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Article ; Online: When Asymptomatic Bacteriuria is not Asymptomatic or "Pseudo-Urinary Tract Infection".

Gomolin, Irving H

Journal of the American Geriatrics Society

2018 Volume 66, Issue 11, Page(s) 2223

MeSH term(s)	Bacteriuria ; Humans ; Urinary Tract Infections
Language	English
Publishing date	2018-10-05
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	80363-7
ISSN	1532-5415 ; 0002-8614
ISSN (online)	1532-5415
ISSN	0002-8614
DOI	10.1111/jgs.15529
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Ud II Zs.168: Show issues

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Article ; Online: Post-acute care nursing home deaths in the COVID era: Potential for attribution bias.

Gomolin, Irving H / Hartley, Douglas A / Polsky, Bruce

Journal of the American Geriatrics Society

2021 Volume 69, Issue 6, Page(s) 1450–1452

MeSH term(s)	Aged ; Bias ; COVID-19/mortality ; Humans ; Nursing Homes ; Subacute Care
Language	English
Publishing date	2021-03-26
Publishing country	United States
Document type	Letter
ZDB-ID	80363-7
ISSN	1532-5415 ; 0002-8614
ISSN (online)	1532-5415
ISSN	0002-8614
DOI	10.1111/jgs.17132
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Article: Mitochondria in Alzheimer's Disease Pathogenesis.

Reiss, Allison B / Gulkarov, Shelly / Jacob, Benna / Srivastava, Ankita / Pinkhasov, Aaron / Gomolin, Irving H / Stecker, Mark M / Wisniewski, Thomas / De Leon, Joshua

Life (Basel, Switzerland)

2024 Volume 14, Issue 2

Abstract: Alzheimer's disease (AD) is a progressive and incurable neurodegenerative disorder that primarily affects persons aged 65 years and above. It causes dementia with memory loss and deterioration in thinking and language skills. AD is characterized by ... ...

Abstract	Alzheimer's disease (AD) is a progressive and incurable neurodegenerative disorder that primarily affects persons aged 65 years and above. It causes dementia with memory loss and deterioration in thinking and language skills. AD is characterized by specific pathology resulting from the accumulation in the brain of extracellular plaques of amyloid-β and intracellular tangles of phosphorylated tau. The importance of mitochondrial dysfunction in AD pathogenesis, while previously underrecognized, is now more and more appreciated. Mitochondria are an essential organelle involved in cellular bioenergetics and signaling pathways. Mitochondrial processes crucial for synaptic activity such as mitophagy, mitochondrial trafficking, mitochondrial fission, and mitochondrial fusion are dysregulated in the AD brain. Excess fission and fragmentation yield mitochondria with low energy production. Reduced glucose metabolism is also observed in the AD brain with a hypometabolic state, particularly in the temporo-parietal brain regions. This review addresses the multiple ways in which abnormal mitochondrial structure and function contribute to AD. Disruption of the electron transport chain and ATP production are particularly neurotoxic because brain cells have disproportionately high energy demands. In addition, oxidative stress, which is extremely damaging to nerve cells, rises dramatically with mitochondrial dyshomeostasis. Restoring mitochondrial health may be a viable approach to AD treatment.
Language	English
Publishing date	2024-01-30
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662250-6
ISSN	2075-1729
ISSN	2075-1729
DOI	10.3390/life14020196
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Article ; Online: Absence of COVID-19 Disease Among Chronically Ventilated Nursing Home Patients.

Gomolin, Irving H / Krichmar, Grigoriy / Siskind, David / Divers, Jasmin / Polsky, Bruce

Journal of the American Medical Directors Association

2021 Volume 22, Issue 12, Page(s) 2500–2503

Abstract: Objective: To describe the experience of COVID-19 disease among chronically ventilated and nonventilated nursing home patients living in 3 separate nursing homes.: Design: Observational study of death, respiratory illness and COVID-19 polymerase ... ...

