Parkinson’s disease (PD) involves the progressive loss of dopaminergic neurons, particularly in the substantia nigra. This neurodegeneration is linked to the abnormal accumulation of α-synuclein, a protein that forms toxic aggregates and spreads between cells, damaging them. At the 20th International Conference on Alzheimer’s and Parkinson’s Diseases (AD/PD), held from March 17 to 21, 2026, in Copenhagen, several strategies were presented that aim to modify the course of the disease and offer real alternatives to purely symptomatic treatments.

Neurodegenerative disease and cognitive decline cannot be explained by a single process. Beta-amyloid plaques, hyperphosphorylated tau, alpha-synuclein, activated microglia and astrocytes, altered receptors such as TREM2, mitochondrial dysfunction, epigenetic changes and cerebrovascular alterations all seem to contribute to the development of dementia in Alzheimer’s disease (AD). While scientists attempt to address each of these elements, prevention is growing as a primary goal.

Entering a cell and watching its entire inner machinery at work, how DNA is copied, how proteins are assembled, or how it splits in two, has been, for decades, an impossible dream. Now, scientists at the University of Illinois have recreated everything that happens inside a cell at molecular scale in an unprecedented computational model. Syn3A is the first 4D digital cell, capable of combining time and space to simultaneously represent all the internal processes that drive the life cycle of a minimal prokaryotic organism.

A therapeutic strategy based on alternative splicing of the MECP2 gene could restore protein levels in Rett syndrome, a neurological disorder caused by mutations in that gene. Scientists at Baylor College of Medicine have successfully tested this approach both in vitro in neurons from Rett patients that produce some functional protein, correcting the altered gene expression and improving neuronal functions, and in vivo in mice.

Computational pathology, which assesses molecular-level features of diseases directly from tissue images (rather than testing the tissue via methods such as staining or sequencing) is making rapid strides.

CAR T cells have been groundbreaking for the treatment of B-cell cancers. But 8 years after Kymriah (tisagenlecleucel, Novartis AG) became the first CAR T-cell therapy to be approved, there are no CAR Ts approved for solid tumors.

The massive cuts to science, global health, and HIV programs that unfolded in 2025 triggered a crisis with worldwide repercussions. The dissolution of USAID, the shutdown of PEPFAR, and the suspension of thousands of NIH research projects led to an immediate collapse of essential services, from HIV prevention to access to treatment. At the 33rd Conference on Retroviruses and Opportunistic Infections (CROI) held Feb. 22-25, 2026, in Denver, scientists, activists, and health professionals presented data illustrating the scale of the damage and warned of a historic setback in the global HIV response.

The effects of aging pose an additional challenge for people with HIV due to the neurological and psychological consequences that persist despite antiretroviral therapy. At the Conference on Retroviruses and Opportunistic Infections (CROI) held Feb. 22-25, 2026, in Denver, the scientific community examined how the virus affects the brain, how the reservoir is established in the CNS, and which genetic, immunological or treatment-related factors influence cognitive health.

Antiretroviral therapies against HIV have been in use for more than 30 years and have enabled people living with HIV to maintain undetectable viral levels. Many of them are aging in good health. However, others present symptoms of cognitive decline. HIV can reach the brain and establish a reservoir there. Yet, it is still unknown what this reservoir is like, which cells are affected, and which comorbidities are typical of aging or are associated with the virus.

The variety of organoids that can be developed in vitro is enabling major advances. Depending on the type of tissues and the research goals, these small 3D cell-based structures that mimic real tissue offer certain advantages over animal models. Scientists at the University of Padova in Italy have created human neuromuscular organoids to reproduce cancer-induced muscle cachexia, a condition that murine models do not accurately replicate.