A model intervention for elder abuse and dementia
alzheimers-disease; curricula; Geriatrics & Gerontology; referral protocols; risk; screening tools; violence
This article describes a 2-year collaborative project in Cleveland, OH, that improved the reporting and management of potential and suspected elder abuse situations involving persons with dementia. Educational curricula for cross-training, screening tools, and referral protocols were developed and tested for staff and volunteers in adult protective services and dementia care. A handbook for caregivers of persons with dementia was produced that enables caregivers to self-identify elder abuse risk and seek appropriate interventions to prevent abuse. Project organization, implementation, and evaluation are discussed along with strategies for replication in other communities.
Anetzberger G J; Palmisano B R; Sanders M; Bass D; Dayton C; Eckert S; Schimer M R
Gerontologist
2000
2000-08
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1093/geront/40.4.492" target="_blank" rel="noreferrer noopener">10.1093/geront/40.4.492</a>
Abnormal Metal Levels In The Primary Visual Pathway Of The Dba/2j Mouse Model Of Glaucoma
alzheimers-disease; amyloid-beta; aqueous-humor; Biochemistry & Molecular Biology; ganglion-cell degeneration; gene-expression; Glaucoma; ICP-MS; iron; microarray analysis; neurodegeneration; neurodegeneration; Retina; Retina; Superior colliculus; synapse
DeToma A S; Dengler-Crish C M; Deb A; Braymer J J; Penner-Hahn J E; Van der Schyf C J; Lim M H; Crish S D
Biometals
2014
2014-12
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1007/s10534-014-9790-z" target="_blank" rel="noreferrer noopener">10.1007/s10534-014-9790-z</a>
AGE-DEPENDENT CHANGES IN OLFACTORY-MEDIATED BEHAVIORAL INVESTIGATIONS IN THE MALE-RAT
Psychology; responses; Neurosciences & Neurology; parkinsons-disease; Behavioral Sciences; recognition; alzheimers-disease; identification; norepinephrine; deficits; bulb; mitral cells; sex odors
Menciowszalek T; Ramirez V D; Dluzen D E
Behavioral and Neural Biology
1992
1992-05
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1016/0163-1047(92)90164-y" target="_blank" rel="noreferrer noopener">10.1016/0163-1047(92)90164-y</a>
Aging differentially alters forms of long-term potentiation in rat hippocampal area CA1
aged fischer-344 rats; alzheimers-disease; calcium channels; concentration-dependent manner; cortex; ltp induction; Neurosciences & Neurology; nmda receptors; Physiology; prefrontal; pyramidal neurons; synaptic transmission; visual cortex
Aging differentially alters forms of long-term potentiation in rat hippocampal area CAl. J. Neurophysiol. 79: 334-341, 1998. Long-term potentiation (LTP) of the Schaffer collateral/commissural inputs to CAI in the hippocampus was shown to consist of N-methyl-D-aspartate receptor (NMDAR) and voltage-dependent calcium channel (VDCC) dependent forms. In this study, the relative contributions of these two forms of LTP in in vitro hippocampal slices from young (2 mo) and old (24 mo) Fischer 344 rats were examined. Excitatory postsynaptic potentials (EPSP) were recorded extracellularly from stratum radiat-um before and after II tetanic stimulus consisting of four 200-Hz, 0.5-s trains given 5 s apart. Under control conditions, a compound LTP consisting of both forms was induced and was similar, in both time course and magnitude, in young and old animals. NMDAR-dependent LTP (nmdaLTP), isolated by the application of 10 mu M nifedipine (a voltage-dependent calcium channel blocker), was significantly reduced in magnitude in aged animals. The VDCC dependent form (vdccLTP), isolated by the application of 50 mu M D,L-2-amino-5-phosphonvalerate (APV), was significantly larger in aged animals. Although both LTP forms reached stable values 40-60 min posttetanus in young animals, in aged animals vdccLTP increased and nmdaLTP decreased during this time. In both young and old animals, the sum of the two isolated LTP forms approximated the magnitude of the compound LTP, and application of APV and nifedipine or genestein (a tyrosine kinase inhibitor) together blocked potentiation. These results suggest that aging causes a shift in synaptic plasticity from NMDAR-dependent mechanisms to VDCC-dependent mechanisms. The data are consistent with previous findings of increased L-type calcium current and decreased NMDAR number In aged CAI cells and may help explain age-related deficits in learning and memory.
