On Possible Relationships between Alzheimer’s Disease, Age-Related Memory Loss and the Development of Animal Models

1987 ◽  
pp. 129-139 ◽  
Author(s):  
Raymond T. Bartus ◽  
R. L. Dean
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Memory Loss ◽  
Age Related

Clinical course of Alzheimer’s disease

2011 ◽  
Author(s):  
Alberto Lleo ◽  
Rafael Blesa
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Daily Living ◽  
Clinical Course ◽  
Neurodegenerative Disorder ◽  
Memory Loss ◽  
Remote Memory ◽  
Initial Symptom ◽  
Delayed Recall ◽  
Age Related

• Alzheimer’s disease is an age-related neurodegenerative disorder, with onset usually in late life, characterized by cognitive impairment, a variety of behavioural symptoms, and restrictions in the activities of daily living• The initial symptom is episodic memory loss, in particular in delayed recall of visual and/or verbal material. Immediate and remote memory is usually preserved in early stages...

Age-Associated Memory Loss: Initial Neuropsychological and Cerebral Metabolic Findings of a Longitudinal Study

1994 ◽  
Vol 6 (1) ◽  
pp. 23-44 ◽  
Author(s):  
Gary W. Small ◽  
Anna Okonek ◽  
Mark A. Mandelkern ◽  
Asenath La Rue ◽  
Linda Chang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Longitudinal Study ◽  
Cognitive Abilities ◽  
Mood State ◽  
Familial Risk ◽  
Memory Loss ◽  
Subjective Memory ◽  
Age Related ◽  
Positron Emission

To determine the relationships between clinical and brain function in persons with a familial risk for Alzheimer's disease, the authors assessed subjective and objective cognitive abilities, mood state, and cerebral glucose metabolism (using positron emission tomography) in 43 persons with age-associated memory impairment, with and without first-degree relatives with a clinical diagnosis of Alzheimer's disease. Subjective complaints of memory loss, mood state ratings, and objective memory measures were similar in persons with a family history of Alzheimer's disease (n = 29) compared to those without such a history (n = 14). Metabolic ratios in the frontal regions correlated with a decrease in a specific type of subjective memory complaint (mnemonics usage; p < .001) and some mood state ratings. These results indicate that parietal and temporal hypometabolism is not evident in persons with mild age-related memory complaints, even when such subjects have a familial risk for Alzheimer's disease. Moreover, self-reports of mnemonics usage may be sensitive indicators of decreased frontal lobe function. Longitudinal study will determine whether such clinical and metabolic measures will predict eventual disease progression.

scholarly journals Overview of Alzheimer’s Disease and Some Therapeutic Approaches Targeting Aβby Using Several Synthetic and Herbal Compounds

2016 ◽  
Vol 2016 ◽  
pp. 1-22 ◽  
Author(s):  
Sandeep Kumar Singh ◽  
Saurabh Srivastav ◽  
Amarish Kumar Yadav ◽  
Saripella Srikrishna ◽  
George Perry
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Neurodegenerative Disease ◽  
Therapeutic Approaches ◽  
Age Related

Alzheimer’s disease (AD) is a complex age-related neurodegenerative disease. In this review, we carefully detail amyloid-βmetabolism and its role in AD. We also consider the various genetic animal models used to evaluate therapeutics. Finally, we consider the role of synthetic and plant-based compounds in therapeutics.

Optimizing Modifiable and Lifestyle-related Factors in the Prevention of Dementia Disorders with Special Reference to Alzheimer, Parkinson and Autism Diseases

2020 ◽  
Vol 16 (6) ◽  
pp. 900-911
Author(s):  
Umesh C. Gupta ◽  
Subhas C. Gupta
Keyword(s):  
Physical Activity ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Environmental Pollutants ◽  
Memory Loss ◽  
Tau Proteins ◽  
Body Parts ◽  
Related Factors ◽  
Age Related ◽  
Major Factors

