatment of MCI with two botanicals, namely extracts from Sideritis scardica (500 mg) or Bacopa monnieri (320 mg) and three combinations thereof using this method in order to find a new treatment. The performance of the d2-test, an arithmetic calculation test (CPT) and a memory-test revealed better performance for the d2-test only in the presence of Sideritis extract or the combinations with Bacopa extract. Quantitative EEG assessment during the different experimental conditions showed massive differences between both extracts. Whereas Sideritis extract and its combination with a low amount of Bacopa extract (160 mg) induced increases of spectral power in fronto-temporal brain areas, Bacopa and the combination of Sideritis with high amounts of Bacopa extract produced attenuation of all waves except for delta in fronto-temporal brain areas. These differences were also documented by quantitative EEG maps in comparison to Placebo. A different action of both extracts was confirmed by discriminant analysis, where Sideritis extract and its combination with low Bacopa grouped together quite at distance to Bacopa and the combination of Sideritis with high Bacopa. A combination of Sideritis extract with a low amount of Bacopa should be tested with daily repetitive dosing for at least 4 weeks as a consequence.

Lipolysaccharide-Induced Neuroinflammation Is Associated with Alzheimer-Like Amyloidogenic Axonal Pathology and Dendritic Degeneration in Rats

Chronic neuroinflammation is thought to play an etiological role in Alzheimer’s disease (AD) which is characterized pathologically by amyloid and tau formation, as well as neuritic dystrophy and synaptic degeneration. The causal relationship between these pathological events is a topic of ongoing research and discussion. Recent data from transgenic AD models point to a tight spatio-temporal link between neuritic and amyloid pathology, with the obligatory enzyme for β-amyloid (Aβ) production, namely β-secretase-1 (BACE1), being overexpressed in axon terminals undergoing dystrophic change. However, the axonal pathology inherent with BACE1 elevation seen in transgenic AD mice may be secondary to increased soluble Aβ in these genetically modified animals. Further, it is unclear whether the inflammation seen in AD is the result of , or the cause of neuritic dystrophy. Here we explored the occurrence of AD-like axonal and dendritic pathology in adult rat brains affected by LPS-induced chronic neuroinflammation. Unilateral intracerebral LPS injection induced prominent inflammatory response in glial cells in the ipsilateral cortex and hippocampal formation. BACE1 protein levels were elevated in the ipsilateral hippocampal lysates in the LPS-treated animals relative to controls. BACE1 immunoreactive dystrophic axons appeared in the LPS-treated ipsilateral cortex and hippocampal formation, colocalizing with increased β-amyloid precursor protein and Aβ antibody (4G8) immunolabeling. Quantitative Golgi studies revealed reduction of dendritic branching points and spine density on cortical layer III and hippocampal CA3 pyramidal neurons in the LPS-treated ipsilateral cerebrum. These findings suggest that Alzheimer-like amyloidogenic axonal pathology and dendritic degeneration occur in wildtype mammalian brain in partnership with neuroinflammation following LPS injection.

Rivastigmine Restores 5-HT_1AReceptor Levels in the Hippocampus of Olfactory Bulbectomized Mice

Rivastigmine, a dual acetylcholinesterase and butyrylcholinesterase inhibitor, is used for symptomatic treatment of patients with mild to moderately severe dementia in Alzheimer’s disease (AD) patients. In the present study, we found that 5-HT1A receptor (5-HT1AR) is downregulated, whereas 5-HT2A receptor (5-HT2AR) is upregulated in the hippocampal dentate gyrus (DG) and CA1 region by olfactory bulbectomy (OBX) in mice. Furthermore, chronic treatment with rivastigmine (1.0 mg/kg) for 2 weeks starting 2 weeks after OBX operation restored the decreased 5-HT1AR and the increased 5-HT2AR levels. To determine whether cholinergic receptor stimulation by rivastigmine is involved in the rivastigmine-induced regulation of 5-HTR levels, we treated the mice with mecamylamine (2.5 mg/kg), or atropine (5.0 mg/kg) with rivastigmine (1.0 mg/kg) once a day for 2 weeks. Notably, the rivastigmine-induced 5-HT1AR upregulation was eliminated by mecamylamine but not by atropine treatments. On the other hand, the restored 5-HT2AR level by rivastigmine was not affected by either mecamylamine or atropine. Treatment with 8-OH-DPAT, a selective 5-HT1AR agonist improved the decreased 5-HT1AR and the increased 5-HT2AR levels in OBX mice. On the other hand, treatment with TCB-2, a potent 5-HT2AR agonist had no effects on the 5-HT1AR and 5-HT2AR dysregulation in OBX mice. Taken together, nicotinic acetylcholine receptor (nAChR) stimulation mediates rivastigmine-induced upregulation of 5-HT1AR. Therefore, we speculate that the increased ACh levels by rivastigmine can stimulate nAChR located on serotonergic nerve terminals and stimulate 5-HT1AR by the enhanced 5-HT release in the hippocampus. The 5-HT1AR stimulation likely mediates the improvement of 5-HT1AR levels as auto-receptor in OBX hippocampus.

