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1

CHARACTERISTICS OF ARABIC HANDWRITING ON GRAPHIC TABLET IN NEURODEGENERATIVE DISEASE: PRELIMINARY RESULTS BETWEEN PATIENTS WITH ALZHEIMER’S DISEASE AND HEALTHY CONTROLS

100%

Ghita A., Ibtissame A., Alae A., Ghizlane K., Mostafa M., Faouzi B. M.

Acta Neuropsychologica

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2022

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vol. 20(1)

53-65

EN

Handwriting is a component of the complex language that came about late in the history of mankind and which develops late in human beings. Numerous works have raised changes in both the graphic and kinematic characteristics of writing. Although, age does not modify the lexical and syntactic parameters of language, it can however modify its spatial structure, especially pressure and speed. Many neurodegenerative pathologies, especially Alzheimer's disease, are characterized by a progressive disorganization of writing. Depending on the cognitive stage of the dementia, the graphic gesture deteriorates as does the spatial construction. Objective: Our study aims at assessing the characteristics of Arabic writing in a healthy Moroccan population and to compare it to people with mild to moderate Alzheimer's disease. Our objective is to help health professionals detect early cognitive deterioration in neurodegenerative diseases by analyzing the graphic gesture. Handwriting is captured on a graphic tablet (WACOM) and is analyzed "online" as a sequence of acquired signals (position, pressure, speed and pen inclination) in Moroccan patients with mild to moderate Alzheimer's disease and these were compared to those of normal volunteers. We performed a first analysis of the results from 18 Alzheimer's patients compared to 18 control subjects. The results reveal differences between the control and Alzheimer's groups. AD subjects had lower speeds and accelerations compared to the control subjects. The time spent on paper and in the air was significantly greater in the AD subjects. This preliminary analysis of the results allowed us to identify distinguishing characteristics through the analysis of different handwriting parameters in order to identify the two groups studied.

2

Neuroprotective effects of dehydroepiandrosterone (DHEA) in rat model of Alzheimer's disease

100%

Aly H. F., Metwally F. M., Ahmed H. H.

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2011

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vol. 58

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issue 4

513-520

EN

The current study was undertaken to elucidate a possible neuroprotective role of dehydroepiandrosterone (DHEA) against the development of Alzheimer's disease in experimental rat model. Alzheimer's disease was produced in young female ovariectomized rats by intraperitoneal administration of AlCl3 (4.2 mg/kg body weight) daily for 12 weeks. Half of these animals also received orally DHEA (250 mg/kg body weight, three times weekly) for 18 weeks. Control groups of animals received either DHAE alone, or no DHEA, or were not ovariectomized. After such treatment the animals were analyzed for oxidative stress biomarkers such as hydrogen peroxide, nitric oxide and malondialdehyde, total antioxidant capacity, reduced glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase and catalase activities, antiapoptotic marker Bcl-2 and brain derived neurotrophic factor. Also brain cholinergic markers (acetylcholinesterase and acetylcholine) were determined. The results revealed significant increase in oxidative stress parameters associated with significant decrease in the antioxidant enzyme activities in Al-intoxicated ovariectomized rats. Significant depletion in brain Bcl-2 and brain-derived neurotrophic factor levels were also detected. Moreover, significant elevations in brain acetylcholinesterase activity accompanied with significant reduction in acetylcholine level were recorded. Significant amelioration in all investigated parameters was detected as a result of treatment of Al-intoxicated ovariectomized rats with DHEA. These results were confirmed by histological examination of brain sections. These results clearly indicate a neuroprotective effect of DHEA against Alzheimer's disease.

3

Molecular cloning and sequencing of rabbit presenilin-1 cDNA fragment.

100%

Al-Khedhairy A. A., Arfin M., Dukhyil A. A. B.

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2002

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vol. 49

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issue 4

1013-1017

EN

Molecular cloning and sequencing of a cDNA encoding rabbit presenilin-1 (Ps1) fragment was performed by reverse transcription polymerase chain reaction (RT-PCR) using primers: 5'-GGA TGA GCA GCT AAT CTA TAC C-3' and 5'-TCC ATT CAG GGA GGT ACT TGA TA-3'. The cDNA fragment revealed 402 nucleotides. The sequence was well conserved and found to be 91, 90, 88, 87 and 78% homologous to that of human, lemur, rat, mouse and chicken, respectively. The cDNA translated into a 130 amino-acid protein fragment. The deduced amino-acid sequence was also well conserved in various species and exhibited 98% similarities with those of rat, lemur and human homologues. However, differences were noticed at residues 145, 168 and 212. This cDNA fragment is quite significant because it is the most conserved portion of Ps1 in various animals and encodes four transmembrane regions (TM2, 3, 4, 5) as defined in human Ps1. Moreover, it includes more than 50% of the sites at which substitutions have been reported in familial Alzheimer's disease (FAD). Therefore, it is suggested that the rabbit can be used as an experimental model for future studies on Ps1 and its physiological functions to work out possible pathways leading to FAD linked neurodegeneration.

