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1.
Brain Nerve ; 71(10): 1081-1088, 2019 Oct.
Artigo em Japonês | MEDLINE | ID: mdl-31588052

RESUMO

During the past 20 years, genome studies for Alzheimer's disease (AD) have elucidated the pathogenesis of AD including the amyloid hypothesis. However, clinical trials of the disease modifying drugs for AD developed based on the amyloid hypothesis have been largely unsuccessful. New genes associated with AD have been identified through comprehensive genome analyses such as genome-wide association studies and whole genome/exome sequencing using next-generation sequencers. With these efforts, new therapeutic targets to AD have been explored. This review summarizes the genetic make-up of AD in terms of both risk and protective factors from the viewpoint of novel therapeutic targets to AD.


Assuntos
Doença de Alzheimer/genética , Doença de Alzheimer/terapia , Testes Genéticos , Predisposição Genética para Doença , Estudo de Associação Genômica Ampla , Humanos , Fatores de Proteção , Fatores de Risco
2.
J Natl Black Nurses Assoc ; 30(1): 40-47, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31465684

RESUMO

The purpose of this article was to help healthcare practitioners understand the dynamics of Alzheimer's care giving and to introduce an evidence-based practice intervention to improve the caregiver's self-efficacy. Over 5 million people in the United States are afflicted with Alzheimer's disease and require a caregiver to assist with all areas of daily activity. Adult care giving is challenging for the caregiver, who is often a family member with little to no knowledge or skill in rendering care. African-American caregivers encounter an even greater challenge by overcoming cultural bias inherent in racial disparity. Evidence-based practice interventions are helpful in successfully rendering care while minimizing stress and burden. Healthcare providers must consider the caregiver, the dynamics of care giving, and cultural norms, in the plan of care to successfully care for the Alzheimer's patient along the trajectory of the disease.


Assuntos
Doença de Alzheimer/terapia , Cuidadores/psicologia , Planejamento de Assistência ao Paciente/organização & administração , Adulto , Afro-Americanos/psicologia , Características Culturais , Prática Clínica Baseada em Evidências , Humanos , Autoeficácia
3.
Nervenarzt ; 90(9): 891-897, 2019 Sep.
Artigo em Alemão | MEDLINE | ID: mdl-31332452

RESUMO

Alzheimer's disease is histopathologically characterized by aggregation of two proteins, namely amyloid-beta peptide and tau protein. Whereas former intervention trials focused particularly on the amyloid pathology, recent therapeutic approaches are directed against the tau pathology. This article summarizes recent progress in anti-tau therapies, especially therapies based on anti-tau immunization and antisense oligonucleotides (ASO).


Assuntos
Doença de Alzheimer , Proteínas tau , Doença de Alzheimer/terapia , Peptídeos beta-Amiloides/metabolismo , Humanos , Imunoterapia , Oligonucleotídeos Antissenso/uso terapêutico , Proteínas tau/antagonistas & inibidores , Proteínas tau/metabolismo
5.
Life Sci ; 231: 116564, 2019 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-31202840

RESUMO

Alzheimer's disease (AD) as a dementia and neurodegenerative disease, is mostly prevalent among people more than 65 years. AD is mostly manifested in the form of degraded mental function, such as losing memory and impaired cognitive function. Due to inefficiency of traditional pharmacological therapeutic approaches with no long-term cure, cell therapy can be considered as a capable approach in AD management. Therapies based on mesenchymal stem cells (MSCs) have provided hopeful results in experimental models regarding several disorders. MSCs enhance the levels of functional recoveries in pathologic experimental models of central nervous system (CNS) and are being investigated in clinical trials in neurological disorders. However, there is limited knowledge on the protective capabilities of MSCs in AD management. Almost, several experiments have suggested positive effects of MSCs and helped to better understand of AD-related dementia mechanism. MSCs have the potential to be used in AD treatment through amyloid-ß peptide (AB), Tau protein and cholinergic system. This review aimed to clarify the promising perspective of MSCs in the context of AD.