Shankar S; Teyler T J; Robbins N
Journal of Neurophysiology
1998
1998-01
Journal Article
<a href="http://doi.org/10.1152/jn.1998.79.1.334" target="_blank" rel="noreferrer noopener">10.1152/jn.1998.79.1.334</a>
Chronic exposure to a glyphosate-containing pesticide leads to mitochondrial dysfunction and increased reactive oxygen species production in Caenorhabditis elegans
C. elegans; Glyphosate; Hydrogen peroxide; Mitochondrial inhibition; oxidative stress; Toxicology; Environmental Sciences & Ecology; Pharmacology & Pharmacy; parkinsons-disease; brain; alzheimers-disease; mechanisms; degeneration; species; neurodegenerative diseases; 6-ohda; C. elegans; complex-i; Herbicide; Reactive oxygen
Glyphosate-containing herbicides are among the most widely-used in the world. Although glyphosate itself is relatively non-toxic, growing evidence suggests that commercial herbicide formulations may lead to increased oxidative stress and mitochondrial inhibition. In order to assess these mechanisms in vivo, we chronically (24 h) exposed Caenorhabditis elegans to various concentrations of the glyphosate-containing herbicide TouchDown (TD). Following TD exposure, we evaluated the function of specific mitochondrial electron transport chain complexes. Initial oxygen consumption studies demonstrated inhibition in mid- and high-TD concentration treatment groups compared to controls. Results from tetramethylrhodamine ethyl ester and ATP assays indicated reductions in the proton gradient and ATP levels, respectively. Additional studies were designed to determine whether TD exposure resulted in increased reactive oxygen species (ROS) production. Data from hydrogen peroxide, but not superoxide or hydroxyl radical, assays showed statistically significant increases in this specific ROS. Taken together, these data indicate that exposure of Caenorhabditis elegans to TD leads to mitochondrial inhibition and hydrogen peroxide production.
Bailey D C; Todt C E; Burchfield S L; Pressley A S; Denney R D; Snapp I B; Negga R; Traynor W L; Fitsanakis V A
Environmental Toxicology and Pharmacology
2018
2018-01
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1016/j.etap.2017.11.005" target="_blank" rel="noreferrer noopener">10.1016/j.etap.2017.11.005</a>
Estrogen-mediated regulation of CYP7B1: A possible role for controlling DHEA levels in human tissues
7-alpha-hydroxylase; alzheimers-disease; bile-acid biosynthesis; Biochemistry & Molecular Biology; CYP7B1; dehydroepiandrosterone 7-hydroxylase; DHEA; Endocrinology & Metabolism; estrogen; fetal development; gene-expression; human oxysterol 7-alpha-hydroxylase; prostate; rat; receptor-beta; sex hormone biosynthesis; transcriptional regulation; vascular dementia
The current study examines regulation of CYP7B1, a DHEA 7 alpha-hydroxylase, by sex hormones. Transfection with estrogen receptor alpha and treatment with 17 P-estradiol in human embryonic kidney 293 cells significantly increased CYP7B1 catalytic activity and mRNA, and stimulated a human CYP7B1 reporter gene. Transfection with estrogen receptor P showed similar but less significant effects. In the absence of receptors, 17 P-estradiol suppressed CYP7B1 activity, suggesting that estrogenic effects may be different in cells not expressing receptors. Quantitation of CYP7B1 mRNA in adult and fetal human tissues showed markedly higher CYP7B1 mRNA levels in fetal tissues compared with the corresponding adult ones, except in the liver. This indicates a tissue-specific, developmental regulation of CYP7B1 and suggests an important function for this enzyme in fetal life. DHEA secreted by fetal adrenals is an essential precursor for placental estrogen formation. Since CYP7B1 diverts DHEA from the sex hormone biosynthetic pathway, estrogen receptor-mediated up-regulatio of CYP7B1 should lead to less DHEA available for sex hormone synthesis and may help to maintain normal levels of estrogens and androgens in human tissues, especially during fetal development. Regulation by estrogens may also be of importance in other processes where CYP7B1 is involved, including cholesterol homeostasis, cellular proliferation, and CNS function. (c) 2006 Elsevier Ltd. All rights reserved.