4

Drug Closure of a Patent Ductus Arteriosus in an Extremely Low Birth Weight Premature Newborn. A Case Report

100%

Kaczyńska A., Broczek K., Sienkiewicz Z., Gotlib J.

Polish Journal of Public Health

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2015

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vol. 124

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issue 4

215-219

EN

The article presents the role of government and non-government organisations in promoting knowledge on Alzheimer's disease in Poland and the European Union. There is a detailed analysis of the EU documents and non-government organisations in promoting knowledge on Alzheimer's disease in Germany, France and Holland. There is a discussion on the National Alzheimer's Plan on the basis of an example of introducing such a plan in Finland. Additionally, the rules of helping people suffering from Alzheimer's disease and their attendants in Poland are presented.

5

Naming disorders in logopenic variant of Primary Progressive Aphasia

100%

Antczak-Kujawin J.

Acta Neuropsychologica

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2019

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vol. 17(1)

87-95

EN

Language functions, particularly disordered lexical skills were diagnosed in the examined woman based on selected diagnostic tests of the Boston Diagnostic Aphasia Examination (BDAE). Furthermore, an experimental version of the author's original test for assessing lexical-semantic performance in dementia was used. The author presents a case study of a 79-year-old woman diagnosed with logopenic variant primary progressive aphasia (lvPPA) secondary to Alzheimer’s disease. The author describes the symptoms of anomie manifested by the study participant and the supplementary strategies she applied in the case of lexical deficits. The analysis of the findings obtained in the course of language function assessment allowed the author to assess the fluency of speech, speech comprehension, repetition and naming. The study participant diagnosed with lvPPA was observed to manifest the following: an absence of motor speech disorders, absence of characteristics of evident agrammatism, preserved comprehension of individual words, preserved semantic knowledge of objects, disordered retrieval of words in spontaneous speech and in attempts to name, and disordered repetition of sentences and phrases. The analysis of the discussed case study allowed the author to discuss the progressive lexical deficits manifested by the lvPPA patient and to record those supplementary strategies that were most frequently applied in the lexical difficulties experienced by the female patient diagnosed with lvPPA.

6

Alzheimer's disease: Its origin at the membrane, evidence and questions.

88%

Buchet R., Pikuła S.

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2000

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vol. 47

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issue 3

725-733

EN

Numerous results on membrane lipid composition from different regions of autopsied Alzheimer's disease brains in comparison with corresponding fractions isolated from control brains revealed significant differences in serine- and ethanolamine-containing glycerophospholipid as well as in glycosphingolipid content. Changes in membrane lipid composition are frequently accompanied by alterations in membrane fluidity, hydrophobic mismatch, lipid signaling pathways, transient formation and disappearance of lipid microdomains, changes in membrane permeability to cations and variations of other membrane properties. In this review we focus on possible implications of altered membrane composition on β-amyloid precursor protein (APP) and on proteolysis of APP leading eventually to the formation of neurotoxic β-amyloid (Aβ) peptides, the major proteinaceous component of extracellular senile plaques, directly involved in Alzheimer's disease pathogenesis.

7

Molecular mechanisms initiating amyloid β-fibril formation in Alzheimer's disease

75%

Kirkitadze M. D., Kowalska A.

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2005

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vol. 52

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issue 2

417-423

EN

The deposition of aggregated amyloid β-protein (Aβ) in the human brain is a major lesion in Alzheimer' disease (AD). The process of Aβ fibril formation is associated with a cascade of neuropathogenic events that induces brain neurodegeneration leading to the cognitive and behavioral decline characteristic of AD. Although a detailed knowledge of Aβ assembly is crucial for the development of new therapeutic approaches, our understanding of the molecular mechanisms underlying the initiation of Aβ fibril formation remains very incomplete. The genetic defects responsible for familial AD influence fibrillogenesis. In a majority of familial cases determined by amyloid precursor protein (APP) and presenilin (PS) mutations, a significant overproduction of Aβ and an increase in the Aβ42/Aβ40 ratio are observed. Recently, it was shown that the two main alloforms of Aβ have distinct biological activity and behaviour at the earliest stage of assembly. In vitro studies demonstrated that Aβ42 monomers, but not Aβ40, form initial and minimal structures (pentamer/hexamer units called paranuclei) that can oligomerize to larger forms. It is now apparent that Aβ oligomers and protofibrils are more neurotoxic than mature Aβ fibrils or amyloid plaques. The neurotoxicity of the prefibrillar aggregates appears to result from their ability to impair fundamental cellular processes by interacting with the cellular membrane, causing oxidative stress and increasing free Ca^(2+)that eventually lead to apoptotic cell death.

