scholarly journals Principles of age-related changes in the canine and feline brain

2014 ◽  
Vol 64 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Nikolaos Papaioannou
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Function ◽  
Morphological Characteristics ◽  
Individual Variability ◽  
Brain Lesions ◽  
Therapeutic Interventions ◽  
Age Related ◽  
Cat Brain ◽  
Aged Dog

Abstract In the aged dog and cat, especially dog, a cognitive decline develops naturally in many different domains, but at the same time it also exhibits human-like individual variability in the aging process. In the aging dog and cat brain lesions develop spontaneously. Dogs share some morphological characteristics with those of Alzheimer’s disease in man. The canine brain with its plaques and tangles which show oxidative changes, forms a spontaneous model for understanding the early changes and their interrelationships in Alzheimer’s disease. Additionally, the aged dog represents a useful model for the development of preventive or therapeutic interventions to improve aged brain function. These interventions can then be translated into human clinical trials.

Types of Age-Related Brain Lesions and Relationship to Neuropathologic Diagnostic Systems of Alzheimer's Disease

2001 ◽  
pp. 65-76 ◽  
Author(s):  
Panteleimon Giannakopoulos ◽  
Enikö Kövari ◽  
Gabriel Gold ◽  
Patrick R. Hof ◽  
Constantin Bouras
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Lesions ◽  
Diagnostic Systems ◽  
Age Related

scholarly journals Microglia in Alzheimer’s Disease: A Target for Therapeutic Intervention

2021 ◽  
Vol 15 ◽  
Author(s):  
Guimei Zhang ◽  
Zicheng Wang ◽  
Huiling Hu ◽  
Meng Zhao ◽  
Li Sun
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Therapeutic Interventions ◽  
Tau Pathology ◽  
Age Related ◽  
Amyloid Accumulation ◽  
Pathophysiological Role ◽  
Inflammatory Drugs ◽  
Β Amyloid

Alzheimer’s disease (AD) is one of the most common types of age-related dementia worldwide. In addition to extracellular amyloid plaques and intracellular neurofibrillary tangles, dysregulated microglia also play deleterious roles in the AD pathogenesis. Numerous studies have demonstrated that unbridled microglial activity induces a chronic neuroinflammatory environment, promotes β-amyloid accumulation and tau pathology, and impairs microglia-associated mitophagy. Thus, targeting microglia may pave the way for new therapeutic interventions. This review provides a thorough overview of the pathophysiological role of the microglia in AD and illustrates the potential avenues for microglia-targeted therapies, including microglial modification, immunoreceptors, and anti-inflammatory drugs.

scholarly journals THE INTERRELATIONSHIP BETWEEN INSULIN-LIKE GROWTH FACTOR 1, APOLIPOPROTEIN E Ε4, LIFESTYLE FACTORS, AND THE AGING BODY AND BRAIN

2020 ◽  
pp. 1-9
Author(s):  
S.A. Galle ◽  
I.K. Geraedts ◽  
J.B. Deijen ◽  
M.V. Milders ◽  
M.L. Drent
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Growth Factor ◽  
Apolipoprotein E ◽  
Cognitive Functioning ◽  
Brain Function ◽  
Healthy Aging ◽  
Insulin Like Growth Factor ◽  
Age Related ◽  
The Impact

Aging is associated with a decrease in body and brain function and with a decline in insulin-like growth factor 1 levels. The observed associations between alterations in insulin-like growth factor 1 levels and cognitive functioning and Mild Cognitive Impairment suggest that altered insulin-like growth factor 1 signaling may accompany Alzheimer’s disease or is involved in the pathogenesis of the disease. Recent animal research has suggested a possible association between insulin-like growth factor 1 levels and the Apolipoprotein E ε4 allele, a genetic predisposition to Alzheimer’s disease. It is therefore hypothesized that a reduction in insulin-like growth factor 1 signaling may moderate the vulnerability to Alzheimer’s disease of human Apolipoprotein E ε4 carriers. We address the impact of age-related decline of insulin-like growth factor 1 levels on physical and brain function in healthy aging and Alzheimer’s disease and discuss the links between insulin-like growth factor 1 and the Apolipoprotein E ε4 polymorphism. Furthermore, we discuss lifestyle interventions that may increase insulin-like growth factor 1 serum levels, including physical activity and adherence to a protein rich diet and the possible benefits to the physical fitness and cognitive functioning of the aging population.

scholarly journals Alzheimer’s disease and the genetics of neuroprotection

2020 ◽  
Author(s):  
Tyler Johnson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Underlying Mechanism ◽  
Therapeutic Interventions ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Pathogenic Variants ◽  
Age Related ◽  
Β Amyloid ◽  
Reduced Risk