Assuntos
Doença de Alzheimer/terapia , Transplante de Células-Tronco Mesenquimais/métodos , Animais , Humanos , Células-Tronco Mesenquimais/citologia , Células-Tronco Mesenquimais/fisiologia , Ensaios Clínicos Controlados Aleatórios como Assunto
6.
Adv Gerontol ; 32(1-2): 112-120, 2019.
Artigo em Russo | MEDLINE | ID: mdl-31228376

RESUMO

The article deals with the important issue of diagnosis and treatment of Alzheimer's disease in the elderly and senile age. Despite the fact that this disease is considered, of course, age-associated pathology, which is the main cause of senile dementia, its diagnosis in Russia is exhibited rather rarely compared with dementia, for example, of vascular origin. This is due, in the author's opinion, not only with the difficulties of in-vivo diagnosis of Alzheimer's disease, but, first of all, with the characteristic of the elderly and senile multiplicity of pathological processes. A significant part of these pathologic processes, as well as Alzheimer's disease, can cause increasing cognitive disorders. Under this condition, dementia is already considered as a multi-factorial disease even in cases where Alzheimer's disease is the leading factor. This position, in turn, requires the expansion of the diagnostic search even in cases of full confidence in the diagnosis of Alzheimer's disease in the elderly and senile age to determine the possible role of other pathological processes in the formation and development of dementia. Ultimately, with limited opportunities for treatment of Alzheimer's disease, this will help in the selection of treatment methods aimed at reducing the role of other etiological and pathogenic moments in the development of dementia of mixed Genesis in the elderly and senile.


Assuntos
Doença de Alzheimer , Transtornos Cognitivos , Idoso , Doença de Alzheimer/complicações , Doença de Alzheimer/diagnóstico , Doença de Alzheimer/terapia , Transtornos Cognitivos/etiologia , Humanos , Federação Russa
7.
Life Sci ; 231: 116483, 2019 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-31102743

RESUMO

Alzheimer's disease (AD) remains one of the greatest global concerns. Current treatment of AD - the acetylcholinesterase inhibitors - provides temporary improvement of cognitive functions, but does not affect the core of the underlying pathological process. There is still the need for alternative approaches, preferably ones based on the upstream events in the AD pathogenesis. The nature of AD pathogenesis remains complicated and not entirely explained. It is assumed to comprise of many interrelated events which can sequentially lead to further pathologies - as a kind of vicious cycle. The solution in this case could be to interact with these processes on multiple levels at the same time. The proposed approach hopes to achieve the state of equilibrium between two pathological pathways via reducing their dynamics on appropriate levels. The first step is to inhibit Tumor Necrosis Factor signaling related to inflammatory response. The second is to take advantage of the influence of insulin signaling on amyloid-ß processing to restore its proper clearance. Employing two only partially-beneficial approaches into a novel approach aims at breaking the "vicious cycle" and eliciting synergistic effect via working on different levels simultaneously. The effect of such therapy could allow physicians to completely inhibit neural damage. The proposed strategy may prove easily introducible as an efficacious clinical approach employing novel anti-TNF agents in combination with anti-diabetic agents. Data is needed on its influence on cognitive functions, any occurrence of adverse effects, and the development of models of optimal doses and their temporal location.


Assuntos
Doença de Alzheimer/fisiopatologia , Doença de Alzheimer/terapia , Diabetes Mellitus/terapia , Inflamação/terapia , Anti-Inflamatórios/uso terapêutico , Cognição , Demência/tratamento farmacológico , Demência/fisiopatologia , Diabetes Mellitus/tratamento farmacológico , Diabetes Mellitus/imunologia , Diabetes Mellitus/metabolismo , Sinergismo Farmacológico , Humanos , Hipoglicemiantes/uso terapêutico , Inflamação/metabolismo , Insulina/metabolismo , Fator de Necrose Tumoral alfa/metabolismo
8.
Zhongguo Zhen Jiu ; 39(5): 551-5, 2019 May 12.
Artigo em Chinês | MEDLINE | ID: mdl-31099230

