Small molecule inhibitor DDQ-treated hippocampal neuronal cells show improved neurite outgrowth and synaptic branching DOI Creative Commons
Jangampalli Adi Pradeepkiran,

Priyanka Rawat,

Arubala P. Reddy

и другие.

Neural Regeneration Research, Год журнала: 2024, Номер 20(9), С. 2624 - 2632

Опубликована: Июнь 19, 2024

JOURNAL/nrgr/04.03/01300535-202509000-00024/figure1/v/2024-11-05T132919Z/r/image-tiff The process of neurite outgrowth and branching is a crucial aspect neuronal development regeneration. Axons dendrites, sometimes referred to as neurites, are extensions neuron’s cellular body that used start networks. Here we explored the effects diethyl (3,4-dihydroxyphenethylamino)(quinolin-4-yl) methylphosphonate (DDQ) on developmental features in HT22 cells. In this work, examined protective DDQ processes synaptic differentiated cells expressing mutant Tau (mTau) cDNA. To investigate characteristics, cell viability, biochemical, molecular, western blotting, immunocytochemistry were used. Neurite evaluated through segmentation measurement neural processes. These can be seen measured with fluorescence microscope by manually tracing measuring length growth. observed quantified fluorescent HT22. DDQ-treated mTau-HT22 (HT22 transfected cDNA Tau) display increased levels synaptophysin, MAP-2, β-tubulin. Additionally, confirmed noted reduced both total p-Tau, well elevated microtubule-associated protein 2, β-tubulin, vesicular acetylcholine transporter, mitochondrial biogenesis protein–peroxisome proliferator-activated receptor-gamma coactivator-1α. mTau-expressed neurons, enhanced characteristics improved outgrowth. Our findings conclude (Alzheimer’s disease) treated have functional characteristics. key finding that, cells, preserves structure may even enhance nerve function mTau inhibition.

Язык: Английский

Exploring Advancements in Early Detection of Alzheimer's Disease with Molecular Assays and Animal Models DOI
Papihra Sethi, Rakesh Bhaskar, Krishna Kumar Singh

и другие.

Ageing Research Reviews, Год журнала: 2024, Номер 100, С. 102411 - 102411

Опубликована: Июль 9, 2024

Язык: Английский

Процитировано

15
The Potential of Mitochondrial Therapeutics in the Treatment of Oxidative Stress and Inflammation in Aging DOI
Jitendra Kumar Sinha,

Khanak Jorwal,

Krishna Kumar Singh

и другие.

Molecular Neurobiology, Год журнала: 2024, Номер unknown

Опубликована: Сен. 4, 2024

Язык: Английский

Процитировано

6
Roles of SIRT3 in cardiovascular and neurodegenerative diseases DOI
Liang Chen, Anqi Zhao, Ying Li

и другие.

Ageing Research Reviews, Год журнала: 2025, Номер unknown, С. 102654 - 102654

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0
Mitophagy in Alzheimer's disease and other metabolic disorders: a focus on mitochondrial-targeted therapeutics DOI

Shadt Skawratananond,

Daniel X Xiong,

Charlie Zhang

и другие.

Ageing Research Reviews, Год журнала: 2025, Номер unknown, С. 102732 - 102732

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0
Aloe‐Emodin Improves Mitophagy in Alzheimer's Disease via Activating the AMPK/PGC‐1α/SIRT3 Signaling Pathway DOI Creative Commons
Yulu Wang, Yanqi Ge,

Siyu Hua

и другие.

CNS Neuroscience & Therapeutics, Год журнала: 2025, Номер 31(3)

Опубликована: Март 1, 2025

Impaired mitophagy results in the accumulation of defective mitochondria that are unable to be cleared effectively Alzheimer's disease (AD). Aloe-emodin (AE), a key component traditional Chinese medicine Rhubarb, exhibits neuroprotective effects against disease, though underlying mechanism remains unclear. Studying aloe-emodin's role enhancing is vital for improving cognitive function and reducing neuronal damage disease. The APP/PS1 double transgenic mice were adopted as models AD assess aloe-emodin upon its impact on hippocampal neurons. Additionally, we investigated regulatory mechanisms proteins within aforementioned pathway, morphological characteristics mitophagy-related proteins. An neuron model was developed using Aβ25-35 evaluate mitochondrial function, protein expression such pathway mitophagy. This approach aims elucidate relation AD. AE activates neurons, improves dysfunction, reduces damage, alleviates symptoms mice. AMPK, PGC-1α SIRT3. Increased SIRT3 promotes regulates When autophagy enhanced, Beclin1, LC3, P62, Parkin, PINK1-related changes. Further vitro experiments showed can enhance cell models. membrane potential, GSH, ROS Ca2+ levels gradually recover, alleviating pathological manifestations Knocking down leads increased reduction HT22 cells. Experimental show activate through AMPK/PGC-1α/SIRT3 alleviate dysfunction AD, reduce

Язык: Английский

Процитировано

0
Therapeutic potential of DDQ in enhancing mitochondrial health and cognitive function in Late-Onset Alzheimer’s disease DOI
Sudhir Kshirsagar,

Rainier Vladlen Alvir,

Jangampalli Adi Pradeepkiran

и другие.

Mitochondrion, Год журнала: 2025, Номер unknown, С. 102036 - 102036

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0
Small molecule DDQ involvement of ERK-mediated signaling pathway with enhanced mitophagy in HT22 cells transfected with mTau DOI
Jangampalli Adi Pradeepkiran, Sudhir Kshirsagar,

Rainier Vladlen Alvir

и другие.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Год журнала: 2025, Номер unknown, С. 167850 - 167850

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0
Small molecule inhibitor DDQ-treated hippocampal neuronal cells show improved neurite outgrowth and synaptic branching DOI Creative Commons
Jangampalli Adi Pradeepkiran,

Priyanka Rawat,

Arubala P. Reddy

и другие.

Neural Regeneration Research, Год журнала: 2024, Номер 20(9), С. 2624 - 2632

Опубликована: Июнь 19, 2024

JOURNAL/nrgr/04.03/01300535-202509000-00024/figure1/v/2024-11-05T132919Z/r/image-tiff The process of neurite outgrowth and branching is a crucial aspect neuronal development regeneration. Axons dendrites, sometimes referred to as neurites, are extensions neuron’s cellular body that used start networks. Here we explored the effects diethyl (3,4-dihydroxyphenethylamino)(quinolin-4-yl) methylphosphonate (DDQ) on developmental features in HT22 cells. In this work, examined protective DDQ processes synaptic differentiated cells expressing mutant Tau (mTau) cDNA. To investigate characteristics, cell viability, biochemical, molecular, western blotting, immunocytochemistry were used. Neurite evaluated through segmentation measurement neural processes. These can be seen measured with fluorescence microscope by manually tracing measuring length growth. observed quantified fluorescent HT22. DDQ-treated mTau-HT22 (HT22 transfected cDNA Tau) display increased levels synaptophysin, MAP-2, β-tubulin. Additionally, confirmed noted reduced both total p-Tau, well elevated microtubule-associated protein 2, β-tubulin, vesicular acetylcholine transporter, mitochondrial biogenesis protein–peroxisome proliferator-activated receptor-gamma coactivator-1α. mTau-expressed neurons, enhanced characteristics improved outgrowth. Our findings conclude (Alzheimer’s disease) treated have functional characteristics. key finding that, cells, preserves structure may even enhance nerve function mTau inhibition.

Язык: Английский

Процитировано

3