The Dietary Sugars Intake: The Role In Alzheimer’s Disease Pathomechanism DOI Creative Commons

Rifka Wangiana Yulia Putri,

Dwi Pratika Anjarwati,

Damar Mashkhun Rizqi

и другие.

Clinical and Research Journal in Internal Medicine, Год журнала: 2023, Номер 4(1), С. 404 - 417

Опубликована: Май 25, 2023

Alzheimer’s disease is a common neurodegenerative that affect elderly and it became serious global burden for years. Despite many studies have been performed, an effective cure was still not be found. Therefore, necessary to only focus on curative methods but also preventive with modifiable risk factors underlying disease, example lifestyle metabolic as potential approach in prevention the future. The excessive dietary sugar intake has suggested factor of diseases such cognitive impairment disease. It may promote declines through some pathways induce alteration gut microbiomes, metabolism immune system. These abnormal processes evoke amyloid β plaque formation neurofibrillary tangles brain cells effect chronic inflammation. Chronic inflammation widely studied hallmark pathology. correlation between cognitive, specifically will summarized.

Язык: Английский

REM Sleep Loss-Induced Elevated Noradrenaline Plays a Significant Role in Neurodegeneration: Synthesis of Findings to Propose a Possible Mechanism of Action from Molecule to Patho-Physiological Changes DOI Creative Commons

Shatrunjai Giri,

Rachna Mehta, Birendra Nath Mallick

и другие.

Brain Sciences, Год журнала: 2023, Номер 14(1), С. 8 - 8

Опубликована: Дек. 21, 2023

Wear and tear are natural processes for all living non-living bodies. All cells organisms metabolically active to generate energy their routine needs, including survival. In the process, exposed oxidative load, metabolic waste, bye-products. an organ, non-neuronal divide replenish lost or damaged cells; however, as neuronal normally do not divide, they need special feature(s) protection, survival, sustenance normal functioning of brain. The neurons grow branch axons dendrites, which contribute formation synapses with near far neurons, basic scaffold complex brain functions. It is necessary that one more instinct physiological process(es) (functions) likely protection maintenance synapses. known rapid eye movement sleep (REMS), autonomic behavior, maintains learning memory its loss causes dysfunctions. this review we correlate role REMS in synaptogenesis, consolidation, degeneration. Further, a mechanism action, will show noradrenaline (NA) at low level, protects from damage growth synaptogenesis. However, upon loss, level NA increases, withdraws apoptosis neurons. We propose latter possibly associated neurodegenerative diseases symptoms.

Язык: Английский

Процитировано

3

Molecular and functional alterations in the cerebral microvasculature in an optimized mouse model of sepsis-associated cognitive dysfunction. DOI Open Access
Paulo Ávila‐Gómez, Yuto Shingai, Sabyasachi Dash

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Июнь 1, 2024

Systemic inflammation has been implicated in the development and progression of neurodegenerative conditions such as cognitive impairment dementia. Recent clinical studies indicate an association between sepsis, endothelial dysfunction, decline. However, investigations role therapeutic potential cerebral microvasculature systemic inflammation-induced dysfunction have limited by lack standardized experimental models for evaluating alterations cognition induced inflammatory response. Herein, we validated a mouse model endotoxemia that recapitulates key pathophysiology related to sepsis-induced including induction acute hyperinflammatory response, blood-brain barrier (BBB) leakage, neurovascular inflammation, memory after recovery from In phase, identified novel molecular (e.g. upregulation plasmalemma vesicle associated protein, driver permeability, pro-coagulant plasminogen activator inhibitor-1, PAI-1) functional perturbations (i.e., albumin small molecule BBB leakage) along with neuroinflammation. Remarkably, elevated levels PAI-1, intra/perivascular fibrin/fibrinogen deposition microglial activation persisted 1 month sepsis. We also highlight neuronal relevance following changes neurofilament phosphorylation decreases postsynaptic density protein 95 brain-derived neurotrophic factor suggesting diffuse axonal injury, synapse degeneration impaired neurotrophism. Our study serves support future mechanistic sepsis-associated identify targets this devastating condition.

