Annals of medicine and surgery (2012) · 2026
Microvascular damage in diabetic nephropathy and the subsequent risk of Alzheimer's disease: a systematic review.
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Mohammed Noura, Alyazan Khalil Taher Al-Jabali Tho, Yassien Nuha, Osman Abufatima Iman, Omer Ibrahim Ahmed Fatima, El Yazal Soukina, Satti Wehiba, Alalamat Nadine, Aamer Abkar Ibrahim Mohammed, Tirelbar Basma, Paudel Leepy, Abdalla Abdelsadig Mahmoud Islam, Humdi Leama, Ali Hajer, Hammad Jaber Amin Mohammed, Abdelrahman Nadir
Аннотация
INTRODUCTION: Diabetic nephropathy (DN), a major microvascular complication of diabetes, is increasingly implicated in systemic vascular dysfunction and may contribute to the pathogenesis of Alzheimer's disease (AD). Microvascular injury is a recognized mechanism in AD, and DN-related damage may raise the risk of cognitive decline.
METHODS: Following the PRISMA 2020 guidelines, we searched PubMed, Scopus, and the Cochrane Library (2000-2025) for studies on DN-related vascular damage and cognitive outcomes. Quality was assessed using the Newcastle-Ottawa Scale and the AXIS tool.
RESULTS: Of 275 records, nine studies were included (cross-sectional and longitudinal, with up to 37.5 years of follow-up). DN was measured via eGFR, albuminuria, the fibrinogen-to-albumin ratio, or ICD codes; cognition via assessed using amyloid PET, neurocognitive tests, or registry data. All studies found that impaired kidney function was associated with a greater risk of AD or cognitive decline.
CONCLUSION: Available evidence links DN-related microvascular damage to a higher risk of AD, suggesting a kidney-brain axis. However, causality remains uncertain and requires longitudinal and mechanistic studies to clarify these pathways.
METHODS: Following the PRISMA 2020 guidelines, we searched PubMed, Scopus, and the Cochrane Library (2000-2025) for studies on DN-related vascular damage and cognitive outcomes. Quality was assessed using the Newcastle-Ottawa Scale and the AXIS tool.
RESULTS: Of 275 records, nine studies were included (cross-sectional and longitudinal, with up to 37.5 years of follow-up). DN was measured via eGFR, albuminuria, the fibrinogen-to-albumin ratio, or ICD codes; cognition via assessed using amyloid PET, neurocognitive tests, or registry data. All studies found that impaired kidney function was associated with a greater risk of AD or cognitive decline.
CONCLUSION: Available evidence links DN-related microvascular damage to a higher risk of AD, suggesting a kidney-brain axis. However, causality remains uncertain and requires longitudinal and mechanistic studies to clarify these pathways.