Tang W J; Eggertsen G; Chiang J Y L; Norlin M
Journal of Steroid Biochemistry and Molecular Biology
2006
2006-07
Journal Article
<a href="http://doi.org/10.1016/j.jsbmb.2006.02.005" target="_blank" rel="noreferrer noopener">10.1016/j.jsbmb.2006.02.005</a>
Inhibition Of Apoptosis In Human Retinal Pigment Epithelial Cells Treated With Benzo(e)pyrene, A Toxic Component Of Cigarette Smoke
alzheimers-disease; dna-damage; experimental glaucoma; genistein; macular degeneration; memantine treatment; mitochondrial dysfunction; Ophthalmology; oxidative stress; protects; resveratrol
Mansoor S; Gupta N; Patil A J; Estrago-Franco M F; Ramirez C; Migon R; Sapkal A; Kuppermann B D; Kenney M C
Investigative Ophthalmology & Visual Science
2010
2010-05
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1167/iovs.09-4121" target="_blank" rel="noreferrer noopener">10.1167/iovs.09-4121</a>
Knockdown of amyloid precursor protein normalizes cholinergic function in a cell line derived from the cerebral cortex of a trisomy 16 mouse: An animal model of Down syndrome
16 mice; abnormalities; acetylcholine; acetylcholine-release; alzheimers-disease; amyloid; antisense; beta-protein; calcium; cell line; Down syndrome; Neurosciences & Neurology; neurotoxicity; peptide; rat hippocampal slices; root ganglion neurons
We have generated immortal neuronal cell lines from normal and trisomy 16 (Ts16) mice, a model for Down syndrome (DS). Ts16 lines overexpress DS-related genes (App, amyloid precursor protein; Sod1, Cu/Zn superoxide dismutase) and show altered cholinergic function (reduced choline uptake, ChAT expression and fractional choline release after stimulation). As previous evidence has related amyloid to cholinergic dysfunction, we reduced APP expression using specific mRNA antisense sequences in our neuronal cell line named CTb, derived from Ts16 cerebral cortex, compared to a cell line derived from a normal animal, named CNh. After transfection, Western blot studies showed APP expression knockdown in CTb cells of 36% (24 hr), 40.4% (48 hr), and 50.2% (72 hr) compared to CNh. Under these reduced APP levels, we studied 3 H-choline uptake in CTb and CNh cells. CTb, as reported previously, expressed reduced choline uptake compared to CNh cells (75%, 90%, and 69% reduction at 1, 2, and 5 min incubation, respectively). At 72 hr of APP knockdown, choline uptake levels were essentially similar in both cell types. Further, fractional release of H-3-choline in response to glutamate, nicotine, and depolarization with KCI showed a progressive increase after APP knockdown, reaching values similar to those of CNh after 72 hr of transfection. The results suggest that APP overexpression in CTb cells contributes to impaired cholinergic function, and that gene knockdown in CTb cells is a relevant tool to study DS-related dysfunction. (c) 2006 Wiley-Liss, Inc.
Opazo P; Saud K; de Saint Pierre M; Cardenas A M; Allen D D; Segura-Aguilar J; Caviedes R; Caviedes P
Journal of Neuroscience Research
2006
2006-11
Journal Article
<a href="http://doi.org/10.1002/jnr.21035" target="_blank" rel="noreferrer noopener">10.1002/jnr.21035</a>
Multifunctional drugs with different CNS targets for neuropsychiatric disorders
alzheimers-disease; alzheimers-disease; amyotrophic lateral sclerosis; Biochemistry & Molecular Biology; depressive illness; designed multiple ligands; hetero-cage compounds; iron chelator; Lewy body disease; monoamine oxidase inhibitor; mptp-induced neurotoxicity; neurodegenerative diseases; Neurosciences & Neurology; nicotinic acetylcholine-receptors; nonsteroidal antiinflammatory drugs; parkinsons-disease; parkinsons-disease; schizophrenia
The multiple disease etiologies that lead to neuropsychiatric disorders, such as Parkinson's and Alzheimer's disease, amyotrophic lateral sclerosis, Huntington disease, schizophrenia, depressive illness and stroke, offer significant challenges to drug discovery efforts aimed at preventing or even reversing the progression of these disorders. Transcriptomic tools and proteomic profiling have clearly indicated that such diseases are multifactorial in origin. Further, they are thought to be initiated by a cascade of molecular events that involve several neurotransmitter systems. In response to this complexity, a new paradigm has recently emerged that challenges the widely held assumption that 'silver bullet' agents are superior to 'dirty drugs' in therapeutic approaches aimed at the prevention or treatment of neuropsychiatric diseases. A similar pattern of drug development has occurred in strategies for the treatment of cancer, AIDS and cardiovascular diseases. In this review, we offer an overview of therapeutic strategies and novel investigative drugs discovered or developed in our own and other laboratories, that address multiple CNS etiological targets associated with an array of neuropsychiatric disorders.