Experimental Analysis of Interacting HT22 Plasma Membrane Cholesterol and β-Amyloid

The peptide β-Amyloid (β-A) is known to be one of the primary factors causing neurodegeneration in the Alzheimer disease. Hence, one would like to know the factors that would increase or decrease the toxicity of β-Amyloid in the brain. One of the factors that are debated in the literature is cholesterol, where it is not clear if modulating the levels of cholesterol would affect the degree of toxicity of β-Amyloid on neuron cells in the brain. In order to investigate this problem, data were collected and analyzed for three types of experiments: 1) Correspondence between cholesterol and methyl-β-cyclodextrin (MβCD) measurements;2) measurements of the relative fluorescence unit (RFU) with respect to MβCD concentration (with/without β-A);and 3) RFU measurements with respect to β-A concentration (with/without MβCD). HT22 hippocampal neurons immortalized with the simian virus SV-40 large T-antigen plasmid vector were used to conduct the experiments. Mito-ID Membrane potential cytotoxicity was used as a measure of mitochondrial potential change. The statistical analysis of the presented experimental results indicates that cholesterol has no statistically significant effect on the degree of toxicity of β-Amyloid.

Evaluation of Anxiety and Depression in Caregivers of Patients Affected by Alzheimer’s Disease

Background: Many studies have been underlined as care giving for people with Alzheimer’s disease (AD) is highly stressful and has significant negative consequences, such as anxiety and depression. Objective: The specific aim of our study is to establish whether a difference exists in the prevalence of depression of family caregivers of Alzheimer’s disease patients and healthy subjects not caregiver. Methods: Study group (n = 60) consists of caregivers of patients affected by Alzheimer’s disease, whereas control group (n = 120) consists of healthy individuals who are not care giving (from at least 5 years). All the subjects were subdivided on the basis of the following independent variables: sex, age, marital status and educational level. The subjects of study and control groups studied have filled in the following tests: IPAT CDQ e IPAT ASQ Tests by Cattell which describe depression and anxiety. Such tests have been validated on the adult and elderly Italian population. Statistical analysis: Student t test has been applied for the comparison between experimental and control groups. Results: The caregivers show higher levels of anxiety (medium to high, P < 0.001) and depression in comparison to the group of control (medium to high, P < 0.001). This result indicates the caregiver shows serious depression. Conclusions: The high levels of depression and anxiety suggest the following considerations: interventions of social and psychological support are fundamental not only to maintain the patient in the family nucleus but also to maintain the caregiver’s psychological health.

Tyrosine kinase receptor B isoforms alter APP and BACE1 endogenous levels independently of BDNF

Brain derived neurotrophic factor (BDNF) levels and signaling via the tyrosine receptor kinase B (TrkB) have been shown to be altered in Alzheimer’s Disease. In addition, it has been reported that the isoforms of TrkB can differentially affect metabolism of amyloid precursor protein (APP). Conversely, Ab, a neurotoxic cleavage product of APP, has been shown to impair TrkB/ BDNF signaling. Therefore, we investigated whether the changes observed in APP metabolism were due to the isoform-specific effects of TrkB on either APP expression, and/or on the expression and activity of ADAM10 and BACE1. Since BDNF levels are decreased in AD, we focused on BDNF independent effects of the TrkB isoforms. We found that TrkB FL increases endogenous APP levels in both HEK293 and SH-SY5Y naive cells. We did not find an increase in ADAM10 activity in HEK293 cells, but an increase in BACE1 levels. Additionally, we have found that TrkB FL is able to increase NFAT3 mediated transcriptional activity and we suggest that this causes transcriptional activation of the BACE1 promoter.