RESUMO

OBJECTIVE: To explore the acupoint selection rules of acupuncture for Alzheimer's disease (AD) in modern clinical practice by complex network technology. METHODS: The relevant articles of clinical trials were retrieved from CNKI published before December 2017. Using Microsoft Excel 2010, the database was established. Using Gephi 0.8.2 software, the complex network mode was built and its topological structure was analyzed. RESULTS: Finally, 81 articles were eligible and 114 acupoint prescriptions were extracted. The constructed complex network of acupoint prescriptions for AD was characteristics as small world effect and scale-free property, the crucial acupoints included Baihui (GV 20), Sishencong (EX-HN 1), Fengchi (GB 20), Yintang (GV 29), Shenmen (HT 7), Shenting (GV 24), Zusanli (ST 36), Fenglong (ST 40) and Taichong (LR 3). In acupoint combination, Baihui (GV 20), Neiguan (PC 6), Shenmen (HT 7) and Sanyinjiao (SP 6) were the most common, and the combination of the distal and nearby points was predominant. Using k-core for acupoint optimization, 29 core acupoints were screened and they were mostly located on the governor vessel and the head and neck, with the highest use frequency. 82.76% of acupoints were specific acupoints and the influential points were dominant. Using community structure partition, these acupoints were classified into two groups, i.e. deficiency syndrome and excess syndrome. CONCLUSION: The selection of local acupoints is the first choice in acupuncture treatment for AD. The combination of distal and nearby points is the most common and the special points are the core. In clinical practice, the great consideration is provided on mind regulation, integration of disease and symptoms, the mutual treatment of the primary and the secondary as well as the deficiency and the excess.


Assuntos
Pontos de Acupuntura , Doença de Alzheimer , Publicações , Doença de Alzheimer/terapia , Bases de Dados Factuais , Humanos
9.
J Biomed Sci ; 26(1): 33, 2019 May 09.
Artigo em Inglês | MEDLINE | ID: mdl-31072403

RESUMO

Alzheimer's disease (AD) is the most common type of dementia and typically manifests through a progressive loss of episodic memory and cognitive function, subsequently causing language and visuospatial skills deficiencies, which are often accompanied by behavioral disorders such as apathy, aggressiveness and depression. The presence of extracellular plaques of insoluble ß-amyloid peptide (Aß) and neurofibrillary tangles (NFT) containing hyperphosphorylated tau protein (P-tau) in the neuronal cytoplasm is a remarkable pathophysiological cause in patients' brains. Approximately 70% of the risk of developing AD can be attributed to genetics. However, acquired factors such as cerebrovascular diseases, diabetes, hypertension, obesity and dyslipidemia increase the risk of AD development. The aim of the present minireview was to summarize the pathophysiological mechanism and the main risk factors for AD. As a complement, some protective factors associated with a lower risk of disease incidence, such as cognitive reserve, physical activity and diet will also be addressed.


Assuntos
Doença de Alzheimer/epidemiologia , Doença de Alzheimer/terapia , Reserva Cognitiva , Dieta , Exercício , Idoso , Idoso de 80 Anos ou mais , Humanos , Incidência , Pessoa de Meia-Idade , Fatores de Proteção , Fatores de Risco
10.
Adv Exp Med Biol ; 1128: 227-248, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31062332

RESUMO

Recently, Alzheimer's disease (AD) is understood as "diabetes of the brain" or "type 3 diabetes." Recent clinical trials of anti-amyloid ß-protein (Aß) therapies have not proved to be successful. Thus, glucose-insulin metabolism in the brain is thought to be an alternative therapeutic target. Various types of antidiabetic drugs such as insulin, thiazolidinediones, dipeptidyl peptidase-4 (DPP4) inhibitors, glucagon-like peptide-1 (GLP-1) agonists, biguanides, and others have been reported to be effective on cognitive impairment in animal models and patients with DM or AD. Here, recent reports are reviewed. While we identified apomorphine (APO) as a novel drug that promoted intracellular Aß degradation and improved memory function in an AD mouse model, more recently, we have revealed that APO treatment improves neuronal insulin resistance and activates insulin-degrading enzyme (IDE), a major Aß-degrading enzyme. In this context, recovery of impaired insulin signaling in AD neurons may be a promising therapeutic strategy for AD dementia.


Assuntos
Doença de Alzheimer/complicações , Doença de Alzheimer/terapia , Apomorfina/uso terapêutico , Diabetes Mellitus , Peptídeos beta-Amiloides , Animais , Humanos , Insulina , Insulisina , Camundongos
11.
Med Sci Monit ; 25: 3329-3335, 2019 May 06.
Artigo em Inglês | MEDLINE | ID: mdl-31056537

RESUMO

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the accumulation of ß-amyloid peptide 1-42 and phosphorylation of tau protein in the brain. Thus far, the transfer mechanism of these cytotoxic proteins between nerve cells remains unclear. Recent studies have shown that nanoscale extracellular vesicles (exosomes) originating from cells may play important roles in this transfer process. In addition, several genetic materials and proteins are also involved in intercellular communication by the secretion of the exosomes. That proposes novel avenues for early diagnosis and biological treatment in AD, based on exosome detection and intervention. In this review, exosome-related pathways of cytotoxic protein intercellular transfer in AD, and the effect of membrane proteins on exosomes targeting cells are first introduced. The advances in exosome-related biomarker detection in AD are summarized. Finally, the advantages and challenges of reducing cytotoxic protein accumulation via exosomal intervention for AD treatment are discussed. It is envisaged that future research in exosomes may well provide new insights into the pathogenesis, diagnosis, and treatment of AD.


