vMRI tail (Segura 2018 cortical thickness), Aβ NPT brain/CSF, dual-syndrome hypothesis (fronto-striatal vs cholinergic posterior), Imaging (Aβ in PD / Forrencys 2018 / Florencys 2016 postmortem), sMRI Definition (SBM / VBM / SbM / DBM), Lewy Body score (composite / clinical / SCORE / Table FC), Pathology section (Hall 2014 postmortem)

(Segura 2018 #2885) Cross sectional - Correlation when displaying the whole PD group indicating that a decrease of MOCA score correlates with an increased rate of cortical thinning (Fig 2 - 근데 whole brain cortical thinning 과의 correlation 분석 없네). Further these correlations were shown to be driven by the group with Parkinson’s disease with MCI. Significant clusters were revealed in the temporal lobe bilaterally, the right occipital medial lobe and the left postcentral gyrus.

	Method
Cortical thickness	(Segura, 2018 #2885)	Method (Global average thickness for both hemispheres was as well as mean lateral ventricular volumes, as well as mean lateral ventricular volume and estimated total intracranial volume (eTIV))
Aβ, NFT	Brain	(Lin, 2015 #835): up to 50% of patients with PDD may exhibit co-incident AD on postmortem studies. (44, 47, 49, 53, 56) (Lin, 2015 #835): plasma Aβ (1-42) (1-40) is consistent across many studies)
	CSF	this reduction is consistent across many studies)

In PD, a typical cortical GM atrophy pattern has not yet been conclusively established. Probably the most consistent finding of vMRI studies is frontal atrophy in PD.

(dual-syndrome hypothesis)

• fronto-striatal (dopaminergically modulated) executive dysfunction, which may not herald the progression of serious cognitive decline, and
• a dementia syndrome characterized by cholinergically mediated memory and visuospatial deficits associated with posterior cortical and temporal lobe dysfunction (38, 39).

Imaging

Aβ in PD	Early PD	LATE PD
Imaging	(Forrencys, 2018 #924): 21% show Aβ activity in several neocortical and subcortical regions (using Aβ path) which is in the same range as control Aβ and equivocal control population, suggesting that PD path itself does not confer a specific risk of increased amyloid metabolic patterns. (Mata patients) show MoCA (24.86 vs 27.21), p (no AD) = 27.61 vs 27.61, MoCA-1.0% vs 8.5%; poble, indicating presence of AD in the range expected for AD (33).
postmortem	(Florencys, 2016 #92621): up to half of patients with PD or dementia with Lewy bodies may show at death sufficient amyloid pathology to support a diagnosis of concurrent Alzheimer's disease (AD) (33).

sMRI

	Definition
(surface based) Cortical thickness	As compared to VBM, CT is more sensitive to cortex changes, possibly because it is less depending on the unfolding and the overall brain size [22, 24] and may better discriminate cortical morphological differences in micro to age- or disease-related regional GM changes than VBM [22, 36]. — the width of gray matter of the surface, the distance in millimeters between white (inner) and pial (outer) surfaces, is between WM (inner) and CSF (outer) (Dahlke, 2013 #2692) More than 99% of the surface is between 1 and 4.5 mm thick. (Smith, 2008) GM is the location of the neuron bodies, but the extent of cortical thickness seems to be related to synaptic density, synaptic pruning and intracranial myelination [2,3,4,5], rather than the number of neurons [5, 6]. T1-weighted MRI of the brain is sufficient to compute cortical thickness in an automated procedure and can be further optimized with additional T2-weighted images [7, 8]. Common algorithms to calculate cortical thickness are publicly available; e.g. under the open-source software package FreeSurfer [9].
(volume-based) Volume based morphometry (VBM)
Source-based morphometry (SbM)	is a multivariate method that makes it possible to identify spatially independent sources of local GM variability that share the same covariance across subjects [25, 26]. The method can identify the patterns (components) of GM alterations and reduces the problem of multiple testing.
Deformation-based morphometry (DBM)	is based on the application of non-linear registration for spatial normalization [27]. The resulting deformation fields provide information about the structural difference between the analyzed brain and the template brain. DBM may be more sensitive to subcortical atrophy than other methods [28], (DBM)