Abstract	Objective: To describe the experience of COVID-19 disease among chronically ventilated and nonventilated nursing home patients living in 3 separate nursing homes. Design: Observational study of death, respiratory illness and COVID-19 polymerase chain reaction (PCR) results among residents and staff during nursing home outbreaks in 2020. Setting and participants: 93 chronically ventilated nursing home patients and 1151 nonventilated patients living among 3 separate nursing homes on Long Island, New York, as of March 15, 2020. Illness, PCR results, and antibody studies among staff are also reported. Measurements: Data were collected on death rate among chronically ventilated and nonventilated patients between March 15 and May 15, 2020, compared to the same time in 2019; prevalence of PCR positivity among ventilated and nonventilated patients in 2020; reported illness, PCR positivity, and antibody among staff. Results: Total numbers of deaths among chronically ventilated nursing home patients during this time frame were similar to the analogous period 1 year earlier (9 of 93 in 2020 vs 8 of 100 in 2019, P = .8), whereas deaths among nonventilated patients were greatly increased (214 of 1151 in 2020 vs 55 of 1189 in 2019, P < .001). No ventilated patient deaths were clinically judged to be COVID-19 related. No clusters of COVID-19 illness could be demonstrated among ventilated patients. Surveillance PCR testing of ventilator patients failed to reveal COVID-19 positivity (none of 84 ventilator patients vs 81 of 971 nonventilator patients, P < .002). Illness and evidence of COVID-19 infection was demonstrated among staff working both in nonventilator and in ventilator units. Conclusions and implications: COVID-19 infection resulted in illness and death among nonventilated nursing home residents as well as among staff. This was not observed among chronically ventilated patients. The mechanics of chronic ventilation appears to protect chronically ventilated patients from COVID-19 disease.
MeSH term(s)	COVID-19 ; Disease Outbreaks ; Humans ; Nursing Homes ; SARS-CoV-2 ; Skilled Nursing Facilities
Language	English
Publishing date	2021-09-29
Publishing country	United States
Document type	Journal Article ; Observational Study
ZDB-ID	2171030-2
ISSN	1538-9375 ; 1525-8610
ISSN (online)	1538-9375
ISSN	1525-8610
DOI	10.1016/j.jamda.2021.09.019
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Zs.A 5971: Show issues

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Article: Therapeutic Potential of P110 Peptide: New Insights into Treatment of Alzheimer's Disease.

Srivastava, Ankita / Johnson, Maryann / Renna, Heather A / Sheehan, Katie M / Ahmed, Saba / Palaia, Thomas / Pinkhasov, Aaron / Gomolin, Irving H / De Leon, Joshua / Reiss, Allison B

Life (Basel, Switzerland)

2023 Volume 13, Issue 11

Abstract: Mitochondrial degeneration in various neurodegenerative diseases, specifically in Alzheimer's disease, involves excessive mitochondrial fission and reduced fusion, leading to cell damage. P110 is a seven-amino acid peptide that restores mitochondrial ... ...

Abstract	Mitochondrial degeneration in various neurodegenerative diseases, specifically in Alzheimer's disease, involves excessive mitochondrial fission and reduced fusion, leading to cell damage. P110 is a seven-amino acid peptide that restores mitochondrial dynamics by acting as an inhibitor of mitochondrial fission. However, the role of P110 as a neuroprotective agent in AD remains unclear. Therefore, we performed cell culture studies to evaluate the neuroprotective effect of P110 on amyloid-β accumulation and mitochondrial functioning. Human SH-SY5Y neuronal cells were incubated with 1 µM and 10 µM of P110, and Real-Time PCR and Western blot analysis were done to quantify the expression of genes pertaining to AD and neuronal health. Exposure of SH-SY5Y cells to P110 significantly increased APP mRNA levels at 1 µM, while BACE1 mRNA levels were increased at both 1 µM and 10 µM. However, protein levels of both APP and BACE1 were significantly reduced at 10 µM of P110. Further, P110 treatment significantly increased ADAM10 and Klotho protein levels at 10 µM. In addition, P110 exposure significantly increased active mitochondria and reduced ROS in live SH-SY5Y cells at both 1 µM and 10 µM concentrations. Taken together, our results indicate that P110 might be useful in attenuating amyloid-β generation and improving neuronal health by maintaining mitochondrial function in neurons.
Language	English
Publishing date	2023-11-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662250-6
ISSN	2075-1729
ISSN	2075-1729
DOI	10.3390/life13112156
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Article ; Online: Alzheimer's Disease Treatment: The Search for a Breakthrough.

Reiss, Allison B / Muhieddine, Dalia / Jacob, Berlin / Mesbah, Michael / Pinkhasov, Aaron / Gomolin, Irving H / Stecker, Mark M / Wisniewski, Thomas / De Leon, Joshua

Medicina (Kaunas, Lithuania)

2023 Volume 59, Issue 6

Abstract: As the search for modalities to cure Alzheimer's disease (AD) has made slow progress, research has now turned to innovative pathways involving neural and peripheral inflammation and neuro-regeneration. Widely used AD treatments provide only symptomatic ... ...