Assuntos
Doença de Alzheimer/patologia , Exossomos/patologia , Doença de Alzheimer/diagnóstico , Doença de Alzheimer/metabolismo , Doença de Alzheimer/terapia , Biomarcadores/metabolismo , Encéfalo/metabolismo , Encéfalo/patologia , Exossomos/metabolismo , Humanos , Fosforilação , Proteínas tau/metabolismo
12.
Expert Opin Investig Drugs ; 28(6): 545-554, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-31094578

RESUMO

INTRODUCTION: Alzheimer's dementia (AD) is the most common form of dementia in the World. Pathologically, it is characterized by extracellular ß-amyloid plaques and intraneuronal neurofibrillary tangles (NFTs). The latter is composed of irregular, pathological forms of the tau protein. Currently, FDA-approved symptomatic treatments are limited to the targeting of cholinergic deficits and glutamatergic dysfunctions. However, as understanding of ß-amyloid plaques and NFTs expands, these dysfunctional proteins represent potential therapeutic interventions. The present review article evaluates active and passive immunotherapies in clinical development for AD to date and their potential to significantly improve the treatment of AD going forward. AREAS COVERED: All clinical trials that have targeted ß-amyloid to date have produced somewhat disappointing results, leading to a shift in intervention focus to targeting tau protein. A key component in understanding the value of targeting tau in therapeutic paradigms has come from the conceptualization of prion-like pathological spread of tau isoforms from neuron to neuron, and referred to as 'tauons'. Immunotherapies currently under investigation include approaches aiming at preventing pathological tau aggregation, stabilizing microtubules, and blocking of tauons. EXPERT OPINION: A multi-targeted approach that would use biologics targeting tau offers great promise to the development of effective AD therapeutic interventions.


Assuntos
Doença de Alzheimer/terapia , Imunoterapia/métodos , Proteínas tau/imunologia , Doença de Alzheimer/imunologia , Doença de Alzheimer/fisiopatologia , Peptídeos beta-Amiloides/metabolismo , Animais , Produtos Biológicos/farmacologia , Humanos , Terapia de Alvo Molecular , Emaranhados Neurofibrilares/metabolismo , Proteínas tau/metabolismo
13.
Int J Mol Sci ; 20(7)2019 Apr 03.
Artigo em Inglês | MEDLINE | ID: mdl-30987146

RESUMO

The average life span steadily grows in humans and in animals kept as pets or left in sanctuaries making the issue of elderly-associated cognitive impairment a hot-spot for scientists. Alzheimer's disease (AD) is the most prevalent cause of progressive mental deterioration in aging humans, and there is a growing body of evidence that similar disorders (Alzheimer's-like diseases, ALD) are observed in animals, more than ever found in senescent individuals. This review reveals up to date knowledge in pathogenesis, hallmarks, diagnostic approaches and modalities in AD faced up with ALD related to different animal species. If found at necropsy, there are striking similarities between senile plaques (SP) and neurofibrillary tangles (NFT) in human and animal brains. Also, the set of clinical symptoms in ALD resembles that observed in AD. At molecular and microscopic levels, the human and animal brain histopathology in AD and ALD shows a great resemblance. AD is fatal, and the etiology is still unknown, although the myriad of efforts and techniques were employed in order to decipher the molecular mechanisms of disease onset and its progression. Nowadays, according to an increasing number of cases reported in animals, apparently, biochemistry of AD and ALD has a lot in common. Described observations point to the importance of extensive in vivo models and extensive pre-clinical studies on aging animals as a suitable model for AD disease.


