The Role of Mitochondrial Dysfunction in Alzheimer’s: Molecular Defects and Mitophagy-Enhancing Approaches DOI Creative Commons
Reem M. Farsi

Life, Год журнала: 2023, Номер 13(4), С. 970 - 970

Опубликована: Апрель 8, 2023

Alzheimer’s disease (AD), a progressive and chronic neurodegenerative syndrome, is categorized by cognitive memory damage caused the aggregations of abnormal proteins, specifically including Tau proteins β-amyloid in brain tissue. Moreover, mitochondrial dysfunctions are principal causes AD, which associated with mitophagy impairment. Investigations exploring pharmacological therapies alongside AD have explicitly concentrated on molecules accomplished preventing/abolishing gatherings abovementioned mitochondria damages. Mitophagy removal dead autophagy process. Damages mitophagy, manner diversified degeneracy resulting an ongoing aggregation malfunctioning mitochondria, were also suggested to support AD. Recently, plentiful reports link between defective This treaty highlights updated outlines modern innovations developments machinery brains. therapeutic nanotherapeutic strategies targeting dysfunction presented this review. Based significant role diminished we suggest that application different approaches aimed at stimulating would be beneficial for or reducing induced

Язык: Английский

Rlip overexpression reduces oxidative stress and mitochondrial dysfunction in Alzheimer's disease: Mechanistic insights DOI Creative Commons
P. Hemachandra Reddy, Sudhir Kshirsagar, Chhanda Bose

и другие.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Год журнала: 2023, Номер 1869(7), С. 166759 - 166759

Опубликована: Май 22, 2023

Язык: Английский

Процитировано

7

Non-canonical pathways associated to Amyloid beta and tau protein dyshomeostasis in Alzheimer’s disease: A narrative review DOI Creative Commons

Anna Maggiore,

Valentina Latina, Maria D’Erme

и другие.

Ageing Research Reviews, Год журнала: 2024, Номер 102, С. 102578 - 102578

Опубликована: Ноя. 13, 2024

Alzheimer's Disease (AD) is the most common form of dementia among elderly people. This disease imposes a significant burden on healthcare system, society, and economy due to increasing global aging population. Current trials with drugs or bioactive compounds aimed at reducing cerebral Amyloid beta (Aβ) plaques tau protein neurofibrillary tangles, which are two main hallmarks this devastating neurodegenerative disease, have not provided results in terms their neuropathological outcomes nor met expected clinical end-points. Ageing, genetic environmental risk factors, along different symptoms suggest that AD complex heterogeneous disorder multiple interconnected pathological pathways rather than single entity. In present review, we highlight discuss various non-canonical, Aβ-independent mechanisms, like gliosis, unhealthy dietary intake, lipid sugar signaling, cerebrovascular damage contribute onset development AD. We emphasize challenging traditional "amyloid cascade hypothesis" may improve our understanding age-related syndrome help fight progressive cognitive decline

Язык: Английский

Процитировано

2

Alzheimer’s Disease and Alzheimer’s Disease-Related Dementias in African Americans: Focus on Caregivers DOI Open Access
Jonathan Kopel, Ujala Sehar,

Moumita Choudhury

и другие.

Healthcare, Год журнала: 2023, Номер 11(6), С. 868 - 868

Опубликована: Март 16, 2023

Alzheimer’s disease (AD) and Disease-Related Dementias (ADRD) are chronic illnesses that highly prevalent in African Americans (AA). AD ADRD caused by multiple factors, such as genetic mutations, modifiable non-modifiable risk lifestyle. Histopathological, morphological, cellular studies revealed how changes implicated ADRD, including synaptic damage, inflammatory responses, hormonal imbalance, mitochondrial abnormalities, neuronal loss, addition to the accumulation of amyloid beta phosphorylated tau brain. The contributions race, ethnicity, location socioeconomic status all have a significant impact on care support services available dementia patients. Furthermore, disparities health entangled with social, economic, environmental variables perpetuate disadvantages among different groups, particularly Americans. As such, it remains important understand various racial ethnic groups perceive, access, experience care. Considering mounting data shows AA may be more susceptible than white people, demographic transition creates hurdles providing adequate from family caregivers. there is growing recognition pose stress caregivers compared people. In this review, we examine current literature concerning

Язык: Английский

Процитировано

5

Caffeine improves mitochondrial dysfunction in the white matter of neonatal rats with hypoxia-ischemia through deacetylation: a proteomic analysis of lysine acetylation DOI Creative Commons
Yajun Zhang, Yuqian Wang,

Haiping Dou

и другие.

Frontiers in Molecular Neuroscience, Год журнала: 2024, Номер 17

Опубликована: Апрель 30, 2024

Aims White matter damage (WMD) is linked to both cerebral palsy and cognitive deficits in infants born prematurely. The focus of this study was examine how caffeine influences the acetylation proteins within neonatal white evaluate its effectiveness treating caused by hypoxia-ischemia. Main methods We employed a method combining affinity enrichment with advanced liquid chromatography mass spectrometry profile from rats grouped into control (Sham), hypoxic-ischemic (HI), caffeine-treated (Caffeine) groups. Key findings Our included 1,999 sites lysine across 1,123 proteins, quantifiable changes noted 1,342 689 proteins. Analysis these patterns identified recurring sequences adjacent sites, notably YKacN, FkacN, G * GkacS. Investigation biological roles through Gene Ontology analysis indicated their involvement variety cellular processes, predominantly mitochondrial locations. Further that tau (Mapt), protein associated microtubules, elevated HI condition; however, treatment appeared mitigate over-modification, thus potentially aiding reducing oxidative stress, inflammation nervous system, improving health. Caffeine inhibited acetylated Mapt sirtuin 2 (SITR2), promoted nuclear translocation, improved dysfunction, which subsequently weakened SIRT2 inhibitor, AK-7. Significance Caffeine-induced may play key role dysfunction inhibiting stress neuroinflammation.

Язык: Английский

Процитировано

1

The Role of Mitochondrial Dysfunction in Alzheimer’s: Molecular Defects and Mitophagy-Enhancing Approaches DOI Creative Commons
Reem M. Farsi

Life, Год журнала: 2023, Номер 13(4), С. 970 - 970

Опубликована: Апрель 8, 2023

Alzheimer’s disease (AD), a progressive and chronic neurodegenerative syndrome, is categorized by cognitive memory damage caused the aggregations of abnormal proteins, specifically including Tau proteins β-amyloid in brain tissue. Moreover, mitochondrial dysfunctions are principal causes AD, which associated with mitophagy impairment. Investigations exploring pharmacological therapies alongside AD have explicitly concentrated on molecules accomplished preventing/abolishing gatherings abovementioned mitochondria damages. Mitophagy removal dead autophagy process. Damages mitophagy, manner diversified degeneracy resulting an ongoing aggregation malfunctioning mitochondria, were also suggested to support AD. Recently, plentiful reports link between defective This treaty highlights updated outlines modern innovations developments machinery brains. therapeutic nanotherapeutic strategies targeting dysfunction presented this review. Based significant role diminished we suggest that application different approaches aimed at stimulating would be beneficial for or reducing induced

Язык: Английский

Процитировано

3