As the world’s leading form of age-related dementia, Alzheimer’s disease (AD) is a devastating neurological disorder associated with severe emotional and economic burdens. Despite years of research, the underlying mechanism behind this disease remains unclear. The current prevailing theory relies on the deposition of toxic amyloid beta (Aβ), which promotes the formation of phosphorylated tau tangles, and together these damaging changes drive the loss of neurons. Much of AD development can be attributed to genetic influences, including pathogenic variants of β-amyloid precursor protein, presenilins 1 and 2, and the presence of apolipoprotein 4. However, there are other subtle, yet significant variations within our genome that contribute to protecting us against AD. Variants of the phospholipase Cγ2 and toll-like receptor 4 genes have been associated with reduced risk of developing AD, as well as increased longevity of patients. These neuroprotective variants can guide the development of future therapeutic interventions for AD, as current strategies have proven lackluster.

scholarly journals Neuropathology of Aging in Cats and its Similarities to Human Alzheimer’s Disease

2021 ◽  
Vol 2 ◽  
Author(s):  
Lorena Sordo ◽  
Alessandra C. Martini ◽  
E. Fiona Houston ◽  
Elizabeth Head ◽  
Danièlle Gunn-Moore
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Early Stage ◽  
Senile Plaques ◽  
Brain Regions ◽  
Hyperphosphorylated Tau ◽  
Age Related ◽  
Cat Brain ◽  
Amyloid Aβ ◽  
Intraneuronal Aβ

Elderly cats develop age-related behavioral and neuropathological changes that ultimately lead to cognitive dysfunction syndrome (CDS). These neuropathologies share similarities to those seen in the brains of humans with Alzheimer’s disease (AD), including the extracellular accumulation of ß-amyloid (Aβ) and intraneuronal deposits of hyperphosphorylated tau, which are considered to be the two major hallmarks of AD. The present study assessed the presence and distribution of Aβ and tau hyperphosphorylation within the cat brain (n = 55 cats), and how the distribution of these proteins changes with age and the presence of CDS. For this, immunohistochemistry was performed on seven brain regions from cats of various ages, with and without CDS (n = 10 with CDS). Cats accumulate both intracytoplasmic and extracellular deposits of Aβ, as well as intranuclear and intracytoplasmic hyperphosphorylated tau deposits. Large extracellular aggregates of Aβ were found in elderly cats, mainly in the cortical brain areas, with occasional hippocampal aggregates. This may suggest that these aggregates start in cortical areas and later progress to the hippocampus. While Aβ senile plaques in people with AD have a dense core, extracellular Aβ deposits in cats exhibited a diffuse pattern, similar to the early stages of plaque pathogenesis. Intraneuronal Aβ deposits were also observed, occurring predominantly in cortical brain regions of younger cats, while older cats had few to no intraneuronal Aβ deposits, especially when extracellular aggregates were abundant. Intracytoplasmic hyperphosphorylated tau was found within neurons in the brains of elderly cats, particularly in those with CDS. Due to their ultrastructural features, these deposits are considered to be pre-tangles, which are an early stage of the neurofibrillary tangles seen in AD. The largest numbers of pre-tangles are found mainly in the cerebral cortex of elderly cats, whereas lower numbers were found in other regions (i.e., entorhinal cortex and hippocampus). For the first time, intranuclear tau was found in both phosphorylated and non-phosphorylated states within neurons in the cat brain. The highest numbers of intranuclear deposits were found in the cortex of younger cats, and this tended to decrease with age. In contrast, elderly cats with pre-tangles had only occasional or no nuclear labelling.

scholarly journals THE ROLE OF METABOLIC SYNDROME IN THE ALZHEIMER’S DISEASE

2021 ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Alzheimer's Disease ◽  
Metabolic Syndrome ◽  
Therapeutic Interventions ◽  
The Metabolic Syndrome ◽  
Age Related ◽  
Therapeutic Measures ◽  
Β Amyloid

INTRODUCTION Alzheimer’s disease (AD) is characterized by progressive cognitive loss coupled with age-related functional impairment. Its two major brands are β-amyloid plaques and neurofibrillary tangles. There is strong evidence for a relationship between Metabolic Syndrome (MS) and AD. Both pathologies are quite prevalent and dependent on aging. OBJECTIVE The present study seeks to understand the role of the metabolic syndrome in the pathophysiology of Alzheimer’s disease and to describe preventive and therapeutic interventions. METHODOLOGY The review was made based on the search for scientific articles in the electronic databases PUBMED and Web of Science, using the descriptors “Alzheimer’s Disease”, “Metabolic Syndrome” DISCUSSION MS is a metabolic breakdown with the potential to damage insulin signaling in the brain, causing insulin resistance, inhibiting β-amyloid clearance and its accumulation, which generates neuroinflammation. In addition, it induces a prothrombotic state with ischemic effects, resulting in oxidative stress and neuroinflammation and progressive local brain atrophies. The components of the metabolic syndrome are related to AD, exacerbating neuroinflammation and insulin resistance. Preventive and therapeutic measures aiming at the MS are promising. CONCLUSION From the analyzes developed in this study, different relationships between the components of MS and AD are perceived, the first being possible causes and / or effects of the second. Since insulin resistance plays a major role in the initiation and perpetuation of cognitive impairment in AD. Furthermore, the components of MS associated with AD, when treated with preventive and therapeutic measures, break this association by promoting rebalancing of the metabolism.

