Plastic changes in the primary somatosensory cortex resulting from degenerate to the nucleus basalis of Meynert and verification of the effectiveness of excercise

2023 Fiscal Year Final Research Report

• Project/Area Number: 21K17497
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 59010:Rehabilitation science-related
• Research Institution: Tsukuba International University
• Principal Investigator: Dezawa Shinnosuke つくば国際大学, 医療保健学部, 助手(移行) (60899699)
• Project Period (FY): 2021-04-01 – 2024-03-31
• Keywords: マイネルト基底核 / アセチルコリン / 感覚過敏

Outline of Final Research Achievements

In Parkinson's disease (PD) and Alzheimer's disease (AD), it is known that pain symptoms can occur in association with the conditions. However, the detailed causes are not yet fully understood. Therefore, in this study, we targeted the basal ganglia and substantia nigra, which are deeply implicated in the onset of PD and AD, and measured pain behaviors and abnormal neural activity resulting from their degeneration using rats. As a result, similar pain behaviors were observed in both degenerated animals, with excessive sensory responses found in the primary somatosensory cortex underlying these behaviors. This abnormal neural activity was temporarily reduced by tDCS, suggesting transient alleviation of pain behaviors.

Free Research Field

神経科学

Academic Significance and Societal Importance of the Research Achievements

パーキンソン病（PD）やアルツハイマー病（AD）に付随して生じる異常な痛みは、詳細な原因が未解明であり、有効な治療法が確立されていない。本研究では、両疾患に深く関わるアセチルコリンやドパミンを脳内に放出する神経核の変性が、感覚野における過剰な神経応答や痛みの発症を招くことを明らかにした。さらにtDCSにより感覚応答を抑制することで、痛み行動が一時的に軽減することも示された。これらの結果は、PDやADにおける痛み発症メカニズムの一端を明らかにするとともに、治療戦略開発のための一助となる可能性を有している。