People are twice as likely to inherit their lifespan as previously thought, new research suggests.

The genetic contribution to how long a person lives is around 50 per cent, based on health databases in Denmark and Sweden. This reflects heritability, the share of lifespan differences due to genes.

For decades, many scientists believed genes and ancestry accounted for between about 10 and 25 per cent of longevity.

The research was led by scientists at the Weizmann Institute in Israel, with the Karolinska Institute in Sweden and Leiden University.

The earlier underestimates arose from limited historic health and mortality data, where deaths due to war, infectious disease, risky or unsafe work, accidents, poor diet and lack of medical care were hard to separate in records.

“For many years, human lifespan was thought to be shaped almost entirely by non-genetic factors, which led to considerable scepticism about the role of genetics in ageing and about the feasibility of identifying genetic determinants of longevity,” said Ben Shenhar of the Weizmann Institute.

Environmental forces such as disease or living conditions can mask or confound potential genetic effects.

Hereditary causes of death, for those not killed first by external causes, mean “processes originating within the body, including genetic mutations, age-related diseases and the decline of physiological function with age.” the researchers said.

“If heritability is high, as we have shown, this creates an incentive to search for gene variants that extend lifespan, in order to understand the biology of ageing and, potentially, to address it therapeutically.” said Shenhar.

Other recent research has pointed to a potential role for taurine, an amino acid, in slowing the ageing process.

Scientists have also highlighted the bowhead whale’s 200-year lifespan, attributed to a cellular protein that may protect against carcinogenic mutations.

Limiting the PTP1B enzyme could slow memory loss in Alzheimer’s, pointing to a potential treatment route, new research suggests.

The enzyme appears to contribute to memory decline in mice by altering how the brain’s immune cells behave, researchers say.

Dialling down PTP1B let microglia clear the protein clumps linked to Alzheimer’s, known as amyloid-beta plaques. Microglia are the brain’s resident immune cells that remove waste.

The study was conducted at Cold Spring Harbor Laboratory, a non-profit in New York, where professor Nicholas Tonks has examined the enzyme since discovering PTP1B in 1988.

Microglia normally sweep up waste in the brain but become less effective as Alzheimer’s, which slowly damages memory and thinking, advances.

The research suggests that PTP1B interacts with spleen tyrosine kinase (SYK), which helps control how microglia respond to damage and remove amyloid-beta.

“Over the course of the disease, these cells become exhausted and less effective,” said Yuxin Cen, the study lead.

“Our results suggest that PTP1B inhibition can improve microglial function, clearing up Aβ plaques,” Cen added.

PTP1B is already known to play a role in metabolic conditions such as obesity and type 2 diabetes, both recognised risk factors for Alzheimer’s disease.

The laboratory is now working to develop PTP1B inhibitors for multiple applications.

For Alzheimer’s disease, Tonks envisages a combination of therapies pairing existing approved drugs with PTP1B inhibitors.

According to the World Health Organisation, cholinesterase inhibitors such as donepezil are currently used to treat Alzheimer’s disease, while NMDA receptor antagonists such as memantine are prescribed for more advanced stages.

“The goal is to slow Alzheimer’s progression and improve the quality of life of the patients,” said Tonks.

More than 55 million people live with dementia globally, with Alzheimer’s disease accounting for up to 70 per cent of cases, according to the WHO.

“It’s a slow bereavement,” said Tonks, whose mother lived with Alzheimer’s.

“You lose the person piece by piece.”