Dementia is a syndrome and an umbrella term that encompasses Alzheimer, Parkinson and autism diseases. These diseases are by far the most common cause of dementia; therefore this investigation will chiefly include these disorders, with a limited discussion of few other disorders related to dementia. Alzheimer’s disease (AD) is characterized by the accumulation of cerebral β-amyloid plaques, tau proteins and memory loss; Parkinson by the deterioration of brain cells which regulate the movement of body parts and produce dopamine; and autism by abnormalities of social disorder and difficulty in communicating and forming relationships. Alzheimer’s disease and cognitive impairment in dementia are age-related and manageable only with early diagnosis and prevention. Data based on several decades of research has shown that the major factors responsible for the induction of inflammation in dementia and many chronic diseases are infections, obesity, alcohol, radiation, environmental pollutants, improper nutrition, lack of physical activity, depression, anxiety, genetic factors, and sleep deprivation. There are some studied preventive measures for dementia including continued physical activity and consuming predominantly a plant-based Mediterranean diet comprising olive oil and foods containing flavonoids and other phytochemicals having strong antioxidant and anti-inflammatory properties and along with management of chronic conditions.

scholarly journals Microglia in Aging and Alzheimer’s Disease: A Comparative Species Review

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1138
Author(s):  
Melissa K. Edler ◽  
Isha Mhatre-Winters ◽  
Jason R. Richardson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Single Species ◽  
Functional Behavior ◽  
Age Related ◽  
Rapid Changes ◽  
The Central Nervous System ◽  
Oxidative Species ◽  
Selection Of

Microglia are the primary immune cells of the central nervous system that help nourish and support neurons, clear debris, and respond to foreign stimuli. Greatly impacted by their environment, microglia go through rapid changes in cell shape, gene expression, and functional behavior during states of infection, trauma, and neurodegeneration. Aging also has a profound effect on microglia, leading to chronic inflammation and an increase in the brain’s susceptibility to neurodegenerative processes that occur in Alzheimer’s disease. Despite the scientific community’s growing knowledge in the field of neuroinflammation, the overall success rate of drug treatment for age-related and neurodegenerative diseases remains incredibly low. Potential reasons for the lack of translation from animal models to the clinic include the use of a single species model, an assumption of similarity in humans, and ignoring contradictory data or information from other species. To aid in the selection of validated and predictive animal models and to bridge the translational gap, this review evaluates similarities and differences among species in microglial activation and density, morphology and phenotype, cytokine expression, phagocytosis, and production of oxidative species in aging and Alzheimer’s disease.

scholarly journals Potential Roles of Sestrin2 in Alzheimer’s Disease: Antioxidation, Autophagy Promotion, and Beyond

Biomedicines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1308
Author(s):  
Shang-Der Chen ◽  
Jenq-Lin Yang ◽  
Yi-Heng Hsieh ◽  
Tsu-Kung Lin ◽  
Yi-Chun Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Diseases ◽  
Memory Loss ◽  
Oxygen Species ◽  
Mechanistic Target Of Rapamycin ◽  
Cell Cycle Reentry ◽  
Age Related ◽  
Reduce Activity

Alzheimer's disease (AD) is the most common age-related neurodegenerative disease. It presents with progressive memory loss, worsens cognitive functions to the point of disability, and causes heavy socioeconomic burdens to patients, their families, and society as a whole. The underlying pathogenic mechanisms of AD are complex and may involve excitotoxicity, excessive generation of reactive oxygen species (ROS), aberrant cell cycle reentry, impaired mitochondrial function, and DNA damage. Up to now, there is no effective treatment available for AD, and it is therefore urgent to develop an effective therapeutic regimen for this devastating disease. Sestrin2, belonging to the sestrin family, can counteract oxidative stress, reduce activity of the mammalian/mechanistic target of rapamycin (mTOR), and improve cell survival. It may therefore play a crucial role in neurodegenerative diseases like AD. However, only limited studies of sestrin2 and AD have been conducted up to now. In this article, we discuss current experimental evidence to demonstrate the potential roles of sestrin2 in treating neurodegenerative diseases, focusing specifically on AD. Strategies for augmenting sestrin2 expression may strengthen neurons, adapting them to stressful conditions through counteracting oxidative stress, and may also adjust the autophagy process, these two effects together conferring neuronal resistance in cases of AD.