8

Circular dichroism and aggregation studies of amyloid β (11-8) fragment and its variants.

75%

Juszczyk P., Kołodziejczyk A. S., Grzonka Z.

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2005

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vol. 52

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issue 2

425-431

EN

Aggregation of Aβ peptides is a seminal event in Alzheimer's disease. Detailed understanding of Aβ assembly would facilitate the targeting and design of fibrillogenesis inhibitors. Here comparative conformational and aggregation studies using CD spectroscopy and thioflavine T fluorescence assay are presented. As a model peptide, the 11-28 fragment of Aβ was used. This model peptide is known to contain the core region responsible for Aβ aggregation. The structural and aggregational behaviour of the peptide was compared with the properties of its variants corresponding to natural, clinically relevant mutants at positions 21-23 (A21G, E22K, E22G, E22Q and D23N). In HFIP (hexafluoro-2-propanol), a strong α-helix inducer, the CD spectra revealed an unexpectedly high amount of β-sheet conformation. The aggregation process of Aβ(11-28) variants provoked by water addition to HFIP was found to be consistent with a model of an α-helix-containing intermediate. The aggregation propensity of all Aβ(11-28) variants was also compared and discussed.

9

Targeting BACE with small inhibitory nucleic acids - a future for Alzheimer's disease therapy?

75%

Nawrot B.

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vol. 51

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issue 2

431-444

EN

β-Secretase, a β-site amyloid precursor protein (APP) cleaving enzyme (BACE), participates in the secretion of β-amyloid peptides (Aβ), the major components of the toxic amyloid plaques found in the brains of patients with Alzheimer's disease (AD). According to the amyloid hypothesis, accumulation of Aβ is the primary influence driving AD pathogenesis. Lowering of Aβ secretion can be achieved by decreasing BACE activity rather than by down-regulation of the APP substrate protein. Therefore, β-secretase is a primary target for anti-amyloid therapeutic drug design. Several approaches have been undertaken to find an effective inhibitor of human β-secretase activity, mostly in the field of peptidomimetic, non-cleavable substrate analogues. This review describes strategies targeting BACE mRNA recognition and its down-regulation based on the antisense action of small inhibitory nucleic acids (siNAs). These include antisense oligonucleotides, catalytic nucleic acids - ribozymes and deoxyribozymes - as well as small interfering RNAs (siRNAs). While antisense oligonucleotides were first used to identify an aspartyl protease with β-secretase activity, all the strategies now demonstrate that siNAs are able to inhibit BACE gene expression in a sequence-specific manner, measured both at the level of its mRNA and at the level of protein. Moreover, knock-down of BACE reduces the intra- and extracellular population of Aβ40 and Aβ42 peptides. An anti-amyloid effect of siNAs is observed in a wide spectrum of cell lines as well as in primary cortical neurons. Thus targeting BACE with small inhibitory nucleic acids may be beneficial for the treatment of Alzheimer's disease and for future drug design.

10

Genetic study of familial cases of Alzheimer's disease.

75%

Kowalska A., Pruchnik-Wolińska D., Florczak J., Modestowicz R., Szczech J., Kozubski W., Rossa G., Wender M.

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vol. 51

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issue 1

245-242

EN

A small number (1-5%) of Alzheimer's disease (AD) cases associated with the early-onset form of the disease (EOAD) appears to be transmitted as a pure genetic, autosomal dominant trait. To date, three genes responsible for familial EOAD have been identified in the human genome: amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2). Mutations in these genes account for a significant fraction (18 to 50%) of familial cases of early onset AD. The mutations affect APP processing causing increased production of the toxic Aβ42 peptide. According to the "amyloid cascade hypothesis", aggregation of the Aβ42 peptide in brain is a primary event in AD pathogenesis. In our study of twenty AD patients with a positive family history of dementia, 15% (3 of 20) of the cases could be explained by coding sequence mutations in the PS1 gene. Although a frequency of PS1 mutations is less than 2% in the whole population of AD patients, their detection has a significant diagnostic value for both genetic counseling and treatment in families with AD.

