美國賓利法尼亞大學(xué)的Daniel Weintraub博士近日在《神經(jīng)學(xué)文獻(xiàn)》（Archives of Neurology）上發(fā)表論文稱，帕金森病患者的腦萎縮與其認(rèn)知能力下降有關(guān),。
在對84名帕金森病患者進(jìn)行研究后發(fā)現(xiàn),，認(rèn)知能力正常的患者其大腦體積與健康者相近；而同認(rèn)知能力正常的患者相比,，有輕度認(rèn)知障礙者其大腦海馬區(qū)顯著萎縮（P=0.001）,，而癡呆水平和認(rèn)知障礙與海馬區(qū)（P=0.004）和內(nèi)側(cè)額葉（P=0.003）的萎縮有相關(guān)性。
輕度認(rèn)知障礙的帕金森病患者呈現(xiàn)出一種與認(rèn)知正常的患者顯著不同的腦萎縮,，而與有嚴(yán)重認(rèn)知障礙的患者相似,。
帕金森病患者發(fā)生癡呆的累積發(fā)病率可高達(dá)80%，還有25%未發(fā)生癡呆的患者可達(dá)到輕度認(rèn)知障礙的標(biāo)準(zhǔn),。而對帕金森性癡呆的生物標(biāo)記研究發(fā)現(xiàn),，癡呆者最易發(fā)生萎縮的部位為頂顳葉和額葉前部皮質(zhì)。
該研究的參與者包括84名帕金森病患者和23名正常人,，分別對其進(jìn)行MRI檢查和神經(jīng)心理測試,。
癡呆量表2測試發(fā)現(xiàn)，61名帕金森病患者認(rèn)知功能正常,，12名有輕度認(rèn)知障礙,，11名有癡呆,。霍普金斯語言學(xué)習(xí)能力測試發(fā)現(xiàn)認(rèn)知功能正常的患者與輕度認(rèn)知障礙者和癡呆者有顯著差異,，癡呆者的認(rèn)知語言學(xué)習(xí)能力得分最低,。
MRI結(jié)果顯示，同認(rèn)知功能正常者相比,，癡呆和輕度認(rèn)知障礙的帕金森病患者大腦海馬區(qū)顯著萎縮,，而癡呆者和輕度認(rèn)知障礙者無顯著差異。癡呆者與認(rèn)知功能正常者相比,，其內(nèi)側(cè)顳葉顯著萎縮,。（生物谷bioon.com）
doi:10.1001/archneurol.2011.725
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Neurodegeneration Across Stages of Cognitive Decline in Parkinson Disease
Daniel Weintraub, MD; Jimit Doshi, MS; Deepthi Koka, MS; Christos Davatzikos, PhD; Andrew D. Siderowf, MD, MSCE; John E. Duda, MD; David A. Wolk, MD;Paul J. Moberg, PhD; Sharon X. Xie, PhD; Christopher M. Clark, MD.
Objective To assess regions and patterns of brain atrophy in patients with Parkinson disease (PD) with normal cognition (PD-NC), mild cognitive impairment (PD-MCI), and dementia-level cognitive deficits (PDD).
Design Images were quantified using a region-of-interest approach and voxel-based morphometry analysis. We used a high-dimensional pattern classification approach to delineate brain regions that collectively formed the Spatial Pattern of Abnormalities for Recognition of PDD.
Setting The Parkinson's Disease and Movement Disorders Center at the University of Pennsylvania.
Subjects Eighty-four PD patients (61 PD-NC, 12 PD-MCI, and 11 PDD) and 23 healthy control subjects (HCs) underwent magnetic resonance imaging of the brain.
Results The PD-NC patients did not demonstrate significant brain atrophy compared with HCs. Compared with PD-NC patients, PD-MCI patients had hippocampal atrophy (β = -0.37; P = .001), and PDD patients demonstrated hippocampal (β = -0.32; P = .004) and additional medial temporal lobe atrophy (β = -0.36;P = .003). The PD-MCI patients had a different pattern of atrophy compared with PD-NC patients (P = .04) and a similar pattern to that of PDD patients (P = .81), characterized by hippocampal, prefrontal cortex gray and white matter, occipital lobe gray and white matter, and parietal lobe white matter atrophy. In nondemented PD patients, there was a correlation between memory-encoding performance and hippocampal volume.
Conclusions Hippocampal atrophy is a biomarker of initial cognitive decline in PD, including impaired memory encoding and storage, suggesting heterogeneity in the neural substrate of memory impairment. Use of a pattern classification approach may allow identification of diffuse regions of cortical gray and white matter atrophy early in the course of cognitive decline.