Van der Schyf C J; Geldenhuys W J; Youdim M B H
Journal of Neurochemistry
2006
2006-11
Journal Article
<a href="http://doi.org/10.1111/j.1471-4159.2006.04141.x" target="_blank" rel="noreferrer noopener">10.1111/j.1471-4159.2006.04141.x</a>
Neuropsychiatric Symptoms in Dementia Patients With and Without a History of Traumatic Brain Injury
alzheimers-disease; association; behavioral disturbances; cache county; inventory; long-term care; Neurosciences & Neurology; prevalence; Psychiatry; quality-of-life; residents; validation
The authors aim to determine if a history of traumatic brain injury (TBI) assessed before dementia onset is associated with a higher risk of neuropsychiatric symptoms after dementia onset. A population-based incident series of people with dementia were assessed for TBI prior to onset of dementia and for neuropsychiatric symptoms after the onset, using the Neuropsychiatric Inventory. Participants with predementia TBI were more likely to exhibit disinhibition (12.7% versus 5.4%, OR = 2.8, p = 0.02), but not other neuropsychiatric symptoms. Traumatic brain injury may increase the risk of disinhibition in patients with dementia. (The Journal of Neuropsychiatry and Clinical Neurosciences 2010; 22: 166-172)
Rao V; Rosenberg P; Miles Q S; Patadia D; Treiber K; Bertrand M; Norton M; Steinberg M; Tschanz J; Lyketsos C
Journal of Neuropsychiatry and Clinical Neurosciences
2010
2010
Journal Article
<a href="http://doi.org/10.1176/jnp.2010.22.2.166" target="_blank" rel="noreferrer noopener">10.1176/jnp.2010.22.2.166</a>
NEUROTROPHIN EXPRESSION IN RAT HIPPOCAMPAL SLICES - A STIMULUS PARADIGM INDUCING LTP IN CA1 EVOKES INCREASES IN BDNF AND NT-3 MESSENGER-RNAS
alzheimers-disease; choline-acetyltransferase activity; dopamine-beta-hydroxylase; factor family; nerve growth-factor; neuronal death; Neurosciences & Neurology; ngf; protein-kinase; receptor; selective induction; tyrosine-hydroxylase
We report that stimulation inducing long-term potentiation (LTP) in the CA1 pyramidal cell layer of the hippocampus evokes significant increases in both BDNF and NT-3 mRNAs in CA1 neurons. No changes in BDNF or NT-3 mRNA levels were seen in the nonstimulated regions of the pyramidal cell layer or the dentate. No change was seen in the levels of NGF mRNA at the time point examined. These results suggest that relatively normal levels of activity may regulate region-specific neurotrophin levels in the hippocampus. Given that known effects of NGF (and presumably of BDNF and NT-3) include elevation of neurotransmitter levels, elevation of sodium channels, and promotion of axonal terminal sprouting, activity-associated changes in neurotrophin levels may play a role in regulating neural connections in the adult as well as the developing nervous system.
Patterson S L; Grover L M; Schwartzkroin P A; Bothwell M
Neuron
1992
1992-12
Journal Article
<a href="http://doi.org/10.1016/0896-6273(92)90067-n" target="_blank" rel="noreferrer noopener">10.1016/0896-6273(92)90067-n</a>
Potential Side Effects and Adverse Events of Antipsychotic Use for Residents With Dementia in Assisted Living: Implications for Prescribers, Staff, and Families.
dementia; Alzheimer's disease; family; SYMPTOMS; medication; Alzheimer’s disease; assisted living; ALZHEIMERS-DISEASE; BENEFITS; CARE; INVOLVEMENT; MEDICATIONS; MORTALITY; NURSING-HOME RESIDENTS; PREVALENCE; RISK
Antipsychotic medications are frequently prescribed to assisted living (AL) residents who have dementia, although there is a lack of information about the potential side effects and adverse events of these medications among this population. Oversight and monitoring by family members is an important component of AL care, and it is important to understand family awareness of antipsychotic use and reports of potential side effects and adverse events. This cross-sectional, descriptive study of family members of 283 residents with dementia receiving antipsychotic medications in 91 AL communities found high rates (93%) of symptoms that could be potential side effects and a 6% rate of potential adverse events. The majority of families were aware their relative was taking an antipsychotic. Findings suggest that obtaining family perspectives of potential side effects and adverse events related to medication use may contribute to overall improvement in the safety of AL residents living with dementia.