Regional patterns of atrophy on MRI in Alzheimer’s disease: Neuropsychological features and progression rates in the ADNI cohort

Background: Discrete clinical and pathological subtypes of Alzheimer’s disease (AD) with variable presentations and rates of progression are well known. These subtypes may have specific patterns of regional brain atrophy, which are identifiable on MRI scans. Methods: To examine distinct regions which had distinct underlying patterns of cortical atrophy, factor analytic techniques applied to structural MRI volumetric data from cognitively normal (CN) (n = 202), amnestic mild cognitive impairment (aMCI) (n = 333) or mild AD (n = 146) subjects, in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database was applied. This revealed the existence of two neocortical (NeoC-1 and NeoC-2), and a limbic cluster of atrophic brain regions. The frequency and clinical correlates of these regional patterns of atrophy were evaluated among the three diagnostic groups, and the rates of progression from aMCI to AD, over 24 months were evaluated. Results: Discernable patterns of regional atrophy were observed in about 29% of CN, 55% of aMCI and 83% of AD subjects. Heterogeneity in clinical presentation and APOE ε4 frequency were associated with regional patterns of atrophy on MRI scans. The most rapid progression rates to dementia among aMCI subjects (n = 224), over a 24-month period, were in those with NeoC-1 regional impairment (68.2%), followed by the Limbic regional impairment (48.8%). The same pattern of results was observed when only aMCI amyloid positive subjects were examined. Conclusions: The neuroimaging results closely parallel findings described recently among AD patients with the hippocampal sparing and limbic subtypes of AD neuropathology at autopsy. We conclude that NeoC-1, Limbic and other patterns of MRI atrophy may be useful markers for predicting the rate of progression of aMCI to AD and could have utility selecting individuals at higher risk for progression in clinical trials.

S100b protects IMR-32 cells against Ab(1-42) induced neurotoxicity via modulation of apoptotic genes expression

Amyloid beta (1-42) peptide is considered responsible for the formation of senile plaques that accumulate in the brain of patients with Alzheimer’s disease (AD). In the past years considerable attention has been focused on identifying new protective substances that prevent or almost retard the appearance of amyloid beta (1-42)-related neurotoxic effects. In this study, human neuroblastoma cells (IMR-32) was used as system model to evaluate the protective role of S100b, a neurotrophic factor and neuronal survival protein, that is highly expressed by reactive astrocytes in close vicinity of beta-amyloid deposits, against amyloid beta (1-42)-dependent toxicity. Our results show that at nanomolar concentrations, S100b protects cells against Aβmediated cytotoxicity, as assessed by MTS vitality test. The protective mechanism seems to be related to the effect on bcl-2 (an anti-apoptotic gene) expression, which is highly down-regulated by amyloid beta (1-42) treatment, while resulted more expressed in the presence of S100b. On the contrary, Bax, a proapoptotic gene, resulted down-regulated by the treatment with S100 compared with the results obtained in the presence of amyloid beta (1-42) peptide. However, at micromolar doses, S100b is toxic for IMR-32 cells and its toxicity adds to that of the Aβpeptide, suggesting that additional molecular mechanisms may be involved in theneurotoxic process.

Modeling Post-Operative Cognitive Dysfunction in Zebrafish

Permanent post-operative cognitive dysfunction (POCD) is a grim outcome to an estimated 6% of elderly surgical patients. Volatile anesthetics impact neuronal tissue independent of effects attributed to the physical trauma of the surgery itself. While it is recognized that all aspects related to surgery may contribute to cognitive loss in some manner, the present paper focuses on the role of volatile anesthetics in promoting POCD. There is an increased risk of onset and progression of Alzheimer’s disease (AD) from POCD, implying that the neuropathogenesis between the two is similar. Human studies, being ethically limited in scope, require animal models as a substitute. While the literature using rodent models contains valuable information, we believe that the accessible and practical zebrafish will greatly enhance our further understanding of the molecular mechanism of POCD as it relates to AD. Disease genes and fundamental neurobehaviors of these teleost fish mirror those of mammals and humans, validating their use as a core research model for AD. Since the gradual senescence seen in zebrafish also resembles that found in humans, we numerically correlated the two lifespans, offering researchers a computational tool. Zebrafish, being aquatic animals, necessitates the use of miscible compounds, such as trifluoroethanol, whose anesthetic potency we are presenting. We also review the rodent and zebrafish literature relevant to POCD. Continued research with the leading-edge zebrafish unlocks the possibility that, in the future, perioperative intervention will prevent POCD.

