Protein misfolding can cause loss of function and lead to diseases such as Alzheimer's and Parkinson's.

Judge against the scientific consensus as of 2025-11-25. True: authoritative biomedical sources (reviews, textbooks, NIH/NIA material) state that protein misfolding can cause a protein to lose its normal function and that misfolding/aggregation is involved in causing diseases including Alzheimer's (e.g. amyloid-beta, tau) and Parkinson's (e.g. alpha-synuclein). Mostly true: misfolding is accepted as central to both diseases, but the sources say the harm there comes mainly from toxic gain of function or aggregation rather than loss of function. The claim says 'can' and 'like', so it does not have to be the sole mechanism. Mixed: the link is established for only one of the two named diseases. Mostly false: sources describe misfolding in these diseases only as a correlate whose causal role is unproven. False: sources show misfolding has no role in these diseases.

Set before the research began.

1. E1 Alzheimer's Disease Fact Sheet National Institute on Aging (NIH) · 5 April 2023

   “During this very early stage of Alzheimer’s, toxic changes are taking place in the brain, including abnormal buildups of proteins that form amyloid plaques and tau tangles.”

2. E2 Alzheimer's Disease Fact Sheet National Institute on Aging (NIH) · 5 April 2023

   “These plaques and tangles in the brain are still considered some of the main features of Alzheimer’s.”

3. E3 Parkinson's Disease National Institute of Neurological Disorders and Stroke (NIH) · 23 July 2026

   “Damaged brain cells in most people with PD have Lewy bodies, abnormal clumps of a protein called alpha-synuclein. Researchers don’t yet know why Lewy bodies form or how they affect PD.”

4. E4 Parkinson's Disease National Institute of Neurological Disorders and Stroke (NIH) · 23 July 2026

   “This led to the discovery that Lewy bodies in the brains of people with PD contain clumps of abnormal alpha-synuclein.”

NIA describes abnormal buildups of amyloid and tau proteins as toxic changes in early Alzheimer's and as main features of the disease (E1, E2). That links abnormal protein accumulation to Alzheimer's and describes these changes as toxic; the quoted material does not address loss of protein function. For Parkinson's, NINDS says damaged cells contain clumps of abnormal alpha-synuclein but that researchers do not yet know why Lewy bodies form or how they affect PD (E3, E4), so the causal link is not established there. The evidence therefore supports the claim for only one of the two named diseases, and no source states that misfolding causes loss of function.