The promising role of natural products in Alzheimer's disease DOI Creative Commons
Michelle Melgarejo da Rosa, Luciclaudio Cassimiro de Amorim, João Victor de Oliveira Alves

et al.

Brain Disorders, Journal Year: 2022, Volume and Issue: 7, P. 100049 - 100049

Published: Aug. 17, 2022

Experimental studies support the discussion of use bioactive products natural as novel antioxidants sources neuroprotection against neurodegeneration. Natural antioxidants, such polyphenols, vitamins, Ginkgo biloba, curcumin, and herbal formulations are thought to reduce oxidative stress have preventive or therapeutic potential in Alzheimer's disease (AD). Extensive a dysfunctional antioxidant system predominant implications pathogenesis AD. To date, treatment AD attenuates symptoms rather than fighting root cause disease. Several revealed animal models However, clinical trials using molecules for not yet conclusive. It has become apparent that modified strategies enhance bioavailability brain permeability designed target free radicals prospective options The present review summarizes effectiveness several molecules, traditional formulations, from Brazilian Caatinga activity attenuating neuropathology reported various models, preclinical trials. On whole, setbacks future perspectives on these regarding bioavailability, formulation, status will also be discussed.

Language: Английский

Comprehensive Review on Alzheimer’s Disease: Causes and Treatment DOI Creative Commons
Zeinab Breijyeh, Rafik Karaman

Molecules, Journal Year: 2020, Volume and Issue: 25(24), P. 5789 - 5789

Published: Dec. 8, 2020

Alzheimer’s disease (AD) is a disorder that causes degeneration of the cells in brain and it main cause dementia, which characterized by decline thinking independence personal daily activities. AD considered multifactorial disease: two hypotheses were proposed as for AD, cholinergic amyloid hypotheses. Additionally, several risk factors such increasing age, genetic factors, head injuries, vascular diseases, infections, environmental play role disease. Currently, there are only classes approved drugs to treat including inhibitors cholinesterase enzyme antagonists N-methyl d-aspartate (NMDA), effective treating symptoms but do not cure or prevent Nowadays, research focusing on understanding pathology targeting mechanisms, abnormal tau protein metabolism, β-amyloid, inflammatory response, free radical damage, aiming develop successful treatments capable stopping modifying course AD. This review discusses currently available future theories development new therapies disease-modifying therapeutics (DMT), chaperones, natural compounds.

Language: Английский

Citations

1858
Behaviour Hallmarks in Alzheimer’s Disease 5xFAD Mouse Model DOI Open Access
Mafalda Soares Pádua, José Luis Guil‐Guerrero, Paula A. Lopes

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(12), P. 6766 - 6766

Published: June 20, 2024

The 5xFAD transgenic mouse model widely used in Alzheimer’s disease (AD) research recapitulates many AD-related phenotypes with a relatively early onset and aggressive age-dependent progression. Besides developing amyloid peptide deposits alongside neuroinflammation by the age of 2 months, as well exhibiting neuronal decline 4 months that intensifies 9 these mice manifest broad spectrum behavioural impairments. In this review, we present extensive repertoire dysfunctions mice, organised into four categories: motor skills, sensory function, learning memory abilities, neuropsychiatric-like symptoms. problems, associated agility reflex movements, balance coordination, skeletal muscle typically arise time reach age. function (such taste, smell, hearing, vision) starts to deteriorate when buildups spread related anatomical structures. cognitive functions, encompassing such visual recognition, associative, spatial working, reference learning, show signs from 6 Concerning symptoms, comprising apathy, anxiety depression, willingness for exploratory behaviour, it is believed motivational changes emerge approximately Unfortunately, numerous studies different laboratories are often contradictory on conclusions drawn identification age, making preclinical rodent models not easily translatable humans. This variability likely due range factors animals themselves, housing husbandry conditions, experimental settings. forthcoming studies, greater clarity details conducting testing could minimise inconsistencies ensure reliability reproducibility results.

Language: Английский

Citations

19
Advance of sporadic Alzheimer's disease animal models DOI
Lili Zhang, Chen Chen,

Marvin SH Mak

et al.

Medicinal Research Reviews, Journal Year: 2019, Volume and Issue: 40(1), P. 431 - 458

Published: July 22, 2019

Alzheimer's disease (AD), the most common form of dementia, is a progressive neurodegenerative disease. In past decades, numbers promising drug candidates showed significant anti-AD effects in preclinical studies but failed clinical trials. One major reasons might be limitation appropriate animal models for evaluating drugs. More than 95% AD cases are sporadic (sAD). However, were mainly tested familial (fAD) models. The diversity between sAD and fAD lead to high failure rate during development Therefore, an ideal model urgently needed Here, we summarized available models, including their methodology, pathologic features, potential underlying mechanisms. limitations these future trends field also discussed.

Language: Английский

Citations

93
Link between Diabetes and Alzheimer’s Disease Due to the Shared Amyloid Aggregation and Deposition Involving Both Neurodegenerative Changes and Neurovascular Damages DOI Open Access
Gabriela Dumitriṭa Stanciu, Veronica Bild, Daniela Carmen Ababei

et al.