Язык: Английский

Процитировано

0

Benincasa Hispida Reversed D-galactose-induced oxidative Stress And Neurodegeneration-Mediated Cognitive Impairment In Aged Rats. DOI Creative Commons
Pooja RC,

Bharathi Dr

Research Square (Research Square), Год журнала: 2023, Номер unknown

Опубликована: Сен. 27, 2023

Abstract Introduction: Age-related cognitive impairment is a common issue that frequently brought on by oxidative stress and neurodegeneration in the brain. D-gal sugar moiety has been linked to aging disorders. This disease's prevalence expected rise linearly 2050. Material & methods: Benincasa hispida , commonly known as wax gourd or winter melon, widely consumed vegetable with various medicinal properties. it belongs family of Cucurbitaceae. study evaluates neuroprotective role hydro-ethanolic seed extract (BH) against D-gal-induced rats. Healthy male rats were divided into six groups: The control group received normal saline, donepezil (2 mg/kg b.w.t., i.p.); (300 +BH (150 o.p.); BH (250 b.wt. Results discussion: Behavioural, brain biochemical, histopathological changes assessed after treatment. results behavioral depicted significantly reduces spontaneous alternation locomotor activity, indicating impairment. Biochemical studies showed increases rat brains. Histopathological disturbs architecture hippocampal cortical cells, degeneration these areas. co-treatment for 42 days attenuated behavioral, neuroanatomic damages caused D-gal; markedly suppressed AChE activity maintained cellular Conclusion: Thus, this shows can protect from adverse effects (e.g., memory loss impairment) modulating stress.

Язык: Английский

Процитировано

1

Age-dependent dysregulation of locus coeruleus firing in a transgenic rat model of Alzheimer’s disease DOI Creative Commons
Michael A. Kelberman, Jacki M. Rorabaugh,

Claire R. Anderson

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2022, Номер unknown

Опубликована: Ноя. 15, 2022

Abstract Accumulation of hyperphosphorylated tau in the locus coeruleus (LC) is a ubiquitous feature prodromal Alzheimer’s disease (AD), and LC neurons degenerate as AD progresses. Tau-mediated dysfunction may contribute to early neuropsychiatric symptoms, while loss integrity associated with conversion cognitive impairment. Hyperphosphorylated alters firing rates other brain regions, but its effects on have not been described. The purpose this study was characterize changes properties when they are only cells containing tau, well later β-amyloid (Aβ) pathology abundant forebrain. Single unit activity recorded from anesthetized wild-type (WT) TgF344-AD rats, which carry APP/PS1 transgene. Similar human AD, these rats develop (at 6 months) prior Aβ or forebrain regions 12-15 months). At baseline, were hypoactive at both ages compared WT littermates, showed elevated spontaneous bursting properties, particularly younger animals. Differences footshock-evoked depended age, 6-month demonstrating aspects hyperactivity, aged transgenic showing hypoactivity relative WT. Tau-induced alterations pathophysiology hyperactivity followed by contributing These results support further investigation into stage-dependent noradrenergic interventions for AD. Highlights Recorded rat model (AD) endogenous akin 6- 15-month had reduced tonic hyperactive response footshock neuron symptoms

Язык: Английский

Процитировано

1

The Dietary Sugars Intake: The Role In Alzheimer’s Disease Pathomechanism DOI Creative Commons

Rifka Wangiana Yulia Putri,

Dwi Pratika Anjarwati,

Damar Mashkhun Rizqi

и другие.

Clinical and Research Journal in Internal Medicine, Год журнала: 2023, Номер 4(1), С. 404 - 417

Опубликована: Май 25, 2023

Alzheimer’s disease is a common neurodegenerative that affect elderly and it became serious global burden for years. Despite many studies have been performed, an effective cure was still not be found. Therefore, necessary to only focus on curative methods but also preventive with modifiable risk factors underlying disease, example lifestyle metabolic as potential approach in prevention the future. The excessive dietary sugar intake has suggested factor of diseases such cognitive impairment disease. It may promote declines through some pathways induce alteration gut microbiomes, metabolism immune system. These abnormal processes evoke amyloid β plaque formation neurofibrillary tangles brain cells effect chronic inflammation. Chronic inflammation widely studied hallmark pathology. correlation between cognitive, specifically will summarized.

Язык: Английский

Процитировано

0