Abstract	As the search for modalities to cure Alzheimer's disease (AD) has made slow progress, research has now turned to innovative pathways involving neural and peripheral inflammation and neuro-regeneration. Widely used AD treatments provide only symptomatic relief without changing the disease course. The recently FDA-approved anti-amyloid drugs, aducanumab and lecanemab, have demonstrated unclear real-world efficacy with a substantial side effect profile. Interest is growing in targeting the early stages of AD before irreversible pathologic changes so that cognitive function and neuronal viability can be preserved. Neuroinflammation is a fundamental feature of AD that involves complex relationships among cerebral immune cells and pro-inflammatory cytokines, which could be altered pharmacologically by AD therapy. Here, we provide an overview of the manipulations attempted in pre-clinical experiments. These include inhibition of microglial receptors, attenuation of inflammation and enhancement of toxin-clearing autophagy. In addition, modulation of the microbiome-brain-gut axis, dietary changes, and increased mental and physical exercise are under evaluation as ways to optimize brain health. As the scientific and medical communities work together, new solutions may be on the horizon to slow or halt AD progression.
MeSH term(s)	Humans ; Alzheimer Disease/drug therapy ; Inflammation/metabolism ; Brain/pathology ; Cytokines/metabolism ; Cognition
Chemical Substances	Cytokines
Language	English
Publishing date	2023-06-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2188113-3
ISSN	1648-9144 ; 1010-660X
ISSN (online)	1648-9144
ISSN	1010-660X
DOI	10.3390/medicina59061084
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Zs.A 6270: Show issues

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Article ; Online: Alzheimer Disease Clinical Trials Targeting Amyloid: Lessons Learned From Success in Mice and Failure in Humans.

Reiss, Allison B / Montufar, Natalie / DeLeon, Joshua / Pinkhasov, Aaron / Gomolin, Irving H / Glass, Amy D / Arain, Hirra A / Stecker, Mark M

The neurologist

2021 Volume 26, Issue 2, Page(s) 52–61

Abstract: Background: The goal of slowing or halting the development of Alzheimer disease (AD) has resulted in the huge allocation of resources by academic institutions and pharmaceutical companies to the development of new treatments. The etiology of AD is ... ...

Abstract	Background: The goal of slowing or halting the development of Alzheimer disease (AD) has resulted in the huge allocation of resources by academic institutions and pharmaceutical companies to the development of new treatments. The etiology of AD is elusive, but the aggregation of amyloid-β and tau peptide and oxidative processes are considered critical pathologic mechanisms. The failure of drugs with multiple mechanisms to meet efficacy outcomes has caused several companies to decide not to pursue further AD studies and has left the field essentially where it has been for the past 15 years. Efforts are underway to develop biomarkers for detection and monitoring of AD using genetic, imaging, and biochemical technology, but this is of minimal use if no intervention can be offered. Review summary: In this review, we consider the natural progression of AD and how it continues despite present attempts to modify the amyloid-related machinery to alter the disease trajectory. We describe the mechanisms and approaches to AD treatment targeting amyloid, including both passive and active immunotherapy as well as inhibitors of enzymes in the amyloidogenic pathway. Conclusion: Lessons learned from clinical trials of amyloid reduction strategies may prove crucial for the leap forward toward novel therapeutic targets to treat AD.
MeSH term(s)	Alzheimer Disease/drug therapy ; Amyloid beta-Peptides ; Animals ; Biomarkers ; Humans ; Mice
Chemical Substances	Amyloid beta-Peptides ; Biomarkers
Language	English
Publishing date	2021-03-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1361380-7
ISSN	2331-2637 ; 1074-7931
ISSN (online)	2331-2637
ISSN	1074-7931
DOI	10.1097/NRL.0000000000000320
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Zs.A 4641: Show issues

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Article ; Online: Alzheimer’s Disease Treatment

Allison B. Reiss / Dalia Muhieddine / Berlin Jacob / Michael Mesbah / Aaron Pinkhasov / Irving H. Gomolin / Mark M. Stecker / Thomas Wisniewski / Joshua De Leon

Medicina, Vol 59, Iss 1084, p

The Search for a Breakthrough

2023 Volume 1084

Abstract: As the search for modalities to cure Alzheimer’s disease (AD) has made slow progress, research has now turned to innovative pathways involving neural and peripheral inflammation and neuro-regeneration. Widely used AD treatments provide only symptomatic ... ...