Journal of Clinical Medicine, Journal Year: 2020, Volume and Issue: 9(6), P. 1713 - 1713

Published: June 3, 2020

Diabetes and Alzheimer’s disease are two highly prevalent diseases among the aging population have become major public health concerns in 21st century, with a significant risk to each other. Both of these increasingly recognized be multifactorial conditions. The terms “diabetes type 3” or “brain diabetes” been proposed recent years provide complete view potential common pathogenic mechanisms between diseases. While insulin resistance deficiency remains salient hallmarks diabetes, cognitive decline non-cognitive abnormalities such as impairments visuospatial function, attention, flexibility, psychomotor speed also present. Furthermore, amyloid aggregation deposition may drivers for diabetes pathology. Here, we offer brief appraisal social impact economic burden chronic insight into amyloidogenesis through considering advances amyloid-β aggregates on pathology islet polypeptide disease. Exploring detailed knowledge molecular interaction amyloidogenic proteins opens new opportunities therapies biomarker development.

Language: Английский

Citations

89
Design, synthesis, in-silico and biological evaluation of novel chalcone derivatives as multi-function agents for the treatment of Alzheimer's disease DOI
Zhipei Sang, Keren Wang, Pengfei Zhang

et al.

European Journal of Medicinal Chemistry, Journal Year: 2019, Volume and Issue: 180, P. 238 - 252

Published: July 12, 2019

Language: Английский

Citations

77
Anthocyanin as a therapeutic in Alzheimer’s disease: A systematic review of preclinical evidences DOI
Swathi Suresh, Rukaiah Fatma Begum,

Ankul Singh S

et al.

Ageing Research Reviews, Journal Year: 2022, Volume and Issue: 76, P. 101595 - 101595

Published: Feb. 23, 2022

Language: Английский

Citations

58
Adult hippocampal neurogenesis and its impairment in Alzheimer’s disease DOI Open Access
Thomas A. Kim,

Michelle D. Syty,

Kaitlyn Wu

et al.

动物学研究, Journal Year: 2022, Volume and Issue: 43(3), P. 481 - 496

Published: Jan. 1, 2022

Adult neurogenesis is the creation of new neurons which integrate into existing neural circuit adult brain. Recent evidence suggests that hippocampal (AHN) persists throughout life in mammals, including humans. These newborn have been implicated to a crucial role brain functions such as learning and memory. Importantly, studies also found impaired neurodegenerative neuropsychiatric diseases. Alzheimer's disease (AD) one most common forms dementia affecting millions people. Cognitive dysfunction symptom AD patients progressive memory loss has attributed degeneration hippocampus. Therefore, there growing interest identifying how affected AD. However, link between cognitive decline changes poorly understood. In this review, we summarized recent literature on AHN its impairments

Language: Английский

Citations

53
Genetic Phenotypes of Alzheimer’s Disease: Mechanisms and Potential Therapy DOI Creative Commons
Meina Quan, Shuman Cao, Qi Wang

et al.

Phenomics, Journal Year: 2023, Volume and Issue: 3(4), P. 333 - 349

Published: April 3, 2023

Abstract Years of intensive research has brought us extensive knowledge on the genetic and molecular factors involved in Alzheimer's disease (AD). In addition to mutations three main causative genes familial AD (FAD) including presenilins amyloid precursor protein genes, studies have identified several as most plausible for onset progression FAD, such triggering receptor expressed myeloid cells 2 , sortilin-related 1 adenosine triphosphate-binding cassette transporter subfamily A member 7 . The apolipoprotein E ε4 allele is reported be strongest risk factor sporadic (SAD), it also plays an important role FAD. Here, we reviewed recent developments that contributed understanding phenotypes FAD compared them with SAD. We further advancements gene therapy discussed future perspectives based phenotypes.

Language: Английский

Citations

34
Recent Advances in Targeting Transition Metals (Copper, Iron, and Zinc) in Alzheimer’s Disease DOI

Raghuraj Singh,

Archna Panghal,

Krishna Jadhav

et al.

Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 61(12), P. 10916 - 10940

Published: May 29, 2024

Language: Английский

Citations

11
Insights on the Use of Transgenic Mice Models in Alzheimer’s Disease Research DOI Open Access
Mafalda Soares Pádua, José Luis Guil‐Guerrero, José A. M. Prates

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(5), P. 2805 - 2805

Published: Feb. 28, 2024

Alzheimer’s disease (AD), the leading cause of dementia, presents a significant global health challenge with no known cure to date. Central our understanding AD pathogenesis is β-amyloid cascade hypothesis, which underlies drug research and discovery efforts. Despite extensive studies, animal models have completely validated this hypothesis. Effective are essential for accurately replicating key pathological features disease, notably formation plaques neurofibrillary tangles. These markers primarily driven by mutations in amyloid precursor protein (APP) presenilin 1 (PS1) genes familial (FAD) tau tangle pathology. Transgenic mice been instrumental research, heavily relying on overexpression mutated APP simulate conditions. However, these do not entirely replicate human condition AD. This review aims provide comprehensive evaluation historical ongoing efforts AD, particularly through use transgenic models. It focused benefits gathered from toxicity broader biological underpinnings Additionally, critically assesses application preclinical testing new therapeutic interventions, highlighting gap between clinical realities. analysis underscores need refinement methodologies bridge enhance translational value studies.

Language: Английский

Citations

10