Lewy Body score

cl Composite score	Clinical score II
	10 yes-or-no questions: a focusing motor symptoms (slow movement, rigidity or stiffness, balance problems with or without falls, and a resting tremor) and 6 covering nonmotor symptoms (excessive daytime sleepiness, episodes of illogical thinking, frequent staring spells, visual hallucinations, acting out dreams, and orthostatic hypotension)
SCORE	Pathologic score II Table 18 Guidelines for evaluation of Lewy body distribution and frequency Cortical Lewy body frequency Assessment is on a semiquantitative scale. In each region, the total number of LB in the designated zones are counted in either H&E or alpha-synuclein immunostained sections with assessment per high-power field. To distinguish 2-3 and 4-globus neocortical neighbors: The numerical score is assessed as follows: Cortical scores for LB assessment are defined as follows. 1. None or rare: The actual scores of the selected genes from the base of the surface in the most extensive 1µ of the section. 2. Cingulate: The whole gyrus. 3. Transtentorial: The cortical ribbon from the depth to the surface of the collateral sulcus Tissue blocks should be selected such that the section is not sectioned tangentially. Table FC. Guidelines for diagnostic ranking criteria Lewy body scores were regionally defined categories Lewy body scores per individual zones are summarized to give a final score and pertinent distribution as follows. Category Transtentorial Cingulate Temporal Frontal Parietal Total Lewy Score-1: 7-Y6 67% 7.5 ; 11.0 neocortical type 카지로, P피2-도 Y6, P, HP type, Y6 distinct region — 18 distinct region continuum (Y가 도 Y가 표시되어 다음. 1 contains 도 (Y가 도 Y가 표시되어 다음. 11.0 transtentorial type / Y6 counter, 11.0 distinct region Source: higher than 1 by any neocortical area generally indicates neocortical disease.

Pathology

			PDD	PDND (PD without dementia)
(Hall, 2014 #2803)	postmortem	N	109	46
		LB score	6.0
		type	neocortical LB pathology was the most important substrate of dementia, confirms the cortical alpha-synopathy as the main pathological substrate of PDD
(Cui, 2012 #?)	postmortem	92 LB measurement (n was 82)	48 (LB measurement n was 39) CL/B/LN pathology is the most consistent correlate of dementia (Severity of CL (CL/B/LN pathology was positively associated with dementia (p = 0.001), with an odds ratio (OR) of 4.06. Left figure: (values in nasal table?) Global Cortical LB/LN (semiquantitative score), PDD: 1.07 (1.07, 2.35) vs PDND: 0.62 (0.47, 1.47). N = 39 (median (IQR)). PDD 가 41.7% 가 PDND (full normalization). PDND 1 50% 만 20.3 자 70%.

demonstrate significant NBM atrophy and cortical cholinergic binding reductions, respectively in patients with PDD compared to both cognitively intact PD patients and control subjects (Hanyu et al., 2002; Hilker et al., 2005; Bohnen et al., 2006; Shimada et al., 2009; Choi et al., 2012). loss of neurons in the nucleus basalis of Meynert leading to cortical cholinergic denervation [9, 171, 186]

Table 3 Pathological correlates of dementia in Parkinson’s disease

| | Controls | Parkinson’s disease | Parkinson’s disease |

Uncertain Spans

location	transcription	uncertainty
Aβ NFT / CSF cell	consistent across many studies)	trailing parenthesis closes a clipped clause; preserved verbatim.
Imaging / Forrencys 2018	MoCA (24.86 vs 27.21), p (no AD) = 27.61 vs 27.61	reads as written; the duplicated 27.61 vs 27.61 may be an OCR artefact; preserved verbatim.
Lewy body score / SCORE row	Lewy Score-1: 7-Y6 67% 7.5 ; 11.0 neocortical type 카지로, P피2-도 Y6, P, HP type, Y6 distinct region — 18 distinct region	mixed Korean / English narrative with OCR artefacts; preserved verbatim.