Assuntos
Doença de Alzheimer/patologia , Envelhecimento/patologia , Doença de Alzheimer/imunologia , Doença de Alzheimer/terapia , Animais , Modelos Animais de Doenças , Humanos , Inflamação/patologia , Modelos Biológicos
14.
J Neuroinflammation ; 16(1): 74, 2019 Apr 05.
Artigo em Inglês | MEDLINE | ID: mdl-30953557

RESUMO

Neuroinflammation is considered one of the cardinal features of Alzheimer's disease (AD). Neuritic plaques composed of amyloid ß and neurofibrillary tangle-laden neurons are surrounded by reactive astrocytes and microglia. Exposure of microglia, the resident myeloid cell of the CNS, to amyloid ß causes these cells to acquire an inflammatory phenotype. While these reactive microglia are important to contain and phagocytose amyloid plaques, their activated phenotype impacts CNS homeostasis. In rodent models, increased neuroinflammation promoted by overexpression of proinflammatory cytokines can cause an increase in hyperphosphorylated tau and a decrease in hippocampal function. The peripheral immune system can also play a detrimental or beneficial role in CNS inflammation. Systemic inflammation can increase the risk of developing AD dementia, and chemokines released directly by microglia or indirectly by endothelial cells can attract monocytes and T lymphocytes to the CNS. These peripheral immune cells can aid in amyloid ß clearance or modulate microglia responses, depending on the cell type. As such, several groups have targeted the peripheral immune system to modulate chronic neuroinflammation. In this review, we focus on the interplay of immunomodulating factors and cell types that are being investigated as possible therapeutic targets for the treatment or prevention of AD.


Assuntos
Doença de Alzheimer , Citocinas/metabolismo , Microglia/fisiologia , Células Mieloides/fisiologia , Doença de Alzheimer/complicações , Doença de Alzheimer/patologia , Doença de Alzheimer/terapia , Animais , Comunicação Celular/fisiologia , Encefalite/etiologia , Humanos
15.
Biomed Res Int ; 2019: 1431760, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30949496

RESUMO

Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive and painless technique that has been applied for the treatments of diverse neurodegenerative disorders. In the current study, its anti-Alzheimer's disease (AD) effect was assessed and the mechanism driving the effect was explored. The AD symptoms were induced via the intracranial injection of Aß 1-42 in mice and then treated with rTMS of 1 Hz or 10 Hz. The anti-AD effect of rTMS was assessed by Morris water maze (MWM), histological staining and western blotting. The results showed that rTMS administrations of both frequencies improved the cognitive function and suppressed neuron apoptosis in AD mice. Moreover, the treatment also increased the brain BDNF, NGF, and doublecortin levels, which represented the increased viability of neurons by rTMS. The injection of Aß 1-42 also increased the expressions of p-GSK-3ß, p-Tau, and p-ß-catenin and suppressed the level of total ß-catenin. After the treatments of rTMS, the level of ß-catenin was restored, indicating the activation of ß-catenin signaling. In conclusion, the findings outlined in the current study demonstrated that the anti-AD effect of rTMS was associated with the activation of ß-catenin, which would promote the survival of neurons.


Assuntos
Doença de Alzheimer , Peptídeos beta-Amiloides/toxicidade , Encéfalo , Fragmentos de Peptídeos/toxicidade , Transdução de Sinais , Estimulação Magnética Transcraniana , beta Catenina/metabolismo , Doença de Alzheimer/induzido quimicamente , Doença de Alzheimer/metabolismo , Doença de Alzheimer/patologia , Doença de Alzheimer/terapia , Animais , Encéfalo/metabolismo , Encéfalo/patologia , Regulação da Expressão Gênica , Humanos , Masculino , Camundongos , Proteínas do Tecido Nervoso/biossíntese
17.
Neurosci Biobehav Rev ; 101: 122-128, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-30946856

RESUMO

INTRODUCTION: Race is an important health determinant and should adequately be considered in research and drug development protocols targeting Alzheimer's disease (AD). METHODS: A systematic review of available randomized controlled trials (RCTs) on the currently marketed treatments for AD was conducted with the aim of 1) documenting the reporting of race, and 2) exploring the impact of race on the efficacy and safety/tolerability of the considered medications. RESULTS: Overall, 59.2% of the 49 retained RCTs reported information concerning the race of participants. Only a striking minority of enrolled patients was constituted of blacks and Hispanics. None on the retained studies reported results on the efficacy and safety/tolerability of the tested treatment separately for racial groups nor performed sensitivity analyses accounting for the race of participants. DISCUSSION: Race has insufficiently been reported in previous interventional studies on AD. Its potential association with the effectiveness and safety/tolerability of the tested medications has completely been neglected.