Therapeutic Interventions for the Suppression of Alzheimer’s Disease: Quest for a Remedy

2015 ◽  
Vol 16 (5) ◽  
pp. 346-353 ◽  
Author(s):  
Naveed Fazili ◽  
Aabgeena Naeem ◽  
Ghulam Ashraf ◽  
Siew Gan ◽  
Mohammad Kamal
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Therapeutic Interventions

Emerging Promise of Immunotherapy for Alzheimer’s Disease: A New Hope for the Development of Alzheimer’s Vaccine

2020 ◽  
Vol 20 (13) ◽  
pp. 1214-1234 ◽  
Author(s):  
Md. Tanvir Kabir ◽  
Md. Sahab Uddin ◽  
Bijo Mathew ◽  
Pankoj Kumar Das ◽  
Asma Perveen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Immune Response ◽  
Neutralizing Antibodies ◽  
Neurodegenerative Disorder ◽  
Symptomatic Relief ◽  
Aβ Oligomers ◽  
Th2 Immune Response ◽  
Age Related ◽  
Anti Inflammatory

Background: Alzheimer's disease (AD) is a chronic neurodegenerative disorder and the characteristics of this devastating disorder include the progressive and disabling deficits in the cognitive functions including reasoning, attention, judgment, comprehension, memory, and language. Objective: In this article, we have focused on the recent progress that has been achieved in the development of an effective AD vaccine. Summary: Currently, available treatment options of AD are limited to deliver short-term symptomatic relief only. A number of strategies targeting amyloid-beta (Aβ) have been developed in order to treat or prevent AD. In order to exert an effective immune response, an AD vaccine should contain adjuvants that can induce an effective anti-inflammatory T helper 2 (Th2) immune response. AD vaccines should also possess the immunogens which have the capacity to stimulate a protective immune response against various cytotoxic Aβ conformers. The induction of an effective vaccine’s immune response would necessitate the parallel delivery of immunogen to dendritic cells (DCs) and their priming to stimulate a Th2-polarized response. The aforesaid immune response is likely to mediate the generation of neutralizing antibodies against the neurotoxic Aβ oligomers (AβOs) and also anti-inflammatory cytokines, thus preventing the AD-related inflammation. Conclusion: Since there is an age-related decline in the immune functions, therefore vaccines are more likely to prevent AD instead of providing treatment. AD vaccines might be an effective and convenient approach to avoid the treatment-related huge expense.

scholarly journals Interactions between sleep disturbances and Alzheimer’s disease on brain function: a preliminary study combining the static and dynamic functional MRI

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kaicheng Li ◽  
Xiao Luo ◽  
Qingze Zeng ◽  
Yerfan Jiaerken ◽  
Shuyue Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Sleep Disturbance ◽  
Brain Function ◽  
Sleep Disturbances ◽  
Brain Activity ◽  
Vascular Risk Factor ◽  
Underlying Mechanism ◽  
Amyloid Pet

AbstractThough sleep disturbance constitutes the risk factor for Alzheimer’s disease (AD), the underlying mechanism is still unclear. This study aims to explore the interaction between sleep disturbances and AD on brain function. We included 192 normal controls, 111 mild cognitive impairment (MCI), and 30 AD patients, with either poor or normal sleep (PS, NS, respectively). To explore the strength and stability of brain activity, we used static amplitude of low-frequency fluctuation (sALFF) and dynamic ALFF (dALFF) variance. Further, we examined white matter hyperintensities (WMH) and amyloid PET deposition, representing the vascular risk factor and AD-related hallmark, respectively. We observed that sleep disturbance significantly interacted with disease severity, exposing distinct effects on sALFF and dALFF variance. Interestingly, PS groups showed the dALFF variance trajectory of initially increased, then decreased and finally increased along the AD spectrum, while showing the opposite trajectory of sALFF. Further correlation analysis showed that the WMH burden correlates with dALFF variance in PS groups. Conclusively, our study suggested that sleep disturbance interacts with AD severity, expressing as effects of compensatory in MCI and de-compensatory in AD, respectively. Further, vascular impairment might act as important pathogenesis underlying the interaction effect between sleep and AD.

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