Parkinson’s disease (PD) is a chronic neurodegenerative disorder with multifactorial etiology. In the past decade, the genetic causes of monogenic forms of familial PD have been defined. However, the etiology and pathogenesis of the majority of sporadic PD cases that occur in outbred populations have yet to be clarified. The recent development of resources such as the International HapMap Project and technological advances in high-throughput genotyping have provided new basis for genetic association studies of common complex diseases, including PD. A new generation of genome-wide association studies will soon offer a potentially powerful approach for mapping causal genes and will likely change treatment and alter our perception of the genetic determinants of PD. However, the execution and analysis of such studies will require great care.

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• Gene Signals and SNPs Associated with Parkinson’s Disease: A Nutrigenomics and Computational Prospective Insights
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  Neuroscience.2023; 533: 77.     CrossRef

Cerebral white matter lesions (CWMLs) have been suggested to be associated with an increased risk of dementia, disability, and death. CWMLs are more common in individuals with Alzheimer’s disease (AD) than in normal elderly individuals of comparable age. Only a few studies have been done to determine whether CWMLs may influence cognitive decline in Parkinson’s disease (PD). Fully developed PD with concurrent AD was reported to likely cause impaired cognition in spite of accumulating evidence suggesting that PD with dementia (PDD) is more closely associated with Lewy body (LB) pathology. Currently, contradictory data on the neuropathology of dementia in PD require further prospective clinicopathological studies in larger cohorts to elucidate the impact of AD and α-synuclein (SCNA) pathologies on the cognitive status in these disorders. Previous reports did not suggest CWMLs to be associated with an increased risk of PDD. After adjusting for age at death, age at onset of PD, and duration of PD, our recent study investigating CWMLs in PDD via autopsy has shown a positive correlation between the burden of CWMLs and PDD. The frequent co-existence of both LB and AD lesions suggests that both pathologies independently or synergistically contribute to both movement disorders and cognitive impairment. The individual and cumulative burden of CWMLs, LB lesions, and AD lesions may synergistically contribute to cognitive decline in LB disorders such as PDD.

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• Cx43 Mediates Resistance against MPP+-Induced Apoptosis in SH-SY5Y Neuroblastoma Cells via Modulating the Mitochondrial Apoptosis Pathway
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  International Journal of Molecular Sciences.2016; 17(11): 1819.     CrossRef
• Gray and White Matter Contributions to Cognitive Frontostriatal Deficits in Non-Demented Parkinson's Disease
  Catherine C. Price, Jared Tanner, Peter T. Nguyen, Nadine A. Schwab, Sandra Mitchell, Elizabeth Slonena, Babette Brumback, Michael S. Okun, Thomas H. Mareci, Dawn Bowers, Stephen D Ginsberg
  PLOS ONE.2016; 11(1): e0147332.     CrossRef
• White Matter Hypoperfusion and Damage in Dementia: Post‐Mortem Assessment
  Seth Love, J Scott Miners
  Brain Pathology.2015; 25(1): 99.     CrossRef

Lewy body pathology (LBP) is the pathological hallmark of Lewy body diseases, such as Parkinson’s disease and Lewy body dementia. Recent studies have shed new light on the role of LBP, the interactions of LBP with concomitant pathologies, and the propagation of LBP from the olfactory bulb and enteric nervous system to the central nervous system. The intrinsic difficulty with identifying clinicopathological correlates could be overcome by improving our understanding of the pathological evolution of LBP.

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• Demencias degenerativas: ¿un dilema de síndromes o de enfermedades?
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• Advances in NURR1-Regulated Neuroinflammation Associated with Parkinson’s Disease
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Lamotrigine (LTG) is associated with a tremor when given in combination with valproic acid; however, a tremor associated with lamotrigine monotherapy is rare. Here, we report a case of positional and action tremor associated with lamotrigine use. Based on the temporal relationship, it is conceivable that lamotrigine increases serotonin transmission or affects basal ganglia dopamine activity, thereby causing the tremor.

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• Antiseizure Drugs and Movement Disorders
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Mood disorders following acute stroke are relatively common. However, restlessness with manic episodes has rarely been reported. Lesions responsible for post-stroke mania can be located in the thalamus, caudate nucleus, and temporal and frontal lobes. We present a patient who exhibited restlessness with manic episodes after an acute infarction in the right parietal lobe, and summarize the case reports involving post-stroke mania. The right parietal stroke causing mania in our case is a novel observation that may help us to understand the mechanisms underlying restlessness with mania following acute stroke.

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• Restlessness with manic episodes induced by right-sided multiple strokes after COVID-19 infection: A case report
  Takahiko Nagamine
  Brain Circulation.2023; 9(2): 112.     CrossRef
• Poststroke Mania During the COVID-19 Pandemic
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  Journal of Nervous & Mental Disease.2023; 211(12): 979.     CrossRef
• Management of psychiatric disorders in patients with stroke and traumatic brain injury
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• Post stroke delirium
  M. A. Savina
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