Assuntos
Doença de Alzheimer/terapia , Grupos Étnicos/estatística & dados numéricos , Disparidades em Assistência à Saúde/estatística & dados numéricos , Grupos Minoritários/estatística & dados numéricos , Coleta de Dados , Humanos , Ensaios Clínicos Controlados Aleatórios como Assunto
18.
Neuron ; 101(5): 839-862, 2019 03 06.
Artigo em Inglês | MEDLINE | ID: mdl-30844402

RESUMO

Gene transfer has long been a compelling yet elusive therapeutic modality. First mainly considered for rare inherited disorders, gene therapy may open treatment opportunities for more challenging and complex diseases such as Alzheimer's or Parkinson's disease. Today, examples of striking clinical proof of concept, the first gene therapy drugs coming onto the market, and the emergence of powerful new molecular tools have broadened the number of avenues to target neurological disorders but have also highlighted safety concerns and technology gaps. The vector of choice for many nervous system targets currently is the adeno-associated viral (AAV) vector due to its desirable safety profile and strong neuronal tropism. In aggregate, the clinical success, the preclinical potential, and the technological innovation have made therapeutic AAV drug development a reality, particularly for nervous system disorders. Here, we discuss the rationale, opportunities, limitations, and progress in clinical AAV gene therapy.


Assuntos
Doença de Alzheimer/terapia , Marcação de Genes/métodos , Terapia Genética/métodos , Doença de Parkinson/terapia , Animais , Dependovirus/genética , Marcação de Genes/efeitos adversos , Terapia Genética/efeitos adversos , Humanos
19.
Neurobiol Aging ; 78: 18-28, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-30851437

RESUMO

Alzheimer's disease (AD) is the most common type of senile dementia. The antiaging gene Klotho is reported to decline in the brain of patients and animals with AD. However, the role of Klotho in the progression of AD remains elusive. The present study explored the effects and underlying mechanism of Klotho in a mouse model of AD. The upregulation of cerebral Klotho expression was mediated by an intracerebroventricular injection of a lentiviral vector that encoded Klotho (LV-KL) in 7-month-old amyloid precursor protein/presenilin 1 transgenic mice. Three months later, LV-KL significantly induced Klotho overexpression in the brain and effectively ameliorated cognitive deficit and AD-like pathology in amyloid precursor protein/presenilin 1 mice. LV-KL induced autophagy activation and protein kinase B/mammalian target of rapamycin inhibition both in AD mice and BV2 murine microglia. These results suggest that the upregulation of Klotho expression in the brain may promote the autophagic clearance of amyloid beta and protect against cognitive deficits in AD mice. These findings highlight the preventive and therapeutic potential of Klotho for the treatment of AD.


Assuntos
Doença de Alzheimer/genética , Doença de Alzheimer/terapia , Encéfalo/metabolismo , Disfunção Cognitiva/genética , Disfunção Cognitiva/terapia , Expressão Gênica , Terapia Genética/métodos , Vetores Genéticos/administração & dosagem , Vetores Genéticos/genética , Glucuronidase/administração & dosagem , Glucuronidase/genética , Lentivirus , Peptídeos beta-Amiloides/metabolismo , Animais , Autofagia , Modelos Animais de Doenças , Vetores Genéticos/farmacologia , Glucuronidase/metabolismo , Glucuronidase/farmacologia , Humanos , Injeções Intraventriculares , Masculino , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Microglia/metabolismo , Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores , Proteínas Proto-Oncogênicas c-akt/metabolismo , Serina-Treonina Quinases TOR/antagonistas & inibidores , Regulação para Cima
20.
Vet Clin North Am Small Anim Pract ; 49(3): 477-499, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30846383

RESUMO

Canine cognitive dysfunction (CCD) is the canine analog of human Alzheimer disease (AD). The pathophysiology of CCD/AD is multifaceted. CCD is common in aged (>8 years) dogs, affecting between 14% and 35% of the pet dog population. Apparent confusion, anxiety, disturbance of the sleep/wake cycle, and decreased interaction with owners are all common clinical signs of CCD. Although there is no cure for CCD, several proven effective therapeutic approaches are available for improving cognitive ability and maintaining a good quality of life; instituting such therapies early in the disease course is likely to have the greatest positive clinical effect.


Assuntos
Doença de Alzheimer/veterinária , Doenças do Cão/diagnóstico , Cuidados Paliativos , Doença de Alzheimer/diagnóstico , Doença de Alzheimer/terapia , Animais , Doenças do Cão/diagnóstico por imagem , Doenças do Cão/fisiopatologia , Doenças do Cão/terapia , Cães , Medicina Veterinária/tendências
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