Beeber AS; Zimmerman S; Wretman CJ; Palmertree S; Patel K; Sloane PD
Journal Of Applied Gerontology : The Official Journal Of The Southern Gerontological Society
2021
2021-06-23
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
journalArticle
<a href="http://doi.org/10.1177/07334648211023678" target="_blank" rel="noreferrer noopener">10.1177/07334648211023678</a>
STRESSORS AND WELL-BEING AMONG CAREGIVERS TO OLDER ADULTS WITH DEMENTIA - THE IN-HOME VERSUS NURSING-HOME EXPERIENCE
alzheimers-disease; burden; care; caregiving stress; family caregiving; family member; Geriatrics & Gerontology; hassles; institutionalization; long-term care; nursing-homes; predictors; scale
Stephens M A P; Kinney J M; Ogrocki P K
Gerontologist
1991
1991-04
Journal Article
<a href="http://doi.org/10.1093/geront/31.2.217" target="_blank" rel="noreferrer noopener">10.1093/geront/31.2.217</a>
The Effects Of Intranasal Infusion Of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (mptp) Upon Catecholamine Concentrations Within Olfactory Bulbs And Corpus Striatum Of Male Mice
adult-rat; alzheimers-disease; brain; dopamine; epithelium; locus coeruleus; locus coeruleus; mouse; Neurosciences & Neurology; neurotoxicity; nigrostriatal; norepinephrine; parkinsons-disease; toxicity; transport; transporter; uptake
Dluzen D E; Kefalas G
Brain Research
1996
1996-11
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1016/s0006-8993(96)00934-1" target="_blank" rel="noreferrer noopener">10.1016/s0006-8993(96)00934-1</a>
Voltage-gated Calcium Channels Provide An Alternate Route For Iron Uptake In Neuronal Cell Cultures
alzheimer-disease; alzheimers-disease; Biochemistry & Molecular Biology; fpl-64176; iron-overload toxicity; metabolism; mouse-brain; nerve growth-factor; neuroblastoma-cells; neurodegeneration; Neurosciences & Neurology; nimodipine; parkinsons-disease; parkinsons-disease; redox-active iron; substantia nigra; transferrin receptor; voltage-gated calcium channels
Gaasch J A; Geldenhuys W J; Lockman P R; Allen D D; Van der Schyf C J
Neurochemical Research
2007
2007-10
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1007/s11064-007-9313-1" target="_blank" rel="noreferrer noopener">10.1007/s11064-007-9313-1</a>
Why should we use multifunctional neuroprotective and neurorestorative drugs for Parkinson's disease?
A(2A) receptor antagonists; adenosine; alzheimers-disease; amyloid precursor protein; antagonist; bcl-2 family-members; designed multiple ligands; double-blind; dual mechanism; iron chelation; ladostigil; M30; mao-b; monoamine-oxidase-b; neurodegenerative diseases; Neurosciences & Neurology; nmda receptor; rasagiline; tea polyphenol (-)-epigallocatechin-3-gallate
Parkinson's disease (PD) is a severe neurodegenerative disorder, with no available drugs able to prevent the neuronal cell loss characteristic in brains of patients suffering from PD. Due to the complex cascade of molecular events involved in the etiology of PD, an innovative approach towards neuroprotection or neurorescue may entail the use of multifunctional pharmaceuticals that target an array of pathological pathways, each of which is believed to contribute to events that ultimately lead to neuronal cell death. Here we discuss examples of novel multifunctional ligands that may have potential as neuroprotective and neurorestorative therapeutics in PD. The compounds discussed originate from synthetic chemistry as well as from natural sources where various moieties, identified in research to possess neuroprotective and neurorestorative properties, have been introduced into the structures of several monomodal drugs, some of which are used in the clinic. (C) 2007 Elsevier B.V. All rights reserved.
Youdim M B H; Geldenhuys W J; Van der Schyf C J
Parkinsonism & Related Disorders
2007
2007
Journal Article
<a href="http://doi.org/10.1016/s1353-8020(08)70017-8" target="_blank" rel="noreferrer noopener">10.1016/s1353-8020(08)70017-8</a>