Mechanisms of memory loss in Aβ and tau mouse models

2005 ◽  
Vol 33 (4) ◽  
pp. 591-594 ◽  
Author(s):  
K.H. Ashe
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Mouse Models ◽  
Molecular Mechanisms ◽  
Cultured Cells ◽  
Memory Loss ◽  
Amyloid Β ◽  
Aβ Amyloid ◽  
Mechanisms Of Memory

Although memory loss is the central symptom of Alzheimer's disease, the pathophysiological mechanisms leading to dementia are poorly understood. It is difficult to answer this issue with studies in humans and impossible in cultured cells. Therefore animal models are needed to elucidate the molecular mechanisms leading to dementia. The chief neuropathological changes during Alzheimer's disease, namely neurofibrillary tangles and amyloid plaques, have helped us to determine which molecules to focus upon in the animal models, specifically Aβ (amyloid β) and tau. This paper presents my perspective on what we have learnt about mechanisms of memory loss from Aβ and tau mouse models of Alzheimer's disease.

scholarly journals Large Artery Stiffness and Brain Health: Insights from Animal Models

2020 ◽  
Author(s):  
Nicholas R Winder ◽  
Emily H Reeve ◽  
Ashley E Walker
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Brain Aging ◽  
Large Artery ◽  
Neurocognitive Dysfunction ◽  
Disease Etiology ◽  
Age Related ◽  
Artery Stiffness ◽  
Underlying Mechanisms

There are no effective treatments available to halt or reverse the progression of age-related cognitive decline and Alzheimer's disease. Thus, there is an urgent need to understand the underlying mechanisms of disease etiology and progression in order to identify novel therapeutic targets. Age-related changes to vasculature, particularly increases in stiffness of the large elastic arteries, are now recognized as important contributors to brain aging. There is a growing body of evidence for an association between greater large artery stiffness and cognitive impairment among both healthy older adults and patients with Alzheimer's disease. However, studies in humans are limited to only correlative evidence while animal models allow researchers to explore the causative mechanisms linking arterial stiffness to neurocognitive dysfunction and disease. Recently, several rodent models of direct modulation of large artery stiffness and the consequent effects on the brain have been reported. Common outcomes among these models have emerged, including evidence that greater large artery stiffness causes cerebrovascular dysfunction associated with increased oxidative stress and inflammatory signaling. The purpose of this mini review is to highlight recent findings associating large artery stiffness with deleterious brain outcomes, with a specific focus on causative evidence obtained from animal models. We will also discuss the gaps in knowledge that remain in our understanding of how large artery stiffness affects brain function and disease outcomes.

scholarly journals Effects of Reactive Oxygen and Nitrogen Species on TrkA Expression and Signalling: Implications for proNGF in Aging and Alzheimer’s Disease

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1983
Author(s):  
Erika Kropf ◽  
Margaret Fahnestock
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Basal Forebrain ◽  
Memory Loss ◽  
Reactive Oxygen ◽  
Neurotrophin Receptor ◽  
Nitrogen Species ◽  
Age Related ◽  
The Brain

Nerve growth factor (NGF) and its precursor form, proNGF, are critical for neuronal survival and cognitive function. In the brain, proNGF is the only detectable form of NGF. Dysregulation of proNGF in the brain is implicated in age-related memory loss and Alzheimer’s disease (AD). AD is characterized by early and progressive degeneration of the basal forebrain, an area critical for learning, memory, and attention. Learning and memory deficits in AD are associated with loss of proNGF survival signalling and impaired retrograde transport of proNGF to the basal forebrain. ProNGF transport and signalling may be impaired by the increased reactive oxygen and nitrogen species (ROS/RNS) observed in the aged and AD brain. The current literature suggests that ROS/RNS nitrate proNGF and reduce the expression of the proNGF receptor tropomyosin-related kinase A (TrkA), disrupting its downstream survival signalling. ROS/RNS-induced reductions in TrkA expression reduce cell viability, as proNGF loses its neurotrophic function in the absence of TrkA and instead generates apoptotic signalling via the pan-neurotrophin receptor p75NTR. ROS/RNS also interfere with kinesin and dynein motor functions, causing transport deficits. ROS/RNS-induced deficits in microtubule motor function and TrkA expression and signalling may contribute to the vulnerability of the basal forebrain in AD. Antioxidant treatments may be beneficial in restoring proNGF signalling and axonal transport and reducing basal forebrain neurodegeneration and related deficits in cognitive function.

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