Abstract	As the search for modalities to cure Alzheimer’s disease (AD) has made slow progress, research has now turned to innovative pathways involving neural and peripheral inflammation and neuro-regeneration. Widely used AD treatments provide only symptomatic relief without changing the disease course. The recently FDA-approved anti-amyloid drugs, aducanumab and lecanemab, have demonstrated unclear real-world efficacy with a substantial side effect profile. Interest is growing in targeting the early stages of AD before irreversible pathologic changes so that cognitive function and neuronal viability can be preserved. Neuroinflammation is a fundamental feature of AD that involves complex relationships among cerebral immune cells and pro-inflammatory cytokines, which could be altered pharmacologically by AD therapy. Here, we provide an overview of the manipulations attempted in pre-clinical experiments. These include inhibition of microglial receptors, attenuation of inflammation and enhancement of toxin-clearing autophagy. In addition, modulation of the microbiome-brain-gut axis, dietary changes, and increased mental and physical exercise are under evaluation as ways to optimize brain health. As the scientific and medical communities work together, new solutions may be on the horizon to slow or halt AD progression.
Keywords	Alzheimer’s disease ; amyloid ; inflammation ; dementia ; drug therapy ; diet ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2023-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Memantine Plasma Concentrations Among Patients With Dementia.

Gomolin, Irving H / Papamichael, Michael J / Fazzari, Melissa J / Rieger, Robert

Journal of clinical psychopharmacology

2017 Volume 37, Issue 1, Page(s) 117–118

MeSH term(s)	Aged ; Aged, 80 and over ; Dementia/drug therapy ; Excitatory Amino Acid Antagonists/administration & dosage ; Excitatory Amino Acid Antagonists/blood ; Female ; Humans ; Male ; Memantine/administration & dosage ; Memantine/blood
Chemical Substances	Excitatory Amino Acid Antagonists ; Memantine (W8O17SJF3T)
Language	English
Publishing date	2017-02
Publishing country	United States
Document type	Letter
ZDB-ID	604631-9
ISSN	1533-712X ; 0271-0749
ISSN (online)	1533-712X
ISSN	0271-0749
DOI	10.1097/JCP.0000000000000645
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Zs.A 1664: Show issues

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Article: Cognitive changes mediated by adenosine receptor blockade in a resveratrol-treated atherosclerosis-prone lupus mouse model.

Kasselman, Lora J / Renna, Heather A / Voloshyna, Iryna / Pinkhasov, Aaron / Gomolin, Irving H / Teboul, Isaac / De Leon, Joshua / Carsons, Steven E / Reiss, Allison B

Journal of traditional and complementary medicine

2022 Volume 12, Issue 5, Page(s) 447–454

Abstract: Background and aim: Resveratrol is a bioactive molecule used in dietary supplements and herbal medicines and consumed worldwide. Prior work showed that resveratrol's anti-atherogenic properties are mediated in part through the adenosine A2A receptor. ... ...

Abstract	Background and aim: Resveratrol is a bioactive molecule used in dietary supplements and herbal medicines and consumed worldwide. Prior work showed that resveratrol's anti-atherogenic properties are mediated in part through the adenosine A2A receptor. The present study explores the potential contribution of adenosine A2A receptor activation to neuroprotective action of resveratrol on cognitive deficits in a model of atherosclerosis-prone systemic lupus erythematosus. Experimental procedure: Using behavioral analysis (open field, static rod, novel object recognition) and QRT-PCR, this study measured working memory, anxiety, motor coordination, and expression of mRNA in the brain. Results and conclusion: Data indicate that resveratrol increases working memory, on average but not statistically, and shows a trend towards improved motor coordination (p = 0.07) in atherosclerosis-prone lupus mice. Additionally, resveratrol tends to increase mRNA levels of SIRT1, decrease vascular endothelial growth factor and CX3CL1 mRNA in the hippocampus. Istradefylline, an adenosine A2A receptor antagonist, antagonizes the effects of resveratrol on working memory (p = 0.04) and the expression of SIRT1 (p = 0.03), vascular endothelial growth factor (p = 0.04), and CX3CL1 (p = 0.03) in the hippocampus.This study demonstrates that resveratrol could potentially be a therapeutic candidate in the modulation of cognitive dysfunction in neuropsychiatric lupus, especially motor incoordination. Further human studies, as well as optimization of resveratrol administration, could confirm whether resveratrol may be an additional resource available to reduce the burden of cognitive impairment associated with lupus. Additionally, further studies need to address the role of A2A blockade in cognitive function among the autoimmune population. Section: 3. Dietary therapy/nutrients supplements. Taxonomy classification by evise: autoimmunity, inflammation, neurology.
Language	English
Publishing date	2022-02-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2709698-1
ISSN	2225-4110
ISSN	2225-4110
DOI	10.1016/j.jtcme.2022.01.006
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