Filipin Levels as Potential Predictors of Alzheimer’s Disease Risk

To date, therapies to prevent or treat Alzheimer’s disease (AD) have largely focused on removing excess aggregation-prone amyloid peptide Aβ from the brain, an approach that has produced disappointing clinical outcomes. An alternative hypothesis proposes that Aβ production and aggregation is a symptom of a larger, systemic disease affecting the regulation of lipids, including cholesterol. In this scenario, lipid dysregulation would likely occur early in the disease process, making it an ideal target for predicting risk of mild cognitive impairment (MCI) to AD conversion. Here, we report that levels of filipin, a fluorescent polyene macrolide widely used as a diagnostic tool for diseases of lipid dysregulation, correlate with cellular damage caused by 27-hydroxycholesterol and with dementia status in human peripheral blood cells. These results provide strong preliminary data suggesting that filipin could be of use in the development of a quick and inexpensive method to measure the risk of AD conversion in patients with MCI, supplementing existing testing strategies that focus on the consequences of Aβ accumulation.

Prevalence of Dementia and Its Associated Factors in Cotonou Teaching Hospital, Benin

Introduction: Dementia constitutes a public health hazard in developing countries. There is little data in the sub-Saharan region of African especially in Benin. Objective: Determining dementia hospitalization prevalence and identifying its associated factors in CNHU-HKM, Cotonou. Method: It was a cross-sectional, prospective, descriptive and analytical research conducted from October 2012 to July 2013 in the neurology department;it involved 251 patients aged 50 and above. Dementia screening was conducted using a modified and adapted Mini Mental Scale Examination (MMSE). Dementia clinical and etiological diagnoses were respectively conducted based on DMS-IV and HACHINSKI criteria. Results: Patients were averagely aged 60.9 ± 8.1. Sex ratio (Male/Female) was 1.07. Dementia prevalence was 8.8%. This rate increased proportionally with age, from 5.3% with patients aged below 60 to 12.7% with patients aged above 60. Degenerative dementia was the most predominant type (50%). Following multi-varied analysis, smoking (RC = 6.05 [IC 95% = 1.26 - 29.38] p = 0.0001) and stroke past records (RC = 6.05 [IC 95% = 1.26 - 29.38] p = 0.001) revealed to be the factors associated with dementia. Conclusion: This research showed that dementia affects a significant part of the aging population in CNHU-HKM. It is imperative to combat its associated factors so as to defuse its prevalence.

CSF tau and amyloid β₄₂levels in Alzheimer’s disease—A meta-analysis

Alzheimer’s disease International (ADI) estimates that there are currently 30 million people with dementia in the world. The main objective was to perform meta-analysis of studies of CSF tau and Amyloid β42 (Aβ42) levels in Alzheimer’s disease (AD) patients and controls. In the present study MEDLINE was reviewed from 1995 to 2009, supplemented by citation analysis from retrieved articles to select case control studies. Descriptive statistics showed that median effect size (raw mean difference) of CSF tau and Aβ42 levels were 301 pg/ml (Range: 22 to 614 pg/ml) and –352 pg/ml (Range: –969 to 203 pg/ml) respectively. The pooled effect size CSF tau and Aβ42 was 289.14 pg/ml (95% CI 253.278 to 325.013 pg/ml) and –329.02 pg/ml (95% CI –387.740 to –270.445 pg/ml) respectively. Heterogeneity in effect size of selected studies was present for both parameters (CSF tau: Q statistics = 1816.596, DF = 40, P = 0.000 and CSF Aβ42: Q-statistics = 1259.358, DF = 24, p 42 levels in AD and controls may be considered as potential biomarker along with the clinical phenotype to perform them during high quality diagnostic testing in dementia.

A Short Review of the Literature on Assistive Technologies for Alzheimer’s Patients and Their Caregivers

Alzheimer’s is one of the most disabling neurocognitive diseases. A person diagnosed with Alzheimer’s slowly loses cognitive function and ultimately becomes entirely dependent upon the caregivers. Caregivers must help the patient in everyday activities ranging from walking to cooking, eating, and so on. In most caregiving facilities, a single caregiver often handles more than one patient, which results in caregiver burnout. Researchers are developing useful technologies to prevent caregiver burnouts and facilitate families in the best possible manner. The goal of this purposive short review of literature is to study the modern tools, devices, and gadgets available to Alzheimer’s patients and caregivers and understand the focus areas for future research. The review identified a range of products and technologies that help in monitoring to diagnosis, aid therapy, and reduce the burden on caregivers. These technologies play a vital role in improving the quality of life for both the patients and the caregivers. The study identified reducing cost of the devices, increasing robustness and dependability of the devices, and various aspects of the assistive technologies, including ethical and privacy issues, as the focus areas for future research.