11

Comorbidities disorders and Alzheimer's disease

63%

Fąfara A., Ciesielska N., Damiza A., Chatys Ż., Bentryn D., Gajos A., Zukow W., Sokołowski R.

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issue 6

57-70

EN

Abstract Introduction. Alzheimer's disease is a chronic, progressive, neurodegenerative disease of the brain initially runs with disorders of higher cortical function, leading to dementia and a complete failure. Among the most important modifiable risk factors stand out: advanced age, genetic predisposition towards dementia and sex.Ch Orob Alzheimer's disease is heterogeneous in terms of clinical, neuropathological, biochemical and molecular level, can take place accompanied by a number of disorders and disease entities. Purpose. Presentation and discussion of disorders, and comorbidity of Alzheimer's disease. Materials and methods. Using a key Alzheimer's disease (Alzheimer's disease), comorbidities (comorbidity) Polish and foreign searched electronic bibliographic databases: Polish Medical Bibliography, EBSCO Host Web, Wiley Online Library, Springer Link, Science Direct, Medline. Results. Finally, analysis of the scientific reports showed that frequently co-existing disorders, and Alzheimer's disease include: disease entities associated with hypoestrogenemia, cognitive and behavioral deficits, depression, diabetes type 2, conversion of ocular disorders and eating habits, sleep, bladder control bladder and bowel, and sexual dysfunction. Conclusions. A multitude of sickness characterized by Alzheimer's disease shows coercion interdisciplinary care for early diagnosis not only cognitive deficits but also often concomitant ophthalmic internal medicine, neurological and psychiatric disorders. = Streszczenie Wstęp. Choroba Alzheimera to przewlekła, postępująca, pierwotnie neurodegeneracyjna choroba mózgu przebiegająca z zaburzeniami wyższych czynności korowych, prowadząca do otępienia i pełnej niesprawności. Wśród niemodyfikowalnych najważniejszych czynników ryzyka wyróżnia się: zaawansowany wiek, uwarunkowania genetyczne w kierunku otępienia oraz płeć. Choroba Alzheimera jest schorzeniem heterogennym pod względem klinicznym, neuropatologicznym, biochemicznym i molekularnym, może przebiegać w towarzystwie licznych zaburzeń oraz jednostek chorobowych. Cel. Przedstawienie i omówienie zaburzeń oraz schorzeń współistniejących z chorobą Alzheimera. Materiał i metody. Posługując się kluczowymi choroba Alzheimera (Alzheimer’s disease), choroby współistniejące (comorbidity) przeszukano polskie oraz zagraniczne elektroniczne bazy bibliograficzne: Polska Bibliografia Lekarska, EBSCO host Web, Wiley Online Library, Springer Link, Science Direct, Medline. Wyniki. Ostatecznie analiza doniesień naukowych wykazała, że do często współistniejących z chorobą Alzheimera zaburzeń oraz schorzeń można zaliczyć: jednostki chorobowe związane z hipoestrogenizmem, deficyty poznawcze i behawioralne, depresje, cukrzyce typu 2, zamiany oczne, a także zaburzenia nawyków żywieniowych, snu, kontroli nad pęcherzem moczowym i jelitami oraz zaburzenia seksualne. Wnioski. Mnogość chorobowa charakteryzująca chorobę Alzheimera ukazuje przymus opieki interdyscyplinarnej w celu wczesnego zdiagnozowania nie tylko deficytów poznawczych ale również często współistniejących okulistycznych, internistycznych, neurologicznych i psychiatrycznych zaburzeń.

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CHARACTERISTICS OF ARABIC HANDWRITING ON GRAPHIC TABLET IN NEURODEGENERATIVE DISEASE: PRELIMINARY RESULTS BETWEEN PATIENTS WITH ALZHEIMER’S DISEASE AND HEALTHY CONTROLS

Neuroprotective effects of dehydroepiandrosterone (DHEA) in rat model of Alzheimer's disease

Molecular cloning and sequencing of rabbit presenilin-1 cDNA fragment.

Drug Closure of a Patent Ductus Arteriosus in an Extremely Low Birth Weight Premature Newborn. A Case Report

Naming disorders in logopenic variant of Primary Progressive Aphasia

Alzheimer's disease: Its origin at the membrane, evidence and questions.

Molecular mechanisms initiating amyloid β-fibril formation in Alzheimer's disease

Circular dichroism and aggregation studies of amyloid β (11-8) fragment and its variants.

Targeting BACE with small inhibitory nucleic acids - a future for Alzheimer's disease therapy?

Genetic study of familial cases of Alzheimer's disease.

Comorbidities disorders and Alzheimer's disease