Reduced striatal tyrosine hydroxylase in incidental Lewy body disease

Abstract

Incidental Lewy body disease (ILBD) is the term used when Lewy bodies are found in the nervous system of subjects without clinically documented parkinsonism or dementia. The prevalence of ILBD in the elderly population has been estimated at between 3.8 and 30%, depending on subject age and anatomical site of sampling. It has been speculated that ILBD represents the preclinical stage of Parkinson's disease (PD) and/or dementia with Lewy bodies (DLB). Studies of ILBD could potentially identify early diagnostic signs of these disorders. At present, however, it is impossible to know whether ILBD is a precursor to PD or DLB or is just a benign finding of normal aging. We hypothesized that, if ILBD represents an early stage of PD or DLB, it should be associated with depletion of striatal dopaminergic markers. Eleven subjects with ILBD and 27 control subjects were studied. The ILBD subjects ranged in age from 74 to 96 years (mean 86.5) while the control subjects' age ranged from 75 to 102 years (mean 86.7). Controls and subjects did not differ in terms of age,

Prevalence of Submandibular Gland Synucleinopathy in Parkinson’s Disease, Dementia with Lewy Bodies and other Lewy Body Disorders

“…All subjects with Lewy body disorders must pass through an ILBD phase, however. Despite the apparently low conversion of ILBD to PD or DLB, it would appear that ILBD is not a completely benign condition, as it is associated with an approximately 50% decrease in striatal dopaminergic markers as well as the clinical biomarker of hyposmia [60–63]. …”

Original article Nigrostriatal pathway degeneration in rats after intraperitoneal administration of proteasome inhibitor MG-132

“…The results of other studies showed that motor signs of PD manifest after the loss of approximately 50% of nigral neurons and 80% of striatal dopamine [4,47]. Two postmortem studies using more rigorous quantitative methods, such as using a tessellation method [17] and dissector-based neuromorphometry [27], found that about 30% of nigral neuronal loss appeared sufficient to cause motor symptoms in PD [2]. However, recent research suggests that the first symptoms of Parkinson's disease may manifest after just a 20% decrease in the number of dopaminergic neurons SNc, which has been shown in animal models where a reduction of about 14 to 23% of nigral neuron count or 14% to 37% of striatal dopamine was sufficient to induce mild parkinsonism [43].…”

When does Parkinson's disease begin?

“…2,45 Recent studies have also shown that iLB cases have reduced striatal dopaminergic immunoreactive markers compared with controls, although not as reduced as in PD. [46][47][48] However, while the prevalence of PD is 1% among those older than 60 years, 49 post-mortem studies have shown that 8-14% of subjects older than 60 years without PD or dementia present iLB in the brainstem nuclei. 43,45,50,51 This 10-time higher frequency of iLB compared with the prevalence of PD may not fit with the concept that iLB cases represent a precursor of the motor stage of PD.…”