Motor neuron disease is a neurodegenerative disease characterized by loss of upper motor neuron in the motor cortex and lower motor neurons in the brain stem and spinal cord. Death occurs 2&#x2013;4 years after the onset of the disease. A complex interplay of cellular processes such as mitochondrial dysfunction, oxidative stress, excitotoxicity, and impaired axonal transport are proposed pathogenetic processes underlying neuronal cell loss. Currently evidence exists for the use of riluzole as a disease modifying drug; multidisciplinary team care approach to patient management; noninvasive ventilation for respiratory management; botulinum toxin B for sialorrhoea treatment; palliative care throughout the course of the disease; and Modafinil use for fatigue treatment. Further research is needed in management of dysphagia, bronchial secretion, pseudobulbar affect, spasticity, cramps, insomnia, cognitive impairment, and communication in motor neuron disease.

U. E. Williams

E. E. Philip-Ephraim

S. K. Oparah

Multidisciplinary Interventions in Motor Neuron Disease

In this study we evaluated the time dependence in cadmium-nicotine interaction and its effect on motor function, anxiety linked behavioural changes, serum electrolytes, and weight after acute and chronic treatment in adult male mice. Animals were separated randomly into four groups of n = 6 animals each. Treatment was done with nicotine, cadmium, or nicotine-cadmium for 21 days. A fourth group received normal saline for the same duration (control). Average weight was determined at 7-day interval for the acute (D1-D7) and chronic (D7-D21) treatment phases. Similarly, the behavioural tests for exploratory motor function (open field test) and anxiety were evaluated. Serum electrolytes were measured after the chronic phase. Nicotine, cadmium, and nicotine-cadmium treatments caused no significant change in body weight after the acute phase while cadmium-nicotine and cadmium caused a decline in weight after the chronic phase. This suggests the role of cadmium in the weight loss observed in tobacco smoke users. Both nicotine and cadmium raised serum Ca2+ concentration and had no significant effect on K+ ion when compared with the control. In addition, nicotine-cadmium treatment increased bioaccumulation of Cd2+ in the serum which corresponded to a decrease in body weight, motor function, and an increase in anxiety.

Duyilemi Chris Ajonijebu

Philip Adeyemi Adeniyi

Adeshina Oloruntoba Adekeye

Babawale Peter Olatunji

Azeez Olakunle Ishola

Olalekan Michael Ogundele

Nicotine-Cadmium Interaction Alters Exploratory Motor Function and Increased Anxiety in Adult Male Mice

Ashima Nehra

Sakshi Chopra

Harsimarpreet Kaur

Comment on &#x201c;Prevalence and Cognitive Bases of Subjective Memory Complaints in Older Adults: Evidence from a Community Sample&#x201d;

Previous studies have shown that glial cell line-derived neurotrophic factor (GDNF) family ligands (GFL) are potent survival factors for dopaminergic neurons and motoneurons with therapeutic potential for Parkinson&#x2019;s disease. However, little is known about direct influences of the GFL on microglia function, which are known to express part of the GDNF receptor system. Using RT-PCR and immunohistochemistrym we investigated the expression of the GDNF family receptor alpha 1 (GFR alpha) and the coreceptor transmembrane receptor tyrosine kinase (RET) in rat microglia in vitro as well as the effect of GFL on the expression of proinflammatory molecules in LPS activated microglia. We could show that GFL are able to regulate microglia functions and suggest that part of the well known neuroprotective action may be related to the suppression of microglial activation. We further elucidated the functional significance and pathophysiological implications of these findings and demonstrate that microglia are target cells of members of the GFL (GDNF and the structurally related neurotrophic factors neurturin (NRTN), artemin (ARTN), and persephin (PSPN)).

Uta Rickert

Steffen Grampp

Henrik Wilms

Jessica Spreu

Friederike Knerlich-Lukoschus

Janka Held-Feindt

Ralph Lucius

Glial Cell Line-Derived Neurotrophic Factor Family Members Reduce Microglial Activation via Inhibiting p38MAPKs-Mediated Inflammatory Responses

Objectives. To estimate the prevalence of subjective memory complaints (SMCs) in a sample of community-dwelling, older adults and to examine cognitive bases of these complaints. Participants. 499 community-dwelling adults, 65 and older. Measurements. A telephone survey consisting of cognitive tests and clinical and sociodemographic variables. SMCs were based on subjects' evaluations and subjects' perceptions of others' evaluations. Analysis. Logistic regression was used to model the risk for SMCs as a function of the cognitive, clinical, and sociodemographic variables. We tested for interactions of the cognitive variables with age, education, and gender. Results. 27.1&#x25; reported memory complaints. Among the younger age, better objective memory performance predicted lower risk for SMCs, while among the older age, better memory had no effect on risk. Among the better-educated people, better global cognitive functioning predicted lower risk for SMCs, while among the less-educated people, better global cognitive functioning had no effect on SMC risk. When predicting others' perceptions, better objective memory was associated with lower risk for SMCs. Conclusion. Objective memory performance and global cognitive functioning are associated with lower risk for SMCs, but these relationships are the strongest for the younger age and those with more education, respectively. Age and education may affect the ability to accurately appraise cognitive functioning.

Thomas Fritsch

McKee J. McClendon

Maggie S. Wallendal

Trevor F. Hyde

Janet D. Larsen

Prevalence and Cognitive Bases of Subjective Memory Complaints in Older Adults: Evidence from a Community Sample

The objective is to examine the risk of dementia in subjects with essential tremor (ET) involved in the Arizona Study of Aging and Neurodegenerative Disorders. All subjects were free of a neurodegenerative diagnosis at baseline and had annual motor, general neurological, and neuropsychological assessments. Subjects with ET were compared with controls for the risk of dementia. There were 83 subjects with ET and 424 subjects without tremor. Mean age at study entry was <svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-1.09097pt;width:54.174999px;" id="M1" height="11.2875" version="1.1" viewBox="0 0 54.174999 11.2875" width="54.174999">
	
		
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</svg> for ET and <svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-1.09097pt;width:54.174999px;" id="M2" height="11.4" version="1.1" viewBox="0 0 54.174999 11.4" width="54.174999">
	
		
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</svg> for controls. Median tremor duration was 5.2 years at study entry. Followup was a median of 5.4 years (range 0.9 to 12.1). The hazard ratio for the association between ET and dementia was 0.79 (95% CI 0.33 to 1.85). The hazard ratio for the association between tremor onset at age 65 or over, versus onset before age 65, was 2.1 (95% CI 0.24 to 18) and the hazard ratio for the association between tremor duration greater than 5 years, versus less than 5 years, was 0.46 (95% CI 0.08 to 2.6). We conclude that all elderly ET was not associated with an increased risk of dementia but that a subset of subjects with older age onset/shorter duration tremor may be at higher risk.

Holly A. Shill

Joseph G. Hentz

Sandra A. Jacobson

Christine Belden

Marwan N. Sabbagh

Thomas G. Beach

Erika Driver-Dunckley

Charles H. Adler

Essential Tremor in the Elderly and Risk for Dementia

NMDA and AMPA-type glutamate receptors and their bound membrane-associated guanylate kinases (MAGUKs) are critical for synapse development and plasticity. We hypothesised that these proteins may play a role in the changes in synapse function that occur in Huntington&#x2019;s disease (HD) and Parkinson&#x2019;s disease (PD). We performed immunohistochemical analysis of human postmortem brain tissue to examine changes in the expression of SAP97, PSD-95, GluA2 and GluN1 in human control, and HD- and PD-affected hippocampus and striatum. Significant increases in SAP97 and PSD-95 were observed in the HD and PD hippocampus, and PSD95 was downregulated in HD striatum. We observed a significant increase in GluN1 in the HD hippocampus and a decrease in GluA2 in HD and PD striatum. Parallel immunohistochemistry experiments in the YAC128 mouse model of HD showed no change in the expression levels of these synaptic proteins. Our human data show that major but different changes occur in glutamatergic proteins in HD versus PD human brains. Moreover, the changes in human HD brains differ from those occurring in the YAC128 HD mouse model, suggesting that unique changes occur at a subcellular level in the HD human hippocampus.

C. Fourie

E. Kim

H. Waldvogel

J. M. Wong

A. McGregor

R. L. M. Faull

J. M. Montgomery

Differential Changes in Postsynaptic Density Proteins in Postmortem Huntington&#x2019;s Disease and Parkinson&#x2019;s Disease Human Brains

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Journal of